One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
A large group of proteins that control APOPTOSIS. This family of proteins includes many ONCOGENE PROTEINS as well as a wide variety of classes of INTRACELLULAR SIGNALING PEPTIDES AND PROTEINS such as CASPASES.
A family of intracellular CYSTEINE ENDOPEPTIDASES that play a role in regulating INFLAMMATION and APOPTOSIS. They specifically cleave peptides at a CYSTEINE amino acid that follows an ASPARTIC ACID residue. Caspases are activated by proteolytic cleavage of a precursor form to yield large and small subunits that form the enzyme. Since the cleavage site within precursors matches the specificity of caspases, sequential activation of precursors by activated caspases can occur.
A short pro-domain caspase that plays an effector role in APOPTOSIS. It is activated by INITIATOR CASPASES such as CASPASE 9. Isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.
A conserved class of proteins that control APOPTOSIS in both VERTEBRATES and INVERTEBRATES. IAP proteins interact with and inhibit CASPASES, and they function as ANTI-APOPTOTIC PROTEINS. The protein class is defined by an approximately 80-amino acid motif called the baculoviral inhibitor of apoptosis repeat.
Membrane proteins encoded by the BCL-2 GENES and serving as potent inhibitors of cell death by APOPTOSIS. The proteins are found on mitochondrial, microsomal, and NUCLEAR MEMBRANE sites within many cell types. Overexpression of bcl-2 proteins, due to a translocation of the gene, is associated with follicular lymphoma.
Splitting the DNA into shorter pieces by endonucleolytic DNA CLEAVAGE at multiple sites. It includes the internucleosomal DNA fragmentation, which along with chromatin condensation, are considered to be the hallmarks of APOPTOSIS.
An in situ method for detecting areas of DNA which are nicked during APOPTOSIS. Terminal deoxynucleotidyl transferase is used to add labeled dUTP, in a template-independent manner, to the 3 prime OH ends of either single- or double-stranded DNA. The terminal deoxynucleotidyl transferase nick end labeling, or TUNEL, assay labels apoptosis on a single-cell level, making it more sensitive than agarose gel electrophoresis for analysis of DNA FRAGMENTATION.
A member of the Bcl-2 protein family and homologous partner of C-BCL-2 PROTO-ONCOGENE PROTEIN. It regulates the release of CYTOCHROME C and APOPTOSIS INDUCING FACTOR from the MITOCHONDRIA. Several isoforms of BCL2-associated X protein occur due to ALTERNATIVE SPLICING of the mRNA for this protein.
An inhibitor of apoptosis protein that is translated by a rare cap-independent mechanism. It blocks caspase-mediated cellular destruction by inhibiting CASPASE 3; CASPASE 7; and CASPASE 9.
A cell line derived from cultured tumor cells.
A flavoprotein that functions as a powerful antioxidant in the MITOCHONDRIA and promotes APOPTOSIS when released from the mitochondria. In mammalian cells AIF is released in response to pro-apoptotic protein members of the bcl-2 protein family. It translocates to the CELL NUCLEUS and binds DNA to stimulate CASPASE-independent CHROMATIN condensation.
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
An APOPTOSIS-regulating protein that is structurally related to CASPASE 8 and competes with CASPASE 8 for binding to FAS ASSOCIATED DEATH DOMAIN PROTEIN. Two forms of CASP8 and FADD-like apoptosis regulating protein exist, a long form containing a caspase-like enzymatically inactive domain and a short form which lacks the caspase-like domain.
A long pro-domain caspase that contains a caspase recruitment domain in its pro-domain region. Caspase 9 is activated during cell stress by mitochondria-derived proapoptotic factors and by CARD SIGNALING ADAPTOR PROTEINS such as APOPTOTIC PROTEASE-ACTIVATING FACTOR 1. It activates APOPTOSIS by cleaving and activating EFFECTOR CASPASES.
Endogenous and exogenous compounds and that either inhibit CASPASES or prevent their activation.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
A long pro-domain caspase that contains a death effector domain in its pro-domain region. Caspase 8 plays a role in APOPTOSIS by cleaving and activating EFFECTOR CASPASES. Activation of this enzyme can occur via the interaction of its N-terminal death effector domain with DEATH DOMAIN RECEPTOR SIGNALING ADAPTOR PROTEINS.
Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)
A transmembrane protein belonging to the tumor necrosis factor superfamily that was originally discovered on cells of the lymphoid-myeloid lineage, including activated T-LYMPHOCYTES and NATURAL KILLER CELLS. It plays an important role in immune homeostasis and cell-mediated toxicity by binding to the FAS RECEPTOR and triggering APOPTOSIS.
Nuclear phosphoprotein encoded by the p53 gene (GENES, P53) whose normal function is to control CELL PROLIFERATION and APOPTOSIS. A mutant or absent p53 protein has been found in LEUKEMIA; OSTEOSARCOMA; LUNG CANCER; and COLORECTAL CANCER.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
Cytochromes of the c type that are found in eukaryotic MITOCHONDRIA. They serve as redox intermediates that accept electrons from MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX III and transfer them to MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX IV.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
A member of the bcl-2 protein family that plays a role in the regulation of APOPTOSIS. Two major isoforms of the protein exist due to ALTERNATIVE SPLICING of the BCL2L1 mRNA and are referred to as Bcl-XS and Bcl-XL.
A protein of the annexin family isolated from human PLACENTA and other tissues. It inhibits cytosolic PHOSPHOLIPASE A2, and displays anticoagulant activity.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
Inhibitors of SERINE ENDOPEPTIDASES and sulfhydryl group-containing enzymes. They act as alkylating agents and are known to interfere in the translation process.
Exogenous and endogenous compounds which inhibit CYSTEINE ENDOPEPTIDASES.
Established cell cultures that have the potential to propagate indefinitely.
Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity.
Technique using an instrument system for making, processing, and displaying one or more measurements on individual cells obtained from a cell suspension. Cells are usually stained with one or more fluorescent dyes specific to cell components of interest, e.g., DNA, and fluorescence of each cell is measured as it rapidly transverses the excitation beam (laser or mercury arc lamp). Fluorescence provides a quantitative measure of various biochemical and biophysical properties of the cell, as well as a basis for cell sorting. Other measurable optical parameters include light absorption and light scattering, the latter being applicable to the measurement of cell size, shape, density, granularity, and stain uptake.
The complex series of phenomena, occurring between the end of one CELL DIVISION and the end of the next, by which cellular material is duplicated and then divided between two daughter cells. The cell cycle includes INTERPHASE, which includes G0 PHASE; G1 PHASE; S PHASE; and G2 PHASE, and CELL DIVISION PHASE.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
Enzymes that catalyze the transfer of multiple ADP-RIBOSE groups from nicotinamide-adenine dinucleotide (NAD) onto protein targets, thus building up a linear or branched homopolymer of repeating ADP-ribose units i.e., POLY ADENOSINE DIPHOSPHATE RIBOSE.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
A transmembrane-protein belonging to the TNF family of intercellular signaling proteins. It is a widely expressed ligand that activates APOPTOSIS by binding to TNF-RELATED APOPTOSIS-INDUCING LIGAND RECEPTORS. The membrane-bound form of the protein can be cleaved by specific CYSTEINE ENDOPEPTIDASES to form a soluble ligand form.
Molecules or ions formed by the incomplete one-electron reduction of oxygen. These reactive oxygen intermediates include SINGLET OXYGEN; SUPEROXIDES; PEROXIDES; HYDROXYL RADICAL; and HYPOCHLOROUS ACID. They contribute to the microbicidal activity of PHAGOCYTES, regulation of signal transduction and gene expression, and the oxidative damage to NUCLEIC ACIDS; PROTEINS; and LIPIDS.
A CELL LINE derived from human T-CELL LEUKEMIA and used to determine the mechanism of differential susceptibility to anti-cancer drugs and radiation.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
Small double-stranded, non-protein coding RNAs (21-31 nucleotides) involved in GENE SILENCING functions, especially RNA INTERFERENCE (RNAi). Endogenously, siRNAs are generated from dsRNAs (RNA, DOUBLE-STRANDED) by the same ribonuclease, Dicer, that generates miRNAs (MICRORNAS). The perfect match of the siRNAs' antisense strand to their target RNAs mediates RNAi by siRNA-guided RNA cleavage. siRNAs fall into different classes including trans-acting siRNA (tasiRNA), repeat-associated RNA (rasiRNA), small-scan RNA (scnRNA), and Piwi protein-interacting RNA (piRNA) and have different specific gene silencing functions.
A short pro-domain caspase that plays an effector role in APOPTOSIS. It is activated by INITIATOR CASPASES such as CASPASE 3 and CASPASE 10. Several isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.
A promyelocytic cell line derived from a patient with ACUTE PROMYELOCYTIC LEUKEMIA. HL-60 cells lack specific markers for LYMPHOID CELLS but express surface receptors for FC FRAGMENTS and COMPLEMENT SYSTEM PROTEINS. They also exhibit phagocytic activity and responsiveness to chemotactic stimuli. (From Hay et al., American Type Culture Collection, 7th ed, pp127-8)
A negative regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
The voltage difference, normally maintained at approximately -180mV, across the INNER MITOCHONDRIAL MEMBRANE, by a net movement of positive charge across the membrane. It is a major component of the PROTON MOTIVE FORCE in MITOCHONDRIA used to drive the synthesis of ATP.
The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.
The B-cell leukemia/lymphoma-2 genes, responsible for blocking apoptosis in normal cells, and associated with follicular lymphoma when overexpressed. Overexpression results from the t(14;18) translocation. The human c-bcl-2 gene is located at 18q24 on the long arm of chromosome 18.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
A multi-domain mitochondrial membrane protein and member of the bcl-2 Protein family. Bak protein interacts with TUMOR SUPPRESSOR PROTEIN P53 and promotes APOPTOSIS.
Glycoproteins found on the membrane or surface of cells.
The pathological process occurring in cells that are dying from irreparable injuries. It is caused by the progressive, uncontrolled action of degradative ENZYMES, leading to MITOCHONDRIAL SWELLING, nuclear flocculation, and cell lysis. It is distinct it from APOPTOSIS, which is a normal, regulated cellular process.
A group of cytochromes with covalent thioether linkages between either or both of the vinyl side chains of protoheme and the protein. (Enzyme Nomenclature, 1992, p539)
A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
A member of the myeloid leukemia factor (MLF) protein family with multiple alternatively spliced transcript variants encoding different protein isoforms. In hematopoietic cells, it is located mainly in the nucleus, and in non-hematopoietic cells, primarily in the cytoplasm with a punctate nuclear localization. MLF1 plays a role in cell cycle differentiation.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
A member of the Bcl-2 protein family that reversibly binds MEMBRANES. It is a pro-apoptotic protein that is activated by caspase cleavage.
Ubiquitous, inducible, nuclear transcriptional activator that binds to enhancer elements in many different cell types and is activated by pathogenic stimuli. The NF-kappa B complex is a heterodimer composed of two DNA-binding subunits: NF-kappa B1 and relA.
Injuries to DNA that introduce deviations from its normal, intact structure and which may, if left unrepaired, result in a MUTATION or a block of DNA REPLICATION. These deviations may be caused by physical or chemical agents and occur by natural or unnatural, introduced circumstances. They include the introduction of illegitimate bases during replication or by deamination or other modification of bases; the loss of a base from the DNA backbone leaving an abasic site; single-strand breaks; double strand breaks; and intrastrand (PYRIMIDINE DIMERS) or interstrand crosslinking. Damage can often be repaired (DNA REPAIR). If the damage is extensive, it can induce APOPTOSIS.
A protein-serine-threonine kinase that is activated by PHOSPHORYLATION in response to GROWTH FACTORS or INSULIN. It plays a major role in cell metabolism, growth, and survival as a core component of SIGNAL TRANSDUCTION. Three isoforms have been described in mammalian cells.
Elements of limited time intervals, contributing to particular results or situations.
An indolocarbazole that is a potent PROTEIN KINASE C inhibitor which enhances cAMP-mediated responses in human neuroblastoma cells. (Biochem Biophys Res Commun 1995;214(3):1114-20)
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
A pro-apoptotic protein and member of the Bcl-2 protein family that is regulated by PHOSPHORYLATION. Unphosphorylated Bad protein inhibits the activity of BCL-XL PROTEIN.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.
Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity.
Members of the class of neutral glycosphingolipids. They are the basic units of SPHINGOLIPIDS. They are sphingoids attached via their amino groups to a long chain fatty acyl group. They abnormally accumulate in FABRY DISEASE.
Tumor necrosis factor receptor family members that are widely expressed and play a role in regulation of peripheral immune responses and APOPTOSIS. The receptors are specific for TNF-RELATED APOPTOSIS-INDUCING LIGAND and signal via conserved death domains that associate with specific TNF RECEPTOR-ASSOCIATED FACTORS in the CYTOPLASM.
A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.
Transport proteins that carry specific substances in the blood or across cell membranes.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
A long pro-domain caspase that contains a caspase recruitment domain in its pro-domain region. Activation of this enzyme can occur via the interaction of its caspase recruitment domain with CARD SIGNALING ADAPTOR PROTEINS. Caspase 2 plays a role in APOPTOSIS by cleaving and activating effector pro-caspases. Several isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.
The first continuously cultured human malignant CELL LINE, derived from the cervical carcinoma of Henrietta Lacks. These cells are used for VIRUS CULTIVATION and antitumor drug screening assays.
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
The action of a drug in promoting or enhancing the effectiveness of another drug.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
A signal-transducing adaptor protein that associates with TNF RECEPTOR complexes. It contains a death effector domain that can interact with death effector domains found on INITIATOR CASPASES such as CASPASE 8 and CASPASE 10. Activation of CASPASES via interaction with this protein plays a role in the signaling cascade that leads to APOPTOSIS.
Proteins whose abnormal expression (gain or loss) are associated with the development, growth, or progression of NEOPLASMS. Some neoplasm proteins are tumor antigens (ANTIGENS, NEOPLASM), i.e. they induce an immune reaction to their tumor. Many neoplasm proteins have been characterized and are used as tumor markers (BIOMARKERS, TUMOR) when they are detectable in cells and body fluids as monitors for the presence or growth of tumors. Abnormal expression of ONCOGENE PROTEINS is involved in neoplastic transformation, whereas the loss of expression of TUMOR SUPPRESSOR PROTEINS is involved with the loss of growth control and progression of the neoplasm.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
ENDOPEPTIDASES which have a cysteine involved in the catalytic process. This group of enzymes is inactivated by CYSTEINE PROTEINASE INHIBITORS such as CYSTATINS and SULFHYDRYL REAGENTS.
A gene silencing phenomenon whereby specific dsRNAs (RNA, DOUBLE-STRANDED) trigger the degradation of homologous mRNA (RNA, MESSENGER). The specific dsRNAs are processed into SMALL INTERFERING RNA (siRNA) which serves as a guide for cleavage of the homologous mRNA in the RNA-INDUCED SILENCING COMPLEX. DNA METHYLATION may also be triggered during this process.
A CARD signaling adaptor protein that plays a role in the mitochondria-stimulated apoptosis (APOPTOSIS, INTRINSIC PATHWAY). It binds to CYTOCHROME C in the CYTOSOL to form an APOPTOSOMAL PROTEIN COMPLEX and activates INITIATOR CASPASES such as CASPASE 9.
A superfamily of PROTEIN-SERINE-THREONINE KINASES that are activated by diverse stimuli via protein kinase cascades. They are the final components of the cascades, activated by phosphorylation by MITOGEN-ACTIVATED PROTEIN KINASE KINASES, which in turn are activated by mitogen-activated protein kinase kinase kinases (MAP KINASE KINASE KINASES).
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.
Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Proteins which bind to DNA. The family includes proteins which bind to both double- and single-stranded DNA and also includes specific DNA binding proteins in serum which can be used as markers for malignant diseases.
Cell surface receptors that bind TUMOR NECROSIS FACTORS and trigger changes which influence the behavior of cells.
Mutant mice homozygous for the recessive gene "nude" which fail to develop a thymus. They are useful in tumor studies and studies on immune responses.
A long pro-domain caspase that has specificity for the precursor form of INTERLEUKIN-1BETA. It plays a role in INFLAMMATION by catalytically converting the inactive forms of CYTOKINES such as interleukin-1beta to their active, secreted form. Caspase 1 is referred as interleukin-1beta converting enzyme and is frequently abbreviated ICE.
Within a eukaryotic cell, a membrane-limited body which contains chromosomes and one or more nucleoli (CELL NUCLEOLUS). The nuclear membrane consists of a double unit-type membrane which is perforated by a number of pores; the outermost membrane is continuous with the ENDOPLASMIC RETICULUM. A cell may contain more than one nucleus. (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)
A human cell line established from a diffuse histiocytic lymphoma (HISTIOCYTIC LYMPHOMA, DIFFUSE) and displaying many monocytic characteristics. It serves as an in vitro model for MONOCYTE and MACROPHAGE differentiation.
Proteins and peptides that are involved in SIGNAL TRANSDUCTION within the cell. Included here are peptides and proteins that regulate the activity of TRANSCRIPTION FACTORS and cellular processes in response to signals from CELL SURFACE RECEPTORS. Intracellular signaling peptide and proteins may be part of an enzymatic signaling cascade or act through binding to and modifying the action of other signaling factors.
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.
A mitogen-activated protein kinase subfamily that regulates a variety of cellular processes including CELL GROWTH PROCESSES; CELL DIFFERENTIATION; APOPTOSIS; and cellular responses to INFLAMMATION. The P38 MAP kinases are regulated by CYTOKINE RECEPTORS and can be activated in response to bacterial pathogens.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
A cyclin-dependent kinase inhibitor that mediates TUMOR SUPPRESSOR PROTEIN P53-dependent CELL CYCLE arrest. p21 interacts with a range of CYCLIN-DEPENDENT KINASES and associates with PROLIFERATING CELL NUCLEAR ANTIGEN and CASPASE 3.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle.
In vivo methods of screening investigative anticancer drugs, biologic response modifiers or radiotherapies. Human tumor tissue or cells are transplanted into mice or rats followed by tumor treatment regimens. A variety of outcomes are monitored to assess antitumor effectiveness.
A 150-kDa MAP kinase kinase kinase that may play a role in the induction of APOPTOSIS. It has specificity for MAP KINASE KINASE 3; MAP KINASE KINASE 4; and MAP KINASE KINASE 6.
A strong oxidizing agent used in aqueous solution as a ripening agent, bleach, and topical anti-infective. It is relatively unstable and solutions deteriorate over time unless stabilized by the addition of acetanilide or similar organic materials.
Linear POLYPEPTIDES that are synthesized on RIBOSOMES and may be further modified, crosslinked, cleaved, or assembled into complex proteins with several subunits. The specific sequence of AMINO ACIDS determines the shape the polypeptide will take, during PROTEIN FOLDING, and the function of the protein.
Proteins that are normally involved in holding cellular growth in check. Deficiencies or abnormalities in these proteins may lead to unregulated cell growth and tumor development.
Phosphotransferases that catalyzes the conversion of 1-phosphatidylinositol to 1-phosphatidylinositol 3-phosphate. Many members of this enzyme class are involved in RECEPTOR MEDIATED SIGNAL TRANSDUCTION and regulation of vesicular transport with the cell. Phosphatidylinositol 3-Kinases have been classified both according to their substrate specificity and their mode of action within the cell.
Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
Immunologic method used for detecting or quantifying immunoreactive substances. The substance is identified by first immobilizing it by blotting onto a membrane and then tagging it with labeled antibodies.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
Proteins found in the nucleus of a cell. Do not confuse with NUCLEOPROTEINS which are proteins conjugated with nucleic acids, that are not necessarily present in the nucleus.
Quaternary ammonium analog of ethidium; an intercalating dye with a specific affinity to certain forms of DNA and, used as diiodide, to separate them in density gradients; also forms fluorescent complexes with cholinesterase which it inhibits.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
CULTURE MEDIA free of serum proteins but including the minimal essential substances required for cell growth. This type of medium avoids the presence of extraneous substances that may affect cell proliferation or unwanted activation of cells.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
A family of cell surface receptors that signal via a conserved domain that extends into the cell CYTOPLASM. The conserved domain is referred to as a death domain due to the fact that many of these receptors are involved in signaling APOPTOSIS. Several DEATH DOMAIN RECEPTOR SIGNALING ADAPTOR PROTEINS can bind to the death domains of the activated receptors and through a complex series of interactions activate apoptotic mediators such as CASPASES.
Lymphocytes responsible for cell-mediated immunity. Two types have been identified - cytotoxic (T-LYMPHOCYTES, CYTOTOXIC) and helper T-lymphocytes (T-LYMPHOCYTES, HELPER-INDUCER). They are formed when lymphocytes circulate through the THYMUS GLAND and differentiate to thymocytes. When exposed to an antigen, they divide rapidly and produce large numbers of new T cells sensitized to that antigen.
Methods of investigating the effectiveness of anticancer cytotoxic drugs and biologic inhibitors. These include in vitro cell-kill models and cytostatic dye exclusion tests as well as in vivo measurement of tumor growth parameters in laboratory animals.
Proteins prepared by recombinant DNA technology.
The process by which chemical compounds provide protection to cells against harmful agents.
The two lipoprotein layers in the MITOCHONDRION. The outer membrane encloses the entire mitochondrion and contains channels with TRANSPORT PROTEINS to move molecules and ions in and out of the organelle. The inner membrane folds into cristae and contains many ENZYMES important to cell METABOLISM and energy production (MITOCHONDRIAL ATP SYNTHASE).
Proteins that control the CELL DIVISION CYCLE. This family of proteins includes a wide variety of classes, including CYCLIN-DEPENDENT KINASES, mitogen-activated kinases, CYCLINS, and PHOSPHOPROTEIN PHOSPHATASES as well as their putative substrates such as chromatin-associated proteins, CYTOSKELETAL PROTEINS, and TRANSCRIPTION FACTORS.
Tumor suppressor genes located on the short arm of human chromosome 17 and coding for the phosphoprotein p53.
The segregation and degradation of damaged or unwanted cytoplasmic constituents by autophagic vacuoles (cytolysosomes) composed of LYSOSOMES containing cellular components in the process of digestion; it plays an important role in BIOLOGICAL METAMORPHOSIS of amphibians, in the removal of bone by osteoclasts, and in the degradation of normal cell components in nutritional deficiency states.
Microscopy of specimens stained with fluorescent dye (usually fluorescein isothiocyanate) or of naturally fluorescent materials, which emit light when exposed to ultraviolet or blue light. Immunofluorescence microscopy utilizes antibodies that are labeled with fluorescent dye.
A CCAAT-enhancer binding protein that is induced by DNA DAMAGE and growth arrest. It serves as a dominant negative inhibitor of other CCAAT-enhancer binding proteins.
Derivatives of phosphatidic acids in which the phosphoric acid is bound in ester linkage to a serine moiety. Complete hydrolysis yields 1 mole of glycerol, phosphoric acid and serine and 2 moles of fatty acids.
Antibiotic substance isolated from streptomycin-producing strains of Streptomyces griseus. It acts by inhibiting elongation during protein synthesis.
Peptides composed of between two and twelve amino acids.
High molecular weight proteins found in the MICROTUBULES of the cytoskeletal system. Under certain conditions they are required for TUBULIN assembly into the microtubules and stabilize the assembled microtubules.
Eukaryotic cell line obtained in a quiescent or stationary phase which undergoes conversion to a state of unregulated growth in culture, resembling an in vitro tumor. It occurs spontaneously or through interaction with viruses, oncogenes, radiation, or drugs/chemicals.
Tumors or cancer of the COLON.
An intracellular signaling system involving the MAP kinase cascades (three-membered protein kinase cascades). Various upstream activators, which act in response to extracellular stimuli, trigger the cascades by activating the first member of a cascade, MAP KINASE KINASE KINASES; (MAPKKKs). Activated MAPKKKs phosphorylate MITOGEN-ACTIVATED PROTEIN KINASE KINASES which in turn phosphorylate the MITOGEN-ACTIVATED PROTEIN KINASES; (MAPKs). The MAPKs then act on various downstream targets to affect gene expression. In mammals, there are several distinct MAP kinase pathways including the ERK (extracellular signal-regulated kinase) pathway, the SAPK/JNK (stress-activated protein kinase/c-jun kinase) pathway, and the p38 kinase pathway. There is some sharing of components among the pathways depending on which stimulus originates activation of the cascade.
Penetrating, high-energy electromagnetic radiation emitted from atomic nuclei during NUCLEAR DECAY. The range of wavelengths of emitted radiation is between 0.1 - 100 pm which overlaps the shorter, more energetic hard X-RAYS wavelengths. The distinction between gamma rays and X-rays is based on their radiation source.
Compounds which inhibit the synthesis of proteins. They are usually ANTI-BACTERIAL AGENTS or toxins. Mechanism of the action of inhibition includes the interruption of peptide-chain elongation, the blocking the A site of ribosomes, the misreading of the genetic code or the prevention of the attachment of oligosaccharide side chains to glycoproteins.
Cellular DNA-binding proteins encoded by the c-myc genes. They are normally involved in nucleic acid metabolism and in mediating the cellular response to growth factors. Elevated and deregulated (constitutive) expression of c-myc proteins can cause tumorigenesis.
A mitogen-activated protein kinase kinase with specificity for JNK MITOGEN-ACTIVATED PROTEIN KINASES; P38 MITOGEN-ACTIVATED PROTEIN KINASES and the RETINOID X RECEPTORS. It takes part in a SIGNAL TRANSDUCTION pathway that is activated in response to cellular stress.
An ERYTHROLEUKEMIA cell line derived from a CHRONIC MYELOID LEUKEMIA patient in BLAST CRISIS.
The N-acetyl derivative of CYSTEINE. It is used as a mucolytic agent to reduce the viscosity of mucous secretions. It has also been shown to have antiviral effects in patients with HIV due to inhibition of viral stimulation by reactive oxygen intermediates.
Human COLORECTAL CARCINOMA cell line.
Regulatory signaling systems that control the progression through the CELL CYCLE. They ensure that the cell has completed, in the correct order and without mistakes, all the processes required to replicate the GENOME and CYTOPLASM, and divide them equally between two daughter cells. If cells sense they have not completed these processes or that the environment does not have the nutrients and growth hormones in place to proceed, then the cells are restrained (or "arrested") until the processes are completed and growth conditions are suitable.
Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.
The artificial induction of GENE SILENCING by the use of RNA INTERFERENCE to reduce the expression of a specific gene. It includes the use of DOUBLE-STRANDED RNA, such as SMALL INTERFERING RNA and RNA containing HAIRPIN LOOP SEQUENCE, and ANTI-SENSE OLIGONUCLEOTIDES.
The process of moving proteins from one cellular compartment (including extracellular) to another by various sorting and transport mechanisms such as gated transport, protein translocation, and vesicular transport.
A family of non-enveloped viruses infecting mammals (MASTADENOVIRUS) and birds (AVIADENOVIRUS) or both (ATADENOVIRUS). Infections may be asymptomatic or result in a variety of diseases.
Short fragments of DNA or RNA that are used to alter the function of target RNAs or DNAs to which they hybridize.
Tumors or cancer of the PROSTATE.
Naturally occurring or synthetic substances that inhibit or retard the oxidation of a substance to which it is added. They counteract the harmful and damaging effects of oxidation in animal tissues.
A broad category of carrier proteins that play a role in SIGNAL TRANSDUCTION. They generally contain several modular domains, each of which having its own binding activity, and act by forming complexes with other intracellular-signaling molecules. Signal-transducing adaptor proteins lack enzyme activity, however their activity can be modulated by other signal-transducing enzymes
The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.
Various physiological or molecular disturbances that impair ENDOPLASMIC RETICULUM function. It triggers many responses, including UNFOLDED PROTEIN RESPONSE, which may lead to APOPTOSIS; and AUTOPHAGY.
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.
Proteins encoded by the mitochondrial genome or proteins encoded by the nuclear genome that are imported to and resident in the MITOCHONDRIA.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
Quaternary salts derived from tetrazoles. They are used in tests to distinguish between reducing sugars and simple aldehydes, for detection of dehydrogenase in tissues, cells, and bacteria, for determination of corticosteroids, and in color photography. (From Mall's Dictionary of Chemistry, 5th ed, p455)
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
The main structural component of the LIVER. They are specialized EPITHELIAL CELLS that are organized into interconnected plates called lobules.
A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine).
Chemical substances, produced by microorganisms, inhibiting or preventing the proliferation of neoplasms.
Tumors or cancer of the human BREAST.
The period of the CELL CYCLE preceding DNA REPLICATION in S PHASE. Subphases of G1 include "competence" (to respond to growth factors), G1a (entry into G1), G1b (progression), and G1c (assembly). Progression through the G1 subphases is effected by limiting growth factors, nutrients, or inhibitors.
A system of cisternae in the CYTOPLASM of many cells. In places the endoplasmic reticulum is continuous with the plasma membrane (CELL MEMBRANE) or outer membrane of the nuclear envelope. If the outer surfaces of the endoplasmic reticulum membranes are coated with ribosomes, the endoplasmic reticulum is said to be rough-surfaced (ENDOPLASMIC RETICULUM, ROUGH); otherwise it is said to be smooth-surfaced (ENDOPLASMIC RETICULUM, SMOOTH). (King & Stansfield, A Dictionary of Genetics, 4th ed)
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
A large family of regulatory proteins that function as accessory subunits to a variety of CYCLIN-DEPENDENT KINASES. They generally function as ENZYME ACTIVATORS that drive the CELL CYCLE through transitions between phases. A subset of cyclins may also function as transcriptional regulators.
A group of phenyl benzopyrans named for having structures like FLAVONES.
The period of the CELL CYCLE following DNA synthesis (S PHASE) and preceding M PHASE (cell division phase). The CHROMOSOMES are tetraploid in this point.
A tripeptide with many roles in cells. It conjugates to drugs to make them more soluble for excretion, is a cofactor for some enzymes, is involved in protein disulfide bond rearrangement and reduces peroxides.
A c-jun amino-terminal kinase that is activated by environmental stress and pro-inflammatory cytokines. Several isoforms of the protein with molecular sizes of 43 and 48 KD exist due to multiple ALTERNATIVE SPLICING.
Human colonic ADENOCARCINOMA cells that are able to express differentiation features characteristic of mature intestinal cells such as the GOBLET CELLS.
A tumor necrosis factor receptor subtype that has specificity for TUMOR NECROSIS FACTOR ALPHA and LYMPHOTOXIN ALPHA. It is constitutively expressed in most tissues and is a key mediator of tumor necrosis factor signaling in the vast majority of cells. The activated receptor signals via a conserved death domain that associates with specific TNF RECEPTOR-ASSOCIATED FACTORS in the CYTOPLASM.
A mitogen-activated protein kinase subfamily that is widely expressed and plays a role in regulation of MEIOSIS; MITOSIS; and post mitotic functions in differentiated cells. The extracellular signal regulated MAP kinases are regulated by a broad variety of CELL SURFACE RECEPTORS and can be activated by certain CARCINOGENS.
Interruption or suppression of the expression of a gene at transcriptional or translational levels.
Compounds that inhibit cell production of DNA or RNA.
Recombinant proteins produced by the GENETIC TRANSLATION of fused genes formed by the combination of NUCLEIC ACID REGULATORY SEQUENCES of one or more genes with the protein coding sequences of one or more genes.
An inorganic and water-soluble platinum complex. After undergoing hydrolysis, it reacts with DNA to produce both intra and interstrand crosslinks. These crosslinks appear to impair replication and transcription of DNA. The cytotoxicity of cisplatin correlates with cellular arrest in the G2 phase of the cell cycle.
The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)
A long pro-domain caspase that contains a death effector domain in its pro-domain region. Activation of this enzyme can occur via the interaction of its N-terminal death effector domain with DEATH DOMAIN RECEPTOR SIGNALING ADAPTOR PROTEINS. Caspase 10 plays a role in APOPTOSIS by cleaving and activating EFFECTOR CASPASES. Several isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.
Binary compounds of oxygen containing the anion O(2-). The anion combines with metals to form alkaline oxides and non-metals to form acidic oxides.
A large multisubunit complex that plays an important role in the degradation of most of the cytosolic and nuclear proteins in eukaryotic cells. It contains a 700-kDa catalytic sub-complex and two 700-kDa regulatory sub-complexes. The complex digests ubiquitinated proteins and protein activated via ornithine decarboxylase antizyme.
An E2F transcription factor that interacts directly with RETINOBLASTOMA PROTEIN and CYCLIN A and activates GENETIC TRANSCRIPTION required for CELL CYCLE entry and DNA synthesis. E2F1 is involved in DNA REPAIR and APOPTOSIS.
White blood cells formed in the body's lymphoid tissue. The nucleus is round or ovoid with coarse, irregularly clumped chromatin while the cytoplasm is typically pale blue with azurophilic (if any) granules. Most lymphocytes can be classified as either T or B (with subpopulations of each), or NATURAL KILLER CELLS.
Intracellular fluid from the cytoplasm after removal of ORGANELLES and other insoluble cytoplasmic components.
The aggregation of soluble ANTIGENS with ANTIBODIES, alone or with antibody binding factors such as ANTI-ANTIBODIES or STAPHYLOCOCCAL PROTEIN A, into complexes large enough to fall out of solution.
An enzyme that catalyzes the hydrolysis of sphingomyelin to ceramide (N-acylsphingosine) plus choline phosphate. A defect in this enzyme leads to NIEMANN-PICK DISEASE. EC 3.1.4.12.
Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).
Electron-accepting molecules in chemical reactions in which electrons are transferred from one molecule to another (OXIDATION-REDUCTION).
The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.
Processes required for CELL ENLARGEMENT and CELL PROLIFERATION.
Inorganic or organic compounds that contain arsenic.

Apoptosis inducing factor (AIF): a phylogenetically old, caspase-independent effector of cell death. (1/444)

Although much emphasis has been laid on the role of caspase in cell death, recent data indicate that, in many instances, mammalian cell death is caspase-independent. Thus, in many examples of mammalian cell death the 'decision' between death and life is upstream or independent of caspase activation. Similarly, it is unclear whether PCD of plants and fungi involves the activation of caspase-like enzymes, and no caspase-like gene has thus far been cloned in these phyla. Apoptosis inducing factor (AIF) is a new mammalian, caspase-independent death effector which, upon apoptosis induction, translocates from its normal localization, the mitochondrial intermembrane space, to the nucleus. Once in the nucleus, AIF causes chromatin condensation and large scale DNA fragmentation to fragments of approximately 50 kbp. The AIF cDNA from mouse and man codes for a protein which possesses three domains (i) an amino-terminal presequence which is removed upon import into the intermembrane space of mitochondria; (ii) a spacer sequence of approximately 27 amino acids; and (iii) a carboxyterminal 484 amino acid oxidoreductase domain with strong homology to oxidoreductases from other vertebrates (X. laevis), non-vertebrate animals (C. elegans, D. melanogaster), plants, fungi, eubacteria, and archaebacteria. Functionally important amino acids involved in the interaction with the prosthetic groups flavin adenine nucleotide and nicotinamide adenine nucleotide are strongly conserved between AIF and bacterial oxidoreductase. Several eukaryotes possess a similar domain organisation in their AIF homologs, making them candidates to be mitochondrial oxidoreductases as well as caspase-independent death effectors. The phylogenetic implications of these findings are discussed.  (+info)

Mitochondria and cell death. Mechanistic aspects and methodological issues. (2/444)

Mitochondria are involved in cell death for reasons that go beyond ATP supply. A recent advance has been the discovery that mitochondria contain and release proteins that are involved in the apoptotic cascade, like cytochrome c and apoptosis inducing factor. The involvement of mitochondria in cell death, and its being cause or consequence, remain issues that are extremely complex to address in situ. The response of mitochondria may critically depend on the type of stimulus, on its intensity, and on the specific mitochondrial function that has been primarily perturbed. On the other hand, the outcome also depends on the integration of mitochondrial responses that cannot be dissected easily. Here, we try to identify the mechanistic aspects of mitochondrial involvement in cell death as can be derived from our current understanding of mitochondrial physiology, with special emphasis on the permeability transition and its consequences (like onset of swelling, cytochrome c release and respiratory inhibition); and to critically evaluate methods that are widely used to monitor mitochondrial function in situ.  (+info)

The novel retinoid 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphtalene carboxylic acid can trigger apoptosis through a mitochondrial pathway independent of the nucleus. (3/444)

The novel retinoid 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphtalene carboxylic acid (AHPN/CD437), a retinoic acid receptor (RAR)gamma activator, has been found to inhibit the growth and to induce apoptosis of a wide variety of malignant cell types including solid tumors and various leukemias. Interestingly, CD437 is able to induce apoptosis in some all-trans-retinoic acid (ATRA)-resistant models. In a number of experimental systems, the early apoptotic stage that precedes nuclear chromatinolysis consists in mitochondrial alterations, including a disruption of the inner mitochondrial transmembrane potential (delta(psi)m) mediated by the mitochondrial permeability transition (MPT). Similarly CD437 causes RPMI 8226, a human myeloma cell line, to undergo a rapid delta(psi)m disruption that precedes other apoptotic alterations such as the generation of reactive oxygen species and DNA fragmentation. The same sequence of events is observed during the CD437-induced apoptosis in L363, a RARgamma-negative human myeloma cell line, as well as RPMI 8226 cytoplasts (anucleate cells). Indeed, RPMI 8226 cells and cytoplasts manifest a similar degree in delta(psi)m loss, phosphatidylserine exposure, and caspase activation in response to CD437, which indicates that nuclear effects cannot account for the apoptogenic potential of CD437. The mitochondrial release of cytochrome c, the activation of caspases as well as nuclear signs of CD437-induced apoptosis are fully prevented by the MPT inhibitory compound cyclosporin A. Purified mitochondria can be directly induced to undergo MPT with CD437 but not with ATRA. In a cell-free in vitro system consisting of exposing mitochondrial supernatants to isolated nuclei, only supernatants from CD437-treated mitochondria provoke chromatin condensation, whereas supernatants from mitochondria treated with ATRA, or with the combination of CD437 and cyclosporin A, remain inactive. In conclusion, these results suggest that the rapid execution of CD437-induced apoptosis is a nucleus-independent (and probably RARgamma-independent) phenomenon involving mitochondria and MPT.  (+info)

Mitochondrio-nuclear translocation of AIF in apoptosis and necrosis. (4/444)

Apoptosis inducing factor (AIF) is a novel apoptotic effector protein that induces chromatin condensation and large-scale ( approximately 50 kbp) DNA fragmentation when added to purified nuclei in vitro. Confocal and electron microscopy reveal that, in normal cells, AIF is strictly confined to mitochondria and thus colocalizes with heat shock protein 60 (hsp60). On induction of apoptosis by staurosporin, c-Myc, etoposide, or ceramide, AIF (but not hsp60) translocates to the nucleus. This suggests that only the outer mitochondrial membrane (which retains AIF in the intermembrane space) but not the inner membrane (which retains hsp60 in the matrix) becomes protein permeable. The mitochondrio-nuclear redistribution of AIF is prevented by a Bcl-2 protein specifically targeted to mitochondrial membranes. The pan-caspase inhibitor Z-VAD. fmk does not prevent the staurosporin-induced translocation of AIF, although it does inhibit oligonucleosomal DNA fragmentation and arrests chromatin condensation at an early stage. ATP depletion is sufficient to cause AIF translocation to the nucleus, and this phenomenon is accelerated by the apoptosis inducer staurosporin. However, in conditions in which both glycolytic and respiratory ATP generation is inhibited, cells fail to manifest any sign of chromatin condensation and advanced DNA fragmentation, thus manifesting a 'necrotic' phenotype. Both in the presence of Z-VAD. fmk and in conditions of ATP depletion, AIF translocation correlates with the appearance of large-scale DNA fragmentation. Altogether, these data are compatible with the hypothesis that AIF is a caspase-independent mitochondrial death effector responsible for partial chromatinolysis.  (+info)

Induction of metabolism-dependent and -independent neutrophil apoptosis by clozapine. (5/444)

Clozapine, an atypical antipsychotic used in the treatment of refractory schizophrenia, causes neutropenia and agranulocytosis in 3 and 0.8% of patients, respectively. Clozapine undergoes bioactivation to a chemically reactive nitrenium ion, which has been shown to cause neutrophil cytotoxicity. To define further the mechanism of cell death, we have investigated the toxicity of clozapine, its stable metabolites, and its chemically reactive nitrenium ion to neutrophils and lymphocytes. Clozapine was able to induce neutrophil apoptosis at therapeutic concentrations (1-3 microM) only when it was bioactivated to the nitrenium ion. The parent drug caused apoptosis at supratherapeutic concentrations (100-300 microM) only. Neutrophil apoptosis induced by the nitrenium ion, but not by the parent drug itself, was inhibited by antioxidants and genistein and was accompanied by cell surface haptenation (assessed by flow cytometry) and glutathione depletion. Dual-color flow cytometry showed that neutrophils that were haptenated were the same cells that underwent apoptosis. No apoptosis of lymphocytes was evident with the nitrenium ion or the parent drug, despite the fact that the former caused cell surface haptenation, glutathione depletion, and loss of membrane integrity. Demethylclozapine, the major stable metabolite in vivo, showed a profile that was similar to, although less marked than that observed with clozapine. N-oxidation of clozapine or replacement of the nitrogen (at position 5) by sulfur produced compounds that were entirely nontoxic to neutrophils. In conclusion, the findings of the study expand on potential mechanisms of clozapine-induced cytotoxicity, which may be of relevance to the major forms of toxicity encountered in patients taking this drug.  (+info)

BNIP3 and genetic control of necrosis-like cell death through the mitochondrial permeability transition pore. (6/444)

Many apoptotic signaling pathways are directed to mitochondria, where they initiate the release of apoptogenic proteins and open the proposed mitochondrial permeability transition (PT) pore that ultimately results in the activation of the caspase proteases responsible for cell disassembly. BNIP3 (formerly NIP3) is a member of the Bcl-2 family that is expressed in mitochondria and induces apoptosis without a functional BH3 domain. We report that endogenous BNIP3 is loosely associated with mitochondrial membrane in normal tissue but fully integrates into the mitochondrial outer membrane with the N terminus in the cytoplasm and the C terminus in the membrane during induction of cell death. Surprisingly, BNIP3-mediated cell death is independent of Apaf-1, caspase activation, cytochrome c release, and nuclear translocation of apoptosis-inducing factor. However, cells transfected with BNIP3 exhibit early plasma membrane permeability, mitochondrial damage, extensive cytoplasmic vacuolation, and mitochondrial autophagy, yielding a morphotype that is typical of necrosis. These changes were accompanied by rapid and profound mitochondrial dysfunction characterized by opening of the mitochondrial PT pore, proton electrochemical gradient (Deltapsim) suppression, and increased reactive oxygen species production. The PT pore inhibitors cyclosporin A and bongkrekic acid blocked mitochondrial dysregulation and cell death. We propose that BNIP3 is a gene that mediates a necrosis-like cell death through PT pore opening and mitochondrial dysfunction.  (+info)

Purification and cloning of an apoptosis-inducing protein derived from fish infected with Anisakis simplex, a causative nematode of human anisakiasis. (7/444)

While investigating the effect of marine products on cell growth, we found that visceral extracts of Chub mackerel, an ocean fish, had a powerful and dose-dependent apoptosis-inducing effect on a variety of mammalian tumor cells. This activity was strikingly dependent on infection of the C. mackerel with the larval nematode, Anisakis simplex. After purification of the protein responsible for the apoptosis-inducing activity, we cloned the corresponding gene and found it to be a flavoprotein. This protein, termed apoptosis-inducing protein (AIP), was also found to possess an endoplasmic reticulum retention signal (C-terminal KDEL sequence) and H2O2-producing activity, indicating that we had isolated a novel reticuloplasimin with potent apoptosis-inducing activity. AIP was induced in fish only after infection with larval nematode and was localized to capsules that formed around larvae to prevent their migration to host tissues. Our results suggest that AIP may function to impede nematode infection.  (+info)

Apoptosis-inducing factor (AIF): a ubiquitous mitochondrial oxidoreductase involved in apoptosis. (8/444)

Apoptosis-inducing factor (AIF) is encoded by one single gene located on the X chromosome. AIF is ubiquitously expressed, both in normal tissues and in a variety of cancer cell lines. The AIF precursor is synthesized in the cytosol and is imported into mitochondria. The mature AIF protein, a flavoprotein (prosthetic group: flavine adenine dinucleotide) with significant homology to plant ascorbate reductases and bacterial NADH oxidases, is normally confined to the mitochondrial intermembrane space. In a variety of different apoptosis-inducing conditions, AIF translocates through the outer mitochondrial membrane to the cytosol and to the nucleus. Ectopic (extra-mitochondrial) AIF induces nuclear chromatin condensation, as well as large scale ( approximately 50 kb) DNA fragmentation. Thus, similar to cytochrome c, AIF is a phylogenetically old, bifunctional protein with an electron acceptor/donor (oxidoreductase) function and a second apoptogenic function. In contrast to cytochrome c, however, AIF acts in a caspase-independent fashion. The molecular mechanisms via which AIF induces apoptosis are discussed.  (+info)

The Genome Sciences Centre sequencing platform is a high-throughput large-scale DNA analysis facility that has been designed to maximize capacity while maintaining efficiency, scalability and flexibility. The platform is one of the largest platforms of its type in Canada and is well recognized internationally.. Current production scale capabilities of the capillary based platform include fosmid end sequencing, PCR amplicon sequencing, plasmid, and BAC end sequencing. We have two Applied Biosytems 3730xls yielding a capacity of 7680 lanes per week, or approx 6 million Q20 bases per week. The GSC sequencing platform prides itself on its flexibility and molecular biology enabling PCR, BAC, fosmid and plasmid DNA preps and several optimized reaction chemistries, allowing us to provide high-quality, high-yield, consistent data generation.. More information on the Illumina Platform.. Through our sequencing validation team we offer several high quality, high throughput targeted sequencing services. We ...
DNA fluorescence in situ hybridization (FISH) is a powerful cytogenetic assay, but conventional sample-preparation methods for FISH do not support large-scale high-throughput data acquisition and analysis, which are potentially useful for several biomedical applications. To address this limitation, we have d
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
View mouse Siva1 Chr12:112644828-112649152 with: phenotypes, sequences, polymorphisms, proteins, references, function, expression
DNA sequence analysis is a multistage process that includes the preparation of DNA, its fragmentation and base analysis, and the interpretation of the resulting sequence information. New technological advances have led to the automation of certain steps in this process and have raised the possibility of large-scale DNA sequencing efforts in the near future [for example, 1 million base pairs (Mb) per year]. New sequencing methodologies, fully automated instrumentation, and improvements in sequencing-related computational resources may render genome-size sequencing projects (100 Mb or larger) feasible during the next 5 to 10 years. ...
Oxygen, Muscle, Skeletal Muscle, Apoptosis, Caspase-3, Cytochrome, Cytochrome C, DNA, DNA Fragmentation, Reactive Oxygen Species, Apoptosis-inducing Factor, Calpain, Cell, Cell Death, Death, Heat, Heat Shock Protein, Heat Shock Protein 70, Membrane, Membrane Potential
There is a worldwide increasing concern over the neurological risks of thimerosal (ethylmercury thiosalicylate) which is an organic mercury compound that is commonly used as an antimicrobial preservative. In this study, we show that thimerosal, at nanomolar concentrations, induces neuronal cell death through the mitochondrial pathway. Thimerosal, in a concentration- and time-dependent manner, decreased cell viability as assessed by calcein-ethidium staining and caused apoptosis detected by Hoechst 33258 dye. Thimerosal-induced apoptosis was associated with depolarization of mitochondrial membrane, generation of reactive oxygen species, and release of cytochrome c and apoptosis-inducing factor (AIF) from mitochondria to cytosol. Although thimerosal did not affect cellular expression of Bax at the protein level, we observed translocation of Bax from cytosol to mitochondria. Finally, caspase-9 and caspase-3 were activated in the absence of caspase-8 activation. Our data suggest that thimerosal ...
Myocyte death occurs in many inherited and acquired cardiomyopathies, including arrhythmogenic cardiomyopathy (ACM), a genetic heart disease plagued by the prevalence of sudden cardiac death. Individuals with ACM and harboring pathogenic desmosomal variants, such as desmoglein-2 (DSG2), often show myocyte necrosis with progression to exercise-associated heart failure. Here, we showed that homozygous Dsg2 mutant mice (Dsg2mut/mut), a model of ACM, die prematurely during swimming and display myocardial dysfunction and necrosis. We detected calcium (Ca2+) overload in Dsg2mut/mut hearts, which induced calpain-1 (CAPN1) activation, association of CAPN1 with mitochondria, and CAPN1-induced cleavage of mitochondrial-bound apoptosis-inducing factor (AIF). Cleaved AIF translocated to the myocyte nucleus triggering large-scale DNA fragmentation and cell death, an effect potentiated by mitochondrial-driven AIF oxidation. Posttranslational oxidation of AIF cysteine residues was due, in part, to a depleted ...
VARECHA, Miroslav et al. Knockdown of apoptosis-inducing factor disrupts function of respiratory complex I. Biocell [online]. 2012, vol.36, n.3, pp.121-126. ISSN 0327-9545.. Recent findings suggest that apoptotic protein apoptosis-inducing factor (AIF) may also play an important non-apoptotic function inside mitochondria. AIF was proposed to be an important component of respiratory chain complex I that is the major producer of superoxide radical. The possible role of AIF is still controversial. Superoxide production could be used as a valuable measure of complex I function, because the majority of superoxide is produced there. Therefore, we employed superoxide-specific mitochondrial fluorescence dye for detection of superoxide production. We studied an impact of AIF knockdown on function of mitochondrial complex I by analyzing superoxide production in selected cell lines. Our results show that tumoral telomerase-positive (TP) AIF knockdown cell lines display significant increase in superoxide ...
All Clarivate Analytics websites use cookies to improve your online experience. They were placed on your computer when you launched this website. You can change your cookie settings through your browser. ...
Synthetic Apoptosis-Inducing Factor, Mitochondrion-Associated, 1 (AIFM1) Peptide. Species: Mammalian. Source: Synthetic. Order product ABIN938567.
Different cell-death mechanisms control many physiological and pathological processes in humans. Mitochondria play important roles in cell death through the release of pro-apoptotic factors such as cytochrome c and apoptosis-inducing factor (AIF), which activate caspase-dependent and caspase-independent cell death, respectively. Poly(ADP-ribose) polymerase 1 (PARP-1) is emerging as an important activator of caspase-independent cell death. PARP-1 generates the majority of long, branched poly(ADP-ribose) (PAR) polymers following DNA damage. Overactivation of PARP-1 initiates a nuclear signal that propagates to mitochondria and triggers the release of AIF. AIF then shuttles from mitochondria to the nucleus and induces peripheral chromatin condensation, large-scale fragmentation of DNA and, ultimately, cytotoxicity. Identification of the pro-death and pro-survival signals in the PARP-1-mediated cell-death program might provide novel therapeutic targets in human diseases.
1)Xin Li#, Guizhong Zhang#, Qian Chen, Yingxue Lin, Junxin Li, Qinggguo Ruan, Youhai Chen, Guang Yu, and Xiaochun Wan*. CD317 Promotes the survival of cancer cells through apoptosis-inducing factor. Journal of Experimental& Clinical Cancer Research, 2016, 35:117; IF=4.357;. (2)Lulu Cui#, Jiacheng Bi#, Dehong Yan, Xiufeng Ye, Mingxing Zheng, Guang Yu, Xiaochun Wan*. JSI-124 inhibits IgE production in an IgE B cell line. BBRC(Biochemical and Biophysical Research Communications). 2017.01.29, 483(1):669-673, IF=2.466;. (3)Jiacheng Bi#, Lulu Cui#, Gang Yu, Xiaolu Yang, Youhai Chen, Xiaochun Wan*. NK cells alleviate lung inflammation by negatively regulating group 2 innate lymphoid cells. The Journal of Immunology. 2017.04.15, 198(8):3336- 3344. IF= 4.856;. (4)Hongling Zhang#, Jiacheng Bi#, Huqiang Yi, Tingting Fan, Qingguo Ruan, Lintao Cai, Youhai H Chen, Xiaochun Wan*. Silencing c-Rel in macrophages dampens Th1 and Th17 immune responses and alleviates experimental autoimmune ...
Sigma-Aldrich offers abstracts and full-text articles by [Mei Yang, Jialing Zhong, Mei Zhao, Jia Wang, Yuyu Gu, Xinghua Yuan, Jianli Sang, Changzhi Huang].
My interests center on development of instrumentation for analyzing and synthesizing proteins and genes (e.g., protein, sequenator, DNA synthesizer, DNA sequenator, protein synthesizer), molecular immunology and autoimmunity, genomics, specifically, large-scale DNA sequence analysis of immune receptor gene families, molecular evolution, cancer biology, and HIV genome analysis.. ...
All of us at SDSC look forward to working with Dr. Subramaniam in his new role as a Distinguished Scientist, said Michael L. Norman, SDSCs interim director. As a true pioneer in bioinformatics and systems biology, Dr. Subramaniam is uniquely qualified to identify new opportunities and propose innovative solutions as SDSC broadens its expertise in these exciting areas of scientific research.. Bioinformatics is the application of statistics and computer sciences to the field of molecular biology. It has been used widely in genomics and genetics, notably in research involving large-scale DNA sequencing.. I am honored to be appointed as an SDSC Distinguished Scientist, said Subramaniam. The new developments at SDSC, notably with its next generation of high-performance computing and data systems, are extraordinarily synergistic with my research plans, and I look forward to extremely valuable and productive collaborations.. In 2008, Subramaniam was awarded the Faculty Excellence in Research ...
Zhu C, Wang X, Deinum J, Huang Z, Gao J, Modjtahedi N, Neagu MR, Nilsson M, Eriksson PS, Hagberg H, Luban J, Kroemer G, Blomgren K. Cyclophilin A participates in the nuclear translocation of apoptosis-inducing factor in neurons after cerebral hypoxia-ischemia. J Exp Med. 2007 Aug 6; 204(8):1741-8 ...
HYD1 is a D-amino acid peptide that was previously shown to inhibit adhesion of prostate cancer cells to the extracellular matrix. In this study, we show that in addition to inhibiting adhesion of multiple myeloma (MM) cells to fibronectin, HYD1 induces cell death in MM cells as a single agent. HYD1-induced cell death was necrotic in nature as shown by: (a) decrease in mitochondrial membrane potential (Δψm), (b) loss of total cellular ATP, and (c) increase in reactive oxygen species (ROS) production. Moreover, HYD1 treatment does not result in apoptotic cell death because it did not trigger the activation of caspases or the release of apoptosis-inducing factor and endonuclease G from the mitochondria, nor did it induce double-stranded DNA breaks. HYD1 did initiate autophagy in cells; however, autophagy was found to be an adaptive response contributing to cell survival rather than the cause of cell death. We were further able to show that N-acetyl-L-cysteine, a thiol-containing free radical ...
The replication initiation factor Cdc6 is cleaved during apoptosis, and expression of a cleavage product is sufficient to induce apoptosis in otherwise unstressed cells. On page 77, Yim et al. report that the cleavage products can act as dominant-negative inhibitors of replication and amplify pro-death signals.. In addition to the previously identified cleavage product, Yim et al. identified a second Cdc6 fragment produced by caspase-3. Both Cdc6 fragments were sufficient to induce cell death without additional pro-apoptotic signals. Moreover, in cells exposed to apoptosis-inducing factors, ectopic expression of the Cdc6 peptides increased the rate of cell death. In contrast, expression of noncleavable Cdc6 suppressed apoptosis, indicating that fragmentation of the protein plays a causal role in the process even in the presence of known triggers.. Truncated Cdc6 interferes with loading of Mcm2 on the chromatin and thus disrupts assembly of the prereplication complex on chromosomes. That in turn ...
I made this for those asking for it. Its easy! Let me know if you need anything else fellow dark souls. * Also you may not have to ... ...
Previous investigations suggest that DL-3-n-butylphthalide (NBP) is a promising multifaceted drug for the treatment of stroke. It is not clear whether NBP can treat traumatic brain injury (TBI) and what could be the mechanisms of therapeutic benefits. To address these issues, TBI was induced by a controlled cortical impact in adult male mice. NBP (100 mg/kg) or saline was intraperitoneally administered within 5 min after TBI. One day after TBI, apoptotic events including caspase-3/9 activation, cytochrome c release from the mitochondria, and apoptosis-inducing factor (AIF) translocation into the nucleus in the pericontusion region were attenuated in NBP-treated mice compared to TBI-saline controls. In the assessment of the nuclear factor kappa-light-chain-enhancer of activated B (NF-κB) pathway, NBP ameliorated the p65 expression and the p-IκB-α/IκB-α ratio, indicating reduced NF-κB activation. Consistently, NBP reduced the upregulation of proinflammatory cytokines such as tumor ...
The Ingvarsson research group is focused on understanding what factors govern the distribution of genetic variation across plant genomes, and how this drives phenotypic variation in traits that are of adaptive or economic importance. We mainly rely on computational analyses of large-scale DNA sequencing data sets but also use data on gene expression and traditional genetic mapping in combination with field and greenhouse experiments. We are especially interested in understanding the genetic architecture of local adaptation in phenology and the relative importance of genetic drift, recombination and natural selection in driving genome-wide patterns of genetic diversity.. The Ingvarsson research group is located at the Department of Plant Biology, Swedish University of Agricultural Sciences in Uppsala, Sweden, although a few people remain at the Department of Ecology and Environmental Sciences, Umeå University where we were located from 2002 to 2016.. ...
Leroy E. Hood, will receive the 2017 NAS Award for Chemistry in Service to Society. Hood is a biotech visionary who has revolutionized biology and medicine in a career that spans five decades. Among his many accomplishments, Hood invented, commercialized, and developed multiple chemical tools that address biological complexity, including the automated DNA sequencer which spearheaded the Human Genome Project.. Hoods earlier research work at Caltech led to the development of four DNA and protein sequencers and synthesizers, all of which became core instruments for contemporary molecular biology. Later, Hoods lab developed the ink-jet oligonucleotide synthesizer, a core technology for DNA chip synthesis and large-scale DNA synthesis, and the first instrument capable of global single-molecule analysis of DNA and RNA molecules.. Beyond these innovations, Hood shepherded a cross-disciplinary approach to chemistry and biology, which led to the establishment of the Science and Technology Center for ...
1. Lipid-induced cell death - Investigation of the mechanism leading to lipotoxicity. 2. Meiotic Processes within the regulation of aging - characterization of the mechanism leading to longevity in yeast and mammalian cells. 3. Autophagy (self-eating) in dying cells - Interconnection of apoptosis and autophagy via a new Bcl-2 family-protein. 4. Identification of a novel yeast caspase - Functional analysis of the raptor- protein regarding the regulation of autophagy and apoptosis. 5. Yeast as a model for neurodegeneration - Parkinson´s, Alzheimer`s, and Huntington`s disease. 6. Caspase independent regulation of cell death - implications of apoptosis-inducing factor AIF1 and its interactom in aging and apoptosis. Contact: Prof. Dr. Frank Madeo. ...
Author(s): Nisar R, Hanson PS, He L, Taylor RW, Blain PG, Morris CM. Publication type: Article. Publication status: Published. Journal: Archives of Toxicology. Year: 2015. Volume: 89. Issue: 10. Pages: 1811-1825. Print publication date: 01/10/2015. Online publication date: 19/02/2015. Acceptance date: 06/01/2015. Date deposited: 01/07/2015. ISSN (print): 0340-5761. ISSN (electronic): 1432-0738. Publisher: Springer. URL: http://dx.doi.org/10.1007/s00204-015-1453-5. DOI: 10.1007/s00204-015-1453-5. PubMed id: 25693864. ...
|strong|Rabbit anti Endonuclease G antibody|/strong| recognizes human endonuclease G, also known as endoG. Endo G is a 297 amino acid, including a 48 amino acid transit peptide ~36 kDa mitochond…
Proper activation of DRs is critical in regulation of T cell development and function. However, the nature of functional receptors, which are expressed on T cells at stages characterized by resistance to the impact of FasL, TNF, and TRAIL, remains to be established. In this study, we have shown that engagement of distinct epitopes on CD99 induced rapid death signaling in the majority of immature T cell lines examined, apparently by a caspase-independent pathway. In contrast, only a few T cell lines were distinctly responsive to apoptosis-inducing anti-Fas and TRAIL. Differences between the Ad20/CD99-mediated death pathway and other novel nonclassical apoptotic pathways were also observed. Thus, our data suggest that CD99 may be a major DR used by the immune system to control T cells at stages before they acquire susceptibility to the impact of death-mediating cytokines of the TNF superfamily.. Previous studies have shown that activation of the CD99 domain specified by mAbs O662, L129, and DN16 ...
LB-18 compound: synthetic drug closely related to lembehyne-A (derived from a marine sponge) induces caspase-independent cell death to human neuroblastoma cells; structure in first source
Parthanatos (a programmed necrosis from PARP1 hyperactivation) is an untapped death mechanism in oncology, and it offers some ideal features for cancer treatments including immunogenicity and its independence from the drug resistance-ridden p53-apoptosis ...
This affordable Grim Reaper scythe lets everyone know their hourglass has run out. Molded plastic High Scythe features a classic silver scythe on a black pole.
This affordable Grim Reaper scythe lets everyone know their hourglass has run out. Molded plastic High Scythe features a classic silver scythe on a black pole.
Shop a large selection of products and learn more about Biomatik CorporationHuman Apoptosis Inducing Factor (AIF) ELISA Kit, 96 tests.
Gentaur molecular products has all kinds of products like :search , Prospecbio \ SDF 1a, His \ CHM-241 for more molecular products just contact us
Natural stone from the Slovakian Mala-Fatra Mountains. High density and very small material removal, for drawing out the cutting edge For honing du...
Sequencing-based approaches have led to new insights about DNA methylation. While many different techniques for genome-scale mapping of DNA methylation have been employed, throughput has been a key limitation for most. To further facilitate the mapping of DNA methylation, we describe a protocol for gel-free multiplexed reduced representation bisulfite sequencing (mRRBS) that reduces the workload dramatically and enables processing of 96 or more samples per week. mRRBS achieves similar CpG coverage to the original RRBS protocol, while the higher throughput and lower cost make it better suited for large-scale DNA methylation mapping studies, including cohorts of cancer samples. ...
Among the candidate cancer-prognostic genes is the p53 tumor suppressor gene, which, when mutated, plays an important role in the development of many types of cancers. To facilitate robust large-scale DNA analysis of microdissected tumor biopsies, we describe a multiplex/nested PCR approach for a simultaneous outer amplification of exons 4-9 of the human p53 gene with parallel amplification of the HLA-DQB1 locus, involving a total of 14 primers. This approach reduces the required number of cells for analysis and avoids any variation in the amplifications of the individual p53 exons during the common outer amplification step. The HLA sequencing allows sample identification because the DQB1 locus is highly polymorphic and is thereby patient-specific. The p53 and HLA amplicons are analyzed by solid-phase sequencing in a semiautomated format. To improve the DNA sequence quality, we used 2-deoxyribonucleoside 5-O-1-thiotriphosphates in the sequencing reactions.. ...
The Genome Sciences Centre sequencing platform is a high-throughput large-scale DNA analysis facility that has been designed to maximize capacity while maintaining efficiency, scalability and flexibility. The platform is one of the largest platforms of its type in Canada and is well recognized internationally.. Current production scale capabilities of the capillary based platform include fosmid end sequencing, PCR amplicon sequencing, plasmid, and BAC end sequencing. We have two Applied Biosytems 3730xls yielding a capacity of 7680 lanes per week, or approx 6 million Q20 bases per week. The GSC sequencing platform prides itself on its flexibility and molecular biology enabling PCR, BAC, fosmid and plasmid DNA preps and several optimized reaction chemistries, allowing us to provide high-quality, high-yield, consistent data generation.. More information on the Illumina Platform.. Through our sequencing validation team we offer several high quality, high throughput targeted sequencing services. We ...
Expression of AIF1 (AIF-1, Em:AF129756.17, IBA1, IRT-1) in liver tissue. Antibody staining with HPA049234 in immunohistochemistry.
Looks like i did it guys! I finally made a build on my own that did a GR 70! (Note i have never done a GR 70 before but specifically wanted to design my own build to do it) I know it might share some similarities to other builds but ultimately the only thing other builds influenced is choosing Mirinae over Bane of the powerful. I needed the healing to keep me alive. I manged to do a GR70 with just over 5 minutes remaining and only 3 deaths. I dont really know how to do a build guide but i just focoused on CHC and CHD as well as max essence. Beyond that the skills and items speak for themselves.. ...
Ibutamoren MK-677 je silný tabletkový stimulant tvorby vlastného rastového hormónu (endogénneho HGH) a silne anabolického hormónu IGF-1 v tele. Športovci tento suplement využívajú predovšetkým pre jeho excelentnú schopnosť pomáhať budovať nové svalové prírastky (dosahovať pozitívnu dusíkovú bilanciu.
Sea icicles forming on undercut lip of the Drygalski Ice Tongue from wave action and freezing seawater, Ross Sea, Antarctica District, Antarctica Region, Antarctica stock photo. Quality New Zealand images by well known photographer Rob Suisted, Natures Pic Images.
Discover how to get to The Westin Trillium House, Blue Mountain. Learn more about taxis, airport shuttles, parking and other means of transportation in Blue Mountains.
Pneumococcus is the most common and aggressive cause of bacterial meningitis and induces a novel apoptosis-inducing factor-dependent (AIF-dependent) form of brain cell apoptosis. Loss of production of two pneumococcal toxins, pneumolysin and H(2)O(2), eliminated mitochondrial damage and apoptosis. Purified pneumolysin or H(2)O(2) induced microglial and neuronal apoptosis in vitro. Both toxins induced increases of intracellular Ca(2+) and triggered the release of AIF from mitochondria. Chelating Ca(2+) effectively blocked AIF release and cell death. In experimental pneumococcal meningitis, pneumolysin colocalized with apoptotic neurons of the hippocampus, and infection with pneumococci unable to produce pneumolysin and H(2)O(2) significantly reduced damage. Two bacterial toxins, pneumolysin and, to a lesser extent, H(2)O(2), induce apoptosis by translocation of AIF, suggesting new neuroprotective strategies for pneumococcal meningitis ...
Its rare that we add a pony into our line-up, but the beautiful type that Harlequin gives his foals caught our attention. At just 12.2 hands, Woodburys Harlequin is an adorable option for sport pony breeders that are looking to emphasize jumping ability. His pedigree includes a high percentage of Welsh and Arabian blood, strongly consolidating his type and expression. Grandsire Neron stood in Holland and was approved with the NRPS. Neron was a very trainable and versatile talent, training both in dressage and jumping. Harlequins dam is herself a graded sports mare who has earned a Ster predicate. She was successful in both dressage, showjumping, and working hunter pony. Her sire, Moelview Mohawk, was highly successful showing in-hand and has produced both in-hand and undersaddle winners.. Harlequin was lightly shown in 2009 and 2010 with resounding success. He won 11 Champion or Reserve Champion placings in-hand and finished second at PoniesUK. Now being shown by a very young junior rider, ...
The SEA/GATOR complex is an essential regulator of the mTORC1 pathway. In mammals the GATOR1 complex is composed of the proteins DEPDC5, NPRL2 and NPRL3. GATOR1 serves as an mTORC1 inhibitor and activates the mTORC1-modulating RagA GTPase. However, several GATOR members have mTORC1 independent functions. Here we characterize mammalian cells overexpressing the GATOR1 component NPRL2. We demonstrate that, in the cells with active p53, ectopic expression of NPRL2 induces NOX2-dependent production of reactive oxygen species and DNA damage. Overexpressed NPRL2 accumulates in the nucleus, together with apoptosis-inducing factor (AIF). These events are accompanied by phosphorylation of p53, activation of a DNA-damage response and cell cycle arrest in G1 phase, followed by apoptosis. In the cells negative for active p53, NPRL2 ectopic expression leads to activation of CHK1 or CHK2 kinases and cell cycle arrest in S or G2/M phases. Combined, these results demonstrate a new role for the NPRL2, distinct from its
Interest in potential cancer chemopreventive and therapeutic properties of dietary ingredients, which are generally more tolerable in the human body ( 15), has increased in recent years, especially for the cancers that usually do not respond well to currently available therapies ( 17). Therefore, it is not surprising that chemoprevention of colon cancer, the leading cancer-related death in Western countries, is becoming more attractive. One of the dietary ingredients that possess anti-inflammatory and/or antioxidant properties is curcumin. Epidemiologic data suggest that curcumin may be responsible for the lower colon cancer rate in India and Southeast Asia ( 39). Based on that and its long history of consumption without any adverse health effects, curcumin is considered to be a safe chemopreventative agent ( 15).. Although it was suggested previously that curcumin-induced apoptosis is mediated through the impairment of the ubiquitin-proteasome pathway ( 40), the exact mechanism was not fully ...
Fingerprint Dive into the research topics of Molecular mechanisms of curcumin-induced cytotoxicity: Induction of apoptosis through generation of reactive oxygen species, down-regulation of Bcl-X,sub,L,/sub, and IAP, the release of cytochrome c and inhibition of Akt. Together they form a unique fingerprint. ...
Precisely blended botanicals to emulate Harlequins flavor & attributes found in nature!. Channel the all-day fun of the pantomiming street jester without losing too much edge on the sense of humor, with the sativa Harlequin. Super-high Myrcene counts allow for a focused and light-hearted experience without too much psychoactive, fast-thinking side effects, making it ideal for novice users or those looking for pain relief. ...
Expression of AIF1 (AIF-1, Em:AF129756.17, IBA1, IRT-1) in kidney tissue. Antibody staining with HPA049234 in immunohistochemistry.
|b|The truth will set you free—if it doesnt get you killed|/b||Br||Br|Savannah Slade is not the person she thought she was. The reading of her fathers will has led her to a world-shattering...|/em||/strong||/b||/i|
|strong|Rowan Summerwaite is ready to finish what she started in |/strong||strong||em|Blood and Blade|/em||/strong||strong|, the next installment in the Goddess with a Blade series by...|/em||/strong||/b||/i|
I just built GIGABYTE GA-P35-DS3R Intel Core 2 Duo E6750 Scythe Infinity HSF eVGA 8800GTS 320MB Superclocked 2x1GB Crucial Ballastix (MicronD9GMH)...
Castedo M, Perfettini JL, Andreau K, Roumier T, Piacentini M, Kroemer G (Dec 2003). "Mitochondrial apoptosis induced by the HIV ... Upon release of cytochrome c to the cytoplasm, the protein binds apoptotic protease activating factor-1 (Apaf-1).[5] ... Role in apoptosis[edit]. Cytochrome c also has an intermediate role in apoptosis, a controlled form of cell death used to kill ... Inhibition of apoptosis[edit]. One of the ways cell apoptosis is activated is by release of cytochrome c from the mitochondria ...
Executioner caspases degrade over 600 cellular components[18] in order to induce the morphological changes for apoptosis. ... There is evidence where it promotes transcription of nuclear factor-κB (NF-κB), a transcription factor that assists in ... Apoptosis[edit]. Apoptosis is a form of programmed cell death where the cell undergoes morphological changes, to minimize its ... The Mechanisms of Apoptosis Kimball's Biology Pages. Simple explanation of the mechanisms of apoptosis triggered by internal ...
Gupta S (2002). "Tumor necrosis factor-alpha-induced apoptosis in T cells from aged humans: a role of TNFR-I and downstream ... "TRAF1 is a substrate of caspases activated during tumor necrosis factor receptor-alpha-induced apoptosis". J. Biol. Chem. 276 ( ... Cowling V, Downward J (October 2002). "Caspase-6 is the direct activator of caspase-8 in the cytochrome c-induced apoptosis ... Guo Y, Srinivasula SM, Druilhe A, Fernandes-Alnemri T, Alnemri ES (April 2002). "Caspase-2 induces apoptosis by releasing ...
In animals apoptosis is induced by caspases and in fungi and plants, apoptosis is induced by arginine and lysine-specific ... There is evidence where it promotes transcription of nuclear factor-κB (NF-κB), a transcription factor that assists in ... Executioner caspases degrade over 600 cellular components[18] in order to induce the morphological changes for apoptosis. ... The Mechanisms of Apoptosis Kimball's Biology Pages. Simple explanation of the mechanisms of apoptosis triggered by internal ...
"Apoptosis-inducing factor CA 2352467 A1". Retrieved 9 August 2015. "Apoptosis-inducing factor CA 2352467 C". Retrieved 9 August ...
"Apoptosis-inducing factor (AIF): a ubiquitous mitochondrial oxidoreductase involved in apoptosis". FEBS Letters. 476 (3): 118- ... Apoptosis-inducing factor 1, mitochondrial is a protein that in humans is encoded by the AIFM1 gene on the X chromosome. This ... "Entrez Gene: AIFM1 apoptosis-inducing factor, mitochondrion-associated, 1". Ferreira P, Villanueva R, Martínez-Júlvez M, ... Candé C, Cohen I, Daugas E, Ravagnan L, Larochette N, Zamzami N, Kroemer G (2002). "Apoptosis-inducing factor (AIF): a novel ...
"Entrez Gene: SIVA1 SIVA1, apoptosis-inducing factor". CS1 maint: discouraged parameter (link) Fortin A, MacLaurin JG, Arbour N ... is sufficient to bind to BCL-XL and sensitize cells to UV radiation induced apoptosis". Apoptosis. 9 (1): 83-95. doi:10.1023/B: ... Siva protein is a zinc-containing intracellular ligand of the CD4 receptor that promotes HIV-1 envelope-induced apoptosis in T- ... 2002). "Siva-1 binds to and inhibits BCL-X(L)-mediated protection against UV radiation-induced apoptosis". Proc. Natl. Acad. ...
... apoptosis by acting on the caspase-dependent pathway and against apoptosis-inducing agents such as tumor necrosis factor-α (TNF ... "Heat-shock protein 70 antagonizes apoptosis-inducing factor". Nat. Cell Biol. 3 (9): 839-43. doi:10.1038/ncb0901-839. PMID ... "Heat shock protein 72 suppresses apoptosis by increasing the stability of X-linked inhibitor of apoptosis protein in renal ... Apoptosis occurs in many physiological and pathological processes. It plays an important role during embryonal development as ...
The research centers on the Harlequin mice, who have a proviral insertion in the apoptosis-inducing factor (AIF) gene. The AIF ... "The harlequin mouse mutation downregulates apoptosis-inducing factor". Nature. 419 (6905): 367-374. Bibcode:2002Natur.419..367K ... Ribosome stalling induced by mutation of a CNS-specific tRNA causes neurodegeneration". Science. 345 (6195): 455-459. doi: ... Her work has highlighted some of the genetic and biochemical factors that are involved in the development of the central ...
"Induction of interferon-alpha and tumor necrosis factor-related apoptosis-inducing ligand in human blood mononuclear cells by ... SeV induces the production of B cell-activating factor by monocytes and by some other cells. Heat-inactivated SeV virus induces ... SeV induces the production of B cell-activating factor by monocytes and by some other cells. Heat-inactivated SeV virus induces ... "The IRF-3 transcription factor mediates Sendai virus-induced apoptosis". Journal of Virology. 74 (8): 3781-92. doi:10.1128/jvi. ...
PAR causes translocation of apoptosis-inducing factor (AIF) from the mitochondria to the nucleus where it induces DNA ... Apoptosis inducing factor Programmed cell death PARP1 David, Karen Kate; Andrabi, Shaida Ahmad; Dawson, Ted Murray; Dawson, ... Binding to Apoptosis-Inducing Factor Is Critical For PAR Polymerase-1-Dependent Cell Death (Parthanatos)". Science Signaling. 4 ... "Apoptosis-Inducing Factor Substitutes for Caspase Executioners in NMDA-Triggered Excitotoxic Neuronal Death". The Journal of ...
"Overexpression of the chromosome 21 transcription factor Ets2 induces neuronal apoptosis". Neurobiology of Disease. 14 (3): 349 ... ETS domain-containing transcription factor ERF is a protein that in humans is encoded by the ERF gene. GRCh38: Ensembl release ... "Entrez Gene: ERF Ets2 repressor factor". Liu D, Pavlopoulos E, Modi W, Moschonas N, Mavrothalassitis G (March 1997). "ERF: ... Bain M, Mendelson M, Sinclair J (January 2003). "Ets-2 Repressor Factor (ERF) mediates repression of the human cytomegalovirus ...
"FOXO proteins regulate tumor necrosis factor-related apoptosis inducing ligand expression. Implications for PTEN mutation in ... 2018) demonstrated that FOXO3a activation in vascular smooth muscle cells induces prominent apoptosis and extracellular matrix ... "The BH3-only protein Puma plays an essential role in cytokine deprivation induced apoptosis of mast cells". Blood. 110 (9): ... "Phosphorylation of forkhead transcription factors by erythropoietin and stem cell factor prevents acetylation and their ...
Moreover, PTP opening induce releasing of caspase-activating factors and apoptosis. Caspase-activating factors induced by ... which is acts as a trigger for apoptosis. MOMP is the process before apoptosis, which is accompanied to permeability of the ... 2012). "PERK is required at the ER-mitochondrial contact sites to convey apoptosis after ROS-based ER stress". Cell Death ... PERK contributes to apoptosis twofold by sustaining the levels of pro-apoptotic C/EBP homologous protein (CHOP). A tight ER- ...
The mitosis promoting factor MPF also regulates DNA-damage induced apoptosis. Negative regulation of MPF by WEE1 causes ... Kruppel-like factor 2 (KLF2) negatively regulates human WEE1, thus increasing sensitivity to DNA-damage induced apoptosis in ... June 2005). "Transcriptional repression of WEE1 by Kruppel-like factor 2 is involved in DNA damage-induced apoptosis". Oncogene ... Besides environmental factors such as nutrients, growth factors and functional load, cell size is also controlled by a cellular ...
Her research team discovered that PAR leads to cell death by facilitating the release of apoptosis inducing factor (AIF) factor ... "Apoptosis-inducing factor mediates poly(ADP-ribose) (PAR) polymer-induced cell death". Proceedings of the National Academy of ... binding to apoptosis-inducing factor is critical for PAR polymerase-1-dependent cell death (parthanatos)". Science Signaling. 4 ... polymerase-1-dependent cell death by apoptosis-inducing factor". Science. 297 (5579): 259-63. Bibcode:2002Sci...297..259Y. doi: ...
"Plasminogen activator inhibitor type 2 inhibits tumor necrosis factor alpha-induced apoptosis. Evidence for an alternate ... gene are associated with basal and tumor necrosis factor-alpha-induced transcription in monocytes". European Journal of ... Due to its position on chromosome 18 close to the bcl-2 protooncogene and several other serpins, PAI-2's role in apoptosis has ... PAI-2 provides protection for cancer cells against plasmin-induced cell death, which can exert a lethal effect on tumors. This ...
"Apoptosis-inducing factor mediates poly(ADP-ribose) (PAR) polymer-induced cell death". Proceedings of the National Academy of ... Also, it plays an integral role in cleavage-induced inactivation. The main role of PARP (found in the cell nucleus) is to ... ATP depletion in a cell leads to lysis and cell death (necrosis). PARP also has the ability to induce programmed cell death, ... This model suggests that this "sugar plug" can also begin the signal for apoptosis. Roles of poly(ADP-ribosyl)ation in plant ...
... apoptosis by acting on the caspase-dependent pathway and against apoptosis-inducing agents such as tumor necrosis factor-α (TNF ... "HSP72 inhibits apoptosis-inducing factor release in ATP-depleted renal epithelial cells". Am. J. Physiol., Cell Physiol. 285 (6 ... "Heat-shock protein 70 antagonizes apoptosis-inducing factor". Nat. Cell Biol. 3 (9): 839-43. doi:10.1038/ncb0901-839. PMID ... "Heat shock protein 72 suppresses apoptosis by increasing the stability of X-linked inhibitor of apoptosis protein in renal ...
2006). "Apoptosis-inducing factor mediates poly(ADP-ribose) (PAR) polymer-induced cell death". Proc Natl Acad Sci U S A. 103 ( ... 2006). "Apoptosis-inducing factor substitutes for caspase executioners in NMDA-triggered excitotoxic neuronal death". J ... 2011). "Poly(ADP-ribose) (PAR) binding to apoptosis-inducing factor is critical for PAR polymerase-1-dependent cell death ( ... 2002). "Mediation of poly(ADP-ribose) polymerase-1-dependent cell death by apoptosis-inducing factor". Science. 297 (5579): 259 ...
... and acts as an autocrine factor to induce apoptosis in endothelial cells. This cytokine is also found to inhibit endothelial ... a novel tumor necrosis factor-like cytokine, induces apoptosis in endothelial cells. Involvement of activation of stress ... "TL1A-induced NF-kappaB activation and c-IAP2 production prevent DR3-mediated apoptosis in TF-1 cells". The Journal of ... Prehn JL, Thomas LS, Landers CJ, Yu QT, Michelsen KS, Targan SR (Apr 2007). "The T cell costimulator TL1A is induced by ...
... an apoptosis-inducing factor-homologous mitochondrion-associated protein, induces caspase-independent apoptosis". J. Biol. Chem ... "Tumor necrosis factor-related apoptosis-inducing ligand receptors signal NF-kappaB and JNK activation and apoptosis through ... They discovered that a signaling cascade can mediate TRAIL-induced NF-κB activation, and TRAIL-induced apoptosis cannot be ... It was named VISA (virus-induced signaling adaptor). It can also interact with TRIF and TRAF6, and plays an essential role in ...
Park MY, Ryu SW, Kim KD, Lim JS, Lee ZW, Kim E (2005). "Fas-associated factor-1 mediates chemotherapeutic-induced apoptosis via ... Overexpression of this gene was shown to induce weak apoptosis. Upon stimulation, this protein was found to translocate from ... "DEDD regulates degradation of intermediate filaments during apoptosis". J. Cell Biol. 158 (6): 1051-66. doi:10.1083/jcb. ... cytoplasm to nucleus and colocalize with UBTF, a basal factor required for RNA polymerase I transcription, in the nucleolus. At ...
Bucur O, Ray S, Bucur MC, Almasan A (May 2006). "APO2 ligand/tumor necrosis factor-related apoptosis-inducing ligand in ... In the field of cell biology, TNF-related apoptosis-inducing ligand (TRAIL), is a protein functioning as a ligand that induces ... These artificial TRAIL mimics bind to DR4/DR5 on cancer cells and induce cell death via both apoptosis and necrosis, which ... tumor necrosis factor receptor superfamily binding. • tumor necrosis factor receptor binding. • receptor binding. • zinc ion ...
4-trisphosphate 5/6-kinase inhibits tumor necrosis factor-induced apoptosis". J. Biol. Chem. 278 (44): 43645-53. doi:10.1074/ ... 4-trisphosphate 5/6-kinase is a protein kinase that phosphorylates the transcription factors c-Jun and ATF-2". J. Biol. Chem. ...
... "mHGTD-P mediates hypoxic neuronal cell death via the release of apoptosis-inducing factor". Neuroscience Letters. 416 (2): 144- ... Human growth and transformation-dependent protein (HGTD-P) is involved in intrinsic apoptosis. Apoptosis, an ancient Greek word ... This protein promotes intrinsic apoptosis in response to hypoxia via interactions with hypoxia-inducible factor-1α (HIF-1α). As ... "MiR-139-5p inhibits HGTD-P and regulates neuronal apoptosis induced by hypoxia-ischemia in neonatal rats". Neurobiology of ...
Li S, Yu W, Hu GF (2012). "Angiogenin inhibits nuclear translocation of apoptosis inducing factor in a Bcl-2-dependent manner ... which subsequently activates other angiogenic factors that induce angiogenesis. However, angiogenin is unique among the many ... Fu H, Feng J, Liu Q, Sun F, Tie Y, Zhu J, Xing R, Sun Z, Zheng X (2008). "Stress induces tRNA cleavage by angiogenin in ... The angiogenic factors associated with Ang may protect the central nervous system and MNs directly. Experiments with wild type ...
... identification of regions that mediate nerve growth factor-induced apoptosis". J. Biol. Chem. 277 (16): 13973-82. doi:10.1074/ ... Yoon K, Jang HD, Lee SY (2004). "Direct interaction of Smac with NADE promotes TRAIL-induced apoptosis". Biochem. Biophys. Res ... "Entrez Gene: NGFRAP1 nerve growth factor receptor (TNFRSF16) associated protein 1". Kimura MT, Irie S, Shoji-Hoshino S, Mukai J ... NGFRAP1 has been shown to interact with YWHAE and Low affinity nerve growth factor receptor. GRCh38: Ensembl release 89: ...
Regulated cell death (apoptosis) is induced by events such as growth factor withdrawal and toxins. It is controlled by ... Rho inhibition induces caspase-9 and caspase-3-dependent apoptosis of cultured human endothelial cells. These proteins are ... Martinez-Caballero S, Dejean LM, Jonas EA, Kinnally KW (June 2005). "The role of the mitochondrial apoptosis induced channel ... Dejean LM, Martinez-Caballero S, Manon S, Kinnally KW (February 2006). "Regulation of the mitochondrial apoptosis-induced ...
... a new member of the tumor necrosis factor family, modulates death ligand-induced apoptosis". Cell Death and Differentiation. 8 ... A proliferation-inducing ligand (APRIL), also known as tumor necrosis factor ligand superfamily member 13 (TNFSF13), is a ... In vitro experiments suggested that this protein may be able to induce apoptosis through its interaction with other TNF ... The protein encoded by this gene is a member of the tumor necrosis factor ligand (TNF) ligand family. This protein is a ligand ...
An induced rebinding model of antigen discrimination. Trends Immunol. 2014, 35 (4): 153-8. PMC 3989030. PMID 24636916. doi: ... Alpha-lactose reverses liver injury via blockade of Tim-3-mediated CD8 apoptosis in sepsis. Clinical Immunology. July 2018, 192 ... Cell-intrinsic transforming growth factor-beta signaling mediates virus-specific CD8+ T cell deletion and viral persistence in ... IL-10 Induces T Cell Exhaustion During Transplantation of Virus Infected Hearts. Cellular Physiology and Biochemistry. 2016, 38 ...
While some of these factors are under personal control, such as diet and obesity, other factors are not, such as increasing age ... Izzedine H, Launay-Vacher V, Deybach C, Bourry E, Barrou B, Deray G (November 2005). "Drug-induced diabetes mellitus". Expert ... resulting in apopotosis of the beta cells.[52] ... Lifestyle factors are important to the development of type 2 ... Dietary factors also influence the risk of developing type 2 diabetes. Consumption of sugar-sweetened drinks in excess is ...
Polysaccharide K can promote apoptosis by inhibiting NF-κB activation, which is normally up-regulated, and inhibiting apoptosis ... It has been shown that HIF-1α can induce the EMT pathway, as well as the Wnt/β-catenin signaling pathway, thus enhancing the ... Yi ZY, Feng LJ, Xiang Z, Yao H (2011). "Vascular endothelial growth factor receptor-1 activation mediates epithelial to ... There are other physiological factors that are associated with cancer development through their interactions with catenins. For ...
HMB supplementation may be useful in the prevention of muscle atrophy induced by bed rest or other factors. Further studies are ... apoptosis, and the regenerative process), whereas it is hypothesized to strongly affect the fourth (mitochondrial dynamics and ... Another factor that contributes to the sustaining of muscle strength in hibernating bears is the occurrence of periodic ... Therefore, one way in which not exercise induces an increase in muscle mass is to down regulate the pathways which have the ...
"Inhibitor of apoptosis proteins (IAPs) and their antagonists regulate spontaneous and tumor necrosis factor (TNF)-induced ... SP can induce the cytokines that are capable of inducing NK-1 transcription factors.[14] ... Chemotherapy induced nausea and vomitingEdit. Further information: Chemotherapy-induced nausea and vomiting and Aprepitant ... "Metalloproteinases and transforming growth factor-alpha mediate substance P-induced mitogen-activated protein kinase activation ...
Some studies have suggested that the renal PAX genes act as pro-survival factors and allow tumor cells to resist apoptosis. ... Down regulation of the PAX gene expression inhibits cell growth and induces apoptosis. This could be a possible avenue for ... "The paired domain-containing factor Pax8 and the homeodomain-containing factor TTF-1 directly interact and synergistically ... "The paired domain-containing factor Pax8 and the homeodomain-containing factor TTF-1 directly interact and synergistically ...
In the brain, B. burgdorferi may induce astrocytes to undergo astrogliosis (proliferation followed by apoptosis), which may ... Urbanization and other anthropogenic factors can be implicated in the spread of Lyme disease to humans. In many areas, ... Borrelia burgdorferi lipoproteins induce both proliferation and apoptosis in rhesus monkey astrocytes". European Journal of ... a form of pathogen-induced autoimmune disease.[97] The production of this reaction might be due to a form of molecular mimicry ...
NMDA induces a calcium flux that allows for synaptic plasticity which is crucial for AHN. ... with beta-catenin and T-cell factor 4 may bypass canonical Wnt signaling to down-regulate adipogenic transcription factors". ... "Relative potency of testosterone and dihydrotestosterone in preventing atrophy and apoptosis in the prostate of the castrated ... "Recruitment of the androgen receptor via serum response factor facilitates expression of a myogenic gene". The Journal of ...
regulation of epidermal growth factor-activated receptor activity. • regulation of resting membrane potential. • regulation of ... Schroeter EH, Kisslinger JA, Kopan R (May 1998). "Notch-1 signalling requires ligand-induced proteolytic release of ... "Two types of human malignant melanoma cell lines revealed by expression patterns of mitochondrial and survival-apoptosis genes ... negative regulation of epidermal growth factor-activated receptor activity. • cell adhesion. • hematopoietic progenitor cell ...
DNA damage-induced oocyte apoptosis depends on the efficiency of the DNA repair machinery that in turn declines with age. ... Sigurdsson S, Van Komen S, Petukhova G, Sung P (Nov 2002). "Homologous DNA pairing by human recombination factors Rad51 and ... Welch C, Chen Y, Stallings RL (2007). "MicroRNA-34a functions as a potential tumor suppressor by inducing apoptosis in ... The Rad51-induced oocyte resistance to apoptosis is likely due to Rad51's central role in homologous recombinational repair of ...
1997). "CD2 induced apoptosis of peripheral T cells.". Transplant. Proc. 29 (5): 2377-8. PMID 9270771. doi:10.1016/S0041-1345( ... Lüscher B (2001). "Function and regulation of the transcription factors of the Myc/Max/Mad network.". Gene 277 (1-2): 1-14. ...
CIAPIN1: Anamorsin (originally, Cytokine induced apoptosis inhibitor 1). *CKLF: Chemokine-like factor ... PMFBP1: encoding protein Polyamine-modulated factor 1-binding protein 1. *POLR3K: encoding enzyme DNA-directed RNA polymerase ... ARL6IP1: encoding protein ADP-ribosylation factor-like protein 6-interacting protein 1 ...
"Sterile 20 kinase phosphorylates histone H2B at serine 10 during hydrogen peroxide-induced apoptosis in S. cerevisiae". Cell. ... SBF is a transcription factor that is activated in late G1 phase, when it dissociates from its repressor Whi5. This occurs when ... The serotonylation potentiates the binding of the general transcription factor TFIID to the TATA box.[49] ... a late acting bystander in apoptosis as yeast carrying mutations of this residue are resistant to hydrogen peroxide-induced ...
Chan-Hui PY, Weaver R (1999). "Human mitogen-activated protein kinase kinase kinase mediates the stress-induced activation of ... 1997). "Stress-signalling kinase Sek1 protects thymocytes from apoptosis mediated by CD95 and CD3". Nature. 385 (6614): 350-3. ... activator SEK-1 and is required for tumor necrosis factor-alpha activation of SAPK in melanoma cells". J. Biol. Chem. UNITED ... activator SEK-1 and is required for tumor necrosis factor-alpha activation of SAPK in melanoma cells". J. Biol. Chem. 272 (5): ...
Prolonged hypoxia induces neuronal cell death via apoptosis, resulting in a hypoxic brain injury.[1][2] ... Jan 2002). "Prevalence and risk factors of silent brain infarcts in the population-based Rotterdam Scan Study". Stroke. 33 (1 ... Nov 2001). "Hypoxia induces apoptosis via two independent pathways in Jurkat cells: differential regulation by glucose". ... Recent research suggests this may be due to an autoimmune response caused by carbon monoxide-induced changes in the myelin ...
Slack SE, Pezet S, McMahon SB, Thompson SW, Malcangio M (October 2004). "Brain-derived neurotrophic factor induces NMDA ... neurotrophic signaling may trigger apoptosis rather than survival pathways in cells expressing the p75 receptor in the absence ... BDNF, brain-derived neurotrophic factor, ANON2, BULN2, Brain-derived neurotrophic factor, brain derived neurotrophic factor. ... Brain-derived neurotrophic factor (BDNF), or abrineurin,[5] is a protein[6] that, in humans, is encoded by the BDNF gene.[7][8] ...
Nelson AM, Gilliland KL, Cong Z, Thiboutot DM (October 2006). "13-cis Retinoic acid induces apoptosis and cell cycle arrest in ... Risk factors for skeletal effects include older age, greater dosage and longer course of treatment. Most bone changes cause no ... Isotretinoin's exact mechanism of action is unknown, but several studies have shown that isotretinoin induces apoptosis ( ... which has been shown to reduce sebum production by inducing apoptosis in sebaceous gland cells, while exhibiting an ...
... apoptosis has been shown to enhance apoptosis caused by chemotherapeutic drugs through autocrine-secreted tumor necrosis factor ... "Autocrine TNFα Signaling Renders Human Cancer Cells Susceptible to Smac-Mimetic-Induced Apoptosis". Cancer Cell. 12 (5): 445-56 ... Paracrine signaling is a form of cell-cell communication in which a cell produces a signal to induce changes in nearby cells, ... One approach used by tumors to upregulate growth and survival is through autocrine production of growth and survival factors. ...
Rapamycin potentiates transforming growth factor beta-induced growth arrest in nontransformed, oncogene-transformed, and human ... Rodriguez R, Meuth M. Chk1 and p21 cooperate to prevent apoptosis during DNA replication fork stress. „Mol. Biol. Cell". 17 (1 ... Yu P, Huang B, Shen M, Lau C, Chan E, Michel J, Xiong Y, Payan DG, Luo Y. p15(PAF), a novel PCNA associated factor with ... overcome Bcl-2 protective function and selectively accumulate the cyclin-dependent kinase inhibitor p27 and induce apoptosis in ...
Kawamura C, Kizaki M, Ikeda Y (2003). "Bone morphogenetic protein (BMP)-2 induces apoptosis in human myeloma cells.". Leuk. ... Chen D, Zhao M, Mundy GR (December 2004). "Bone morphogenetic proteins". Growth Factors 22 (4): 233-41. PMID 15621726. doi: ... "Bovine osteogenic protein is composed of dimers of OP-1 and BMP-2A, two members of the transforming growth factor-beta ...
2002). "EBV regulates c-MYC, apoptosis, and tumorigenicity in Burkitt's lymphoma". Curr. Top. Microbiol. Immunol. 258: 153-60. ... Lüscher B (2001). "Function and regulation of the transcription factors of the Myc/Max/Mad network". Gene 277 (1-2): 1-14. PMID ... Coller HA, Forman JJ, Legesse-Miller A (2007). ""Myc'ed Messages": Myc Induces Transcription of E2F1 while Inhibiting Its ... a widespread euchromatic program in the human genome partially independent of its role as a classical transcription factor". ...
Degradation of Aux/IAA proteins derepresses transcription factors in the auxin-response factor (ARF) family and induces ARF- ... ApoptosisEdit. Both internal and external signals can lead to the induction of apoptosis, or programmed cell death. The ... Proteasome inhibitors have effective anti-tumor activity in cell culture, inducing apoptosis by disrupting the regulated ... "26S proteasome inhibition induces apoptosis and limits growth of human pancreatic cancer". Journal of Cellular Biochemistry. 82 ...
... where they induce IFN production with the presence of a particular transcription factor and activate transcription factor 2. ... When host cells die, either by programmed cell death (also called apoptosis) or by cell injury due to a bacterial or viral ... inducing dimerization of transcription factors IRF3 and IRF7, which are translocated in the nucleus, ... Chemical factors produced during inflammation (histamine, bradykinin, serotonin, leukotrienes, and prostaglandins) sensitize ...
2004). "The glutamine-rich region of the HIV-1 Tat protein is involved in T-cell apoptosis". J. Biol. Chem. 279 (46): 48197- ... Pathogenesis of HIV-induced lesions of the brain, correlations with HIV-associated disorders and modifications according to ... 2004). "Identification of modifiable factors that affect the genetic diversity of the transmitted HIV-1 population". AIDS 18 (4 ... Bentwich Z, Kalinkovich, A, Weisman Z (1995). "Immune activation is a dominant factor in the pathogenesis of African AIDS.". ...
TRAF-2 mediates CD30-induced nuclear factor kappa B activation". Proceedings of the National Academy of Sciences of the United ... It is a positive regulator of apoptosis, and also has been shown to limit the proliferative potential of autoreactive CD8 ... tumor necrosis factor-activated receptor activity. • nerve growth factor binding. Cellular component. • cytoplasm. • integral ... "Tumor necrosis factor receptor-associated factor (TRAF) 5 and TRAF2 are involved in CD30-mediated NFkappaB activation". The ...
The second strategy is to inhibit autophagy and thus induce apoptosis.[85] ... There is evidence that emphasizes the role of autophagy both as a tumor suppressor as well as a factor in tumor cell survival. ... significantly inhibited cell proliferation by inducing autophagic cell death rather than typical apoptosis in a HepG2 human ... Tavassoly, Iman (2015). Dynamics of Cell Fate Decision Mediated by the Interplay of Autophagy and Apoptosis in Cancer Cells. ...
In order to induce an immune response, it needs to be attached to a large carrier molecule such as a protein (a complex of ... If activated cytotoxic CD8+ T cells recognize them, the T cells secrete various toxins that cause the lysis or apoptosis of the ... These algorithms consider factors such as the likelihood of proteasomal processing, transport into the endoplasmic reticulum, ... Furthermore, for a peptide to induce an immune response (activation of T-cells by antigen-presenting cells) it must be a large ...
"12/15-Lipoxygenase Contributes to Platelet-derived Growth Factor-induced Activation of Signal Transducer and Activator of ... Platelet-derived growth factor (PDGF) is one among numerous growth factors that regulate cell growth and division. In ... Other growth factors in this family include vascular endothelial growth factors B and C (VEGF-B, VEGF-C)[16][17] which are ... "Vascular endothelial growth factor: A new member of the platelet-derived growth factor gene family". Biochemical and ...
transcription factor complex. • bicellular tight junction. • nucleoplasm. • nucleolus. • perinuclear region of cytoplasm. • ... Overview of signal transduction pathways involved in apoptosis. (CDK4 in the (pink) nucleus) ... "Cyclin-dependent kinases are inactivated by a combination of p21 and Thr-14/Tyr-15 phosphorylation after UV-induced DNA damage ... Phosphorylation of RB1 allows dissociation of the transcription factor E2F from the RB/E2F complexes and the subsequent ...
... apoptosis of neurons by a mechanism involving activation of the transcription factor NF-kappaB which induces the expression of ... TNF, DIF, TNF-alpha, TNFA, TNFSF2, Tumour necrosis factor, TNF-α, tumor necrosis factor, TNLG1F, Tumor necrosis factor alpha. ... Tumor necrosis factor (TNF, tumor necrosis factor alpha, TNFα, cachexin, or cachectin) is a cell signaling protein (cytokine) ... reported another cytotoxic factor produced by macrophages and named it tumor necrosis factor (TNF).[14] Both factors were ...
Apoptosis-inducing factor (AIF): caspase-independent after all.. Candé C1, Vahsen N, Garrido C, Kroemer G. ...
Here we report the identification and cloning of an apoptosis-inducing factor, AIF, which is sufficient to induce apoptosis of ... Molecular characterization of mitochondrial apoptosis-inducing factor.. Susin SA1, Lorenzo HK, Zamzami N, Marzo I, Snow BE, ... it is normally confined to mitochondria but translocates to the nucleus when apoptosis is induced. Recombinant AIF causes ... It induces purified mitochondria to release the apoptogenic proteins cytochrome c and caspase-9. Microinjection of AIF into the ...
Compare Anti-SIVA1 apoptosis inducing factor Antibody Products from leading suppliers on Biocompare. View specifications, ... Anti-SIVA1 apoptosis inducing factor Antibody Products. Anti-SIVA1 apoptosis inducing factor antibodies are available from ... Your search returned 130 SIVA1 apoptosis inducing factor Antibodies across 24 suppliers. ... The protein may also be known as CD27BP, Siva-1, Siva-2, apoptosis regulatory protein Siva, and CD27-binding (Siva) protein. ...
... pylori-induced apoptosis in human gastric cancer cells mediated via the release of apoptosis-inducing factor from mitochondria ... Apoptosis-inducing factor, mitochondria-associated 3 is a protein that in humans is encoded by the AIFM3 gene. GRCh38: Ensembl ... "Entrez Gene: Apoptosis inducing factor, mitochondria associated 3". Retrieved 2017-10-24. Xie Q, Lin T, Zhang Y, Zheng J, ... induces apoptosis and enhances radiosensitivity in hypoxic human hepatoma cells in vitro". Exp. Cell Res. 318 (8): 944-54. doi: ...
Shop a large selection of products and learn more about Biomatik CorporationHuman Apoptosis Inducing Factor (AIF) ELISA Kit, 96 ... The Human Apoptosis Inducing Factor (AIF) ELISA Kit allows for quantitative determination of Apoptosis Inducing Factor in Serum ... Cross Activity: No significant cross-reactivity or interference between Apoptosis Inducing Factor and analogues was observed. ...
J:117434 Prasad KV, et al., CD27, a member of the tumor necrosis factor receptor family, induces apoptosis and binds to Siva, a ...
Both were biologically active, inducing apoptosis of both hu … ... To evaluate the utility of tumor necrosis factor-related ... apoptosis-inducing ligand (TRAIL) as a cancer therapeutic, we created leucine zipper (LZ) forms of human (hu) and murine (mu) ... Tumoricidal activity of tumor necrosis factor-related apoptosis-inducing ligand in vivo Nat Med. 1999 Feb;5(2):157-63. doi: ... To evaluate the utility of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) as a cancer therapeutic, we created ...
Apoptosis-inducing factor 1, mitochondrialImported. ,p>Information which has been imported from another database using ... tr,E9PRR0,E9PRR0_HUMAN Apoptosis-inducing factor 1, mitochondrial OS=Homo sapiens OX=9606 GN=AIFM1 PE=4 SV=1 ...
Apoptosis-Inducing Factor), Authors: João Agostinho Machado-Neto, Fabiola Traina. Published in: Atlas Genet Cytogenet Oncol ... SIVA1 (SIVA1, Apoptosis-Inducing Factor). Written. 2013-10. João Agostinho Machado-Neto, Fabiola Traina. ... CD27, a member of the tumor necrosis factor receptor family, induces apoptosis and binds to Siva, a proapoptotic protein.. ... SIVA1 overexpression induces apoptosis (Py et al., 2004), while SIVA1 inhibition reduces apoptosis (Resch et al., 2009).. ...
A flavoprotein that functions as a powerful antioxidant in the MITOCHONDRIA and promotes APOPTOSIS when released from the ... AIF Apoptosis Regulatory Protein; Apoptosis-Inducing Factor; Mitochondrial Apoptosis-Inducing Factor; Apoptosis-Inducing Factor ... Apoptosis Inducing Factor. Subscribe to New Research on Apoptosis Inducing Factor A flavoprotein that functions as a powerful ... 11/01/2005 - "Tumour necrosis factor-induced death of adult human oligodendrocytes is mediated by apoptosis inducing factor.". ...
... and nuclear translocation of apoptosis-inducing factor (AIF) in montelukast-treated lung cancer cells. Montelukast also ... In conclusion, montelukast induced lung cancer cell death via the nuclear translocation of AIF. This study confirmed the chemo- ... Montelukast inhibited cell proliferation and colony formation and induced the cell death of lung cancer cells. Further ... apoptosis-inducing factor; asthma cysteinyl leukotriene receptor antagonists; montelukast; lung cancer; apoptosis-inducing ...
The apoptosis of endothelial cells induced by cytokines and/or oxidized low-density … ... High-density lipoproteins protect endothelial cells from tumor necrosis factor-alpha-induced apoptosis Biochem Biophys Res ... The apoptosis of endothelial cells induced by cytokines and/or oxidized low-density lipoproteins, etc. may provide a ... Here we report that HDL prevent the apoptosis of human umbilical venous endothelial cells (HUVECs) induced by tumor necrosis ...
... apoptosis-inducing factor, mitochondrion-associated, 2), Authors: Miroslav Varecha. Published in: Atlas Genet Cytogenet Oncol ... AIFM2 (apoptosis-inducing factor, mitochondrion-associated, 2). Written. 2009-06. Miroslav Varecha. ... A novel p53-inducible apoptogenic gene, PRG3, encodes a homologue of the apoptosis-inducing factor (AIF).. ... The human apoptosis-inducing protein AMID is an oxidoreductase with a modified flavin cofactor and DNA binding activity.. ...
TRAIL, tumor necrosis factor-related apoptosis-inducing ligand. Tumor necrosis factor (TNF)-related apoptosis-inducing ligand ( ... Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) selectively induces apoptosis of tumor cells but not most ... Apoptosis induced in normal human hepatocytes by tumor necrosis factor-related apoptosis-inducing ligand.Nat Med6:564-567,2000 ... Thomas WD, Hersey P: TNF-related apoptosis-inducing ligand (TRAIL) induces apoptosis in Fas ligand-resistant melanoma cells and ...
XAF1 mediates tumor necrosis factor-alpha-induced apoptosis and X-linked inhibitor of apoptosis cleavage by acting through the ... Tumor suppressor XIAP-Associated factor 1 (XAF1) cooperates with tumor necrosis factor-related apoptosis-inducing ligand to ... Tumor suppressor XIAP-Associated factor 1 (XAF1) cooperates with tumor necrosis factor-related apoptosis-inducing ligand to ... inhibitor of apoptosis-associated factor-1 as an interferon-stimulated gene that augments TRAIL Apo2L-induced apoptosis. J Biol ...
Flavonoids have been shown to sensitize cancer cells to TRAIL-induced apoptosis. The aim of this study was to examine the ... The synthetic flavanones enhanced TRAIL-induced apoptosis in HeLa cells through increased expression of TRAIL-R2 death receptor ... The apoptosis was detected by annexin V-FITC fluorescence staining in flow cytometry and microscopy. Death receptor (TRAIL-R1/ ... Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is considered as the most promising anticancer agent in the TNF ...
... critical for the sensitization of leukemic cells to tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis ... the potential of recombinant human apoptosis ligand 2/tumor necrosis factor-related apoptosis-inducing ligand (rhApo2L/TRAIL ... inhibitors and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) synergistically induces mitochondrial damage and ... Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is currently being investigated as a therapeutic agent for a ...
Apoptosis-Inducing Factor Is a Key Factor in Neuronal Cell Death Propagated by BAX-Dependent and BAX-Independent Mechanisms. ... Apoptosis-Inducing Factor Is a Key Factor in Neuronal Cell Death Propagated by BAX-Dependent and BAX-Independent Mechanisms ... Apoptosis-Inducing Factor Is a Key Factor in Neuronal Cell Death Propagated by BAX-Dependent and BAX-Independent Mechanisms ... Apoptosis-Inducing Factor Is a Key Factor in Neuronal Cell Death Propagated by BAX-Dependent and BAX-Independent Mechanisms ...
Critical roles of tumor necrosis factor-related apoptosis-inducing ligand in type 1 diabetes. Diabetes 2003;52:2274-2278 ... Tumour necrosis factor-related apoptosis-inducing ligand sequentially activates pro-survival and pro-apoptotic pathways in SK-N ... Blockade of tumor necrosis factor-related apoptosis-inducing ligand exacerbates type 1 diabetes in NOD mice. Diabetes 2003;52: ... While a large amount of data are available about tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) as an ...
Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) in central nervous system inflammation. J. Mol. Med. (Berlin ... Lack of tumor necrosis factor-related apoptosis-inducing ligand but presence of its receptors in the human brain. J. Neurosci. ... Xiao, M.L., Liu, J.Q. & Chen, C. Effect of tumor necrosis factor-related apoptosis-inducing ligand on developing human ... Effect of tumor necrosis factor-related apoptosis-inducing ligand on developing human oligodendrocytes in culture. *M. -L. Xiao ...
... and Apoptosis by Activating Nuclear Factor B. Yimou Wu, Hong Qiu, Yanhua Zeng, Xiaoxing You, Zhongliang Deng, Minjun Yu, and ... The DNA-binding activity of nuclear factor-. B (NF-. B) was assessed by electrophoretic mobility shift assay (EMSA). Results ... Cell apoptosis was also detected by Annexin V-FITC-propidium iodide (PI) staining and acridine orange (AO)-ethidium bromide (EB ... genitalium-derived LP may be an important etiological factor of certain diseases due to the ability of LP to produce ...
Epidermal growth factor receptor inhibition by tyrphostin 51 induces apoptosis in luteinized granulosa cells. by Shah M Khan, ... Epidermal growth factor receptor inhibition by tyrphostin 51 induces apoptosis in luteinized granulosa cells.. The Journal of ... Epidermal growth factor receptor inhibition by tyrphostin 51 induces apoptosis in luteinized granulosa cells. ... Growth factors may be involved in the control of ovarian cell fate and could contribute to regulation of ovarian cell apoptosis ...
Synthetic Apoptosis-Inducing Factor, Mitochondrion-Associated, 1 (AIFM1) Peptide. Species: Mammalian. Source: Synthetic. Order ... Apoptosis-Inducing Factor, Mitochondrion-Associated, 1 (AIFM1) Peptide Peptide AIFM1 Origin: Mammalian Source: Synthetic BP, ... Apoptosis-Inducing Factor, Mitochondrion-Associated, 1 (AIFM1) (AA 183-195) peptide Peptide ... In addition, AIFM1 induces mitochondria to release the apoptogenic proteins cytochrome c and caspase-9.. Molecular Weight. 66 ...
Tunicamycin enhances tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis in human prostate cancer cells ... Combination of isoliquiritigenin and tumor necrosis factor-related apoptosis-inducing ligand induces apoptosis in colon cancer ... Tumor necrosis factor-related apoptosis-inducing ligand : a novel mechanism for Bacillus Calmette-Guerin-induced antitumor ... Halocynthiaxanthin and peridinin sensitize colon cancer cell lines to tumor necrosis factor-related apoptosis-inducing ligand ...
Apoptosis : an international journal on programmed cell death 2013-5-16 Apoptosis-inducing factor (AIF) and leukocyte elastase ... namely apoptosis-inducing factor and leukocyte elastase inhibitor derived DNase II interact and can cooperate to induce cell ... Programmed cell death is an important factor in tissue homeostasis. Lot of work has been performed to characterize the caspase- ...
Cotreatment with histone deacetylase inhibitor LAQ824 enhances Apo-2L/tumor necrosis factor-related apoptosis inducing ligand- ... induced death inducing signaling complex activity and apoptosis of human acute leukemia cells. Download Prime PubMed App to ... TNF-Related Apoptosis-Inducing LigandReceptors, Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor ... factor_related_apoptosis_inducing_ligand_induced_death_inducing_signaling_complex_activity_and_apoptosis_of_human_acute_ ...
... apoptosis and loss of mitochondrial membrane potential. Download Prime PubMed App to iPhone, iPad, or Android ... Chemotherapeutic agents sensitize sarcoma cell lines to tumor necrosis factor-related apoptosis-inducing ligand-induced caspase ... Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is considered to induce apoptosis in a variety of cancer cells ... Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is considered to induce apoptosis in a variety of cancer cells ...
... and NF-κB activation requires IκBα ... In this study, we investigated whether adriamycin induced myocardium apoptosis through activation of nuclear factor κB in rat. ... Adriamycin induces myocardium apoptosis through activation of nuclear factor κB in rat. ... Myocardial apoptosis was detected by DNA fragmentation assay and TUNEL assay; Location and distribution of p-IκBα was observed ...
Apoptosis induced in normal human hepatocytes by tumor necrosis factor-related apoptosis-inducing ligand. Nat. Med., 6: 564-567 ... Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been reported to specifically kill malignant cells but to ... Antitumor Activity and Bystander Effects of the Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL) Gene Shunsuke ... Gliniak B., Le T. Tumor necrosis factor-related apoptosis-inducing ligands antitumor activity in vivo is enhanced by the ...
NO mediates islet apoptosis induced by IL-1β and IFN-γ. (a) NO donors induce apoptosis in rat islets. Islets were left ... Analysis of the Role of NO in Cytokine-induced Apoptosis.. To examine whether NO could directly induce apoptosis, islets were ... γ-induced Apoptosis Is Mediated by NO.. Our data demonstrate that A20 can protect islets from cytokine-induced apoptosis. ... A20 Inhibits Cytokine-Induced Apoptosis and Nuclear Factor κB-Dependent Gene Activation in Islets. Shane T. Grey, Maria B. ...
  • To evaluate the utility of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) as a cancer therapeutic, we created leucine zipper (LZ) forms of human (hu) and murine (mu) TRAIL to promote and stabilize the formation of trimers. (nih.gov)
  • Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) selectively induces apoptosis of tumor cells but not most normal cells. (diabetesjournals.org)
  • In the second model, we treated normal and TRAIL-deficient C57BL/6 mice with multiple low-dose streptozotocin to induce diabetes. (diabetesjournals.org)
  • Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a type 2 membrane protein of the TNF superfamily. (diabetesjournals.org)
  • It preferentially induces apoptosis of tumor cells but not most normal cells ( 1 ), with the exception of hepatocytes ( 2 ), neural cells ( 3 ), and thymocytes ( 4 , 5 ), which are sensitive to TRAIL-induced apoptosis. (diabetesjournals.org)
  • TRAIL receptor 1 (TRAIL-R1 or death receptor 4) ( 6 ) and TRAIL receptor 2 (TRAIL-R2, death receptor 5, TRICK2, or KILLER) ( 7 , 8 ) have cytoplasmic death domains, and can activate both caspases and nuclear factor (NF)-κB pathways. (diabetesjournals.org)
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is considered as the most promising anticancer agent in the TNF superfamily because of its selective cytotoxicity against tumor cells versus normal primary cells. (mdpi.com)
  • Flavonoids have been shown to sensitize cancer cells to TRAIL-induced apoptosis. (mdpi.com)
  • The synthetic flavanones enhanced TRAIL-induced apoptosis in HeLa cells through increased expression of TRAIL-R2 death receptor and reduction of mitochondrial membrane potential. (mdpi.com)
  • Szliszka E, Kostrzewa-Susłow E, Bronikowska J, Jaworska D, Janeczko T, Czuba ZP, Krol W. Synthetic Flavanones Augment the Anticancer Effect of Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL). (mdpi.com)
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is currently being investigated as a therapeutic agent for a variety of malignancies, as it triggers apoptosis specifically in transformed cells. (hindawi.com)
  • However, TRAIL use as a stand alone therapeutic is hampered by the fact that many primary tumor cells are resistant to TRAIL-mediated apoptosis. (hindawi.com)
  • We found that HDAC inhibition in B-CLL cells led to increased TRAIL receptor expression, increased caspase activation, decreased expression of antiapoptotic regulators such as Bcl-2, and ultimately, enhanced TRAIL-induced apoptosis. (hindawi.com)
  • The TNF family member tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is an apoptotic mediator that has received much attention, due to its ability to bring about cell death specifically in tumor cells without affecting untransformed cells or tissues [ 1 - 3 ]. (hindawi.com)
  • In humans, TRAIL interaction with either of two death-domain containing receptors, TRAIL-R1 (DR4) or TRAIL-R2 (DR5), leads to apoptosis in target cells [ 4 - 7 ]. (hindawi.com)
  • Both TRAIL-R1 and -R2 have been found on a wide variety of primary tumor cells and tumor cell lines, making TRAIL-induced apoptosis ideal for therapeutic intervention in a number of malignancies. (hindawi.com)
  • Despite this potential, TRAIL use as a stand-alone therapeutic has been hampered by the fact that many primary tumor cells are inherently resistant to TRAIL-mediated apoptosis, despite expressing extracellular TRAIL receptors [ 16 ]. (hindawi.com)
  • Not surprisingly, then, prior studies have shown that B-CLL cells are resistant to TRAIL-induced apoptosis [ 19 ]. (hindawi.com)
  • The reasons for this are unclear, but may include a combination of the following: reduced expression of the death-inducing receptors TRAIL -R1 and -R2, reduced expression of downstream caspase 8, or overexpression of antiapoptotic molecules such as FLIP. (hindawi.com)
  • To circumvent this inherent resistance to TRAIL-mediated apoptosis, we sought to determine the extent to which using TRAIL in combination with histone deacetylase inhibitor (HDACi) administration could bring about apoptosis in primary B-CLL cells. (hindawi.com)
  • OBJECTIVE To evaluate the potential therapeutic effect of recombinant human tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) treatment in a model of type 1 diabetes. (diabetesjournals.org)
  • CONCLUSIONS Overall, these data demonstrate that the administration of recombinant TRAIL ameliorates the severity of STZ-induced type 1 diabetes, and this effect was accompanied by the upregulation of SOCS1 expression. (diabetesjournals.org)
  • While a large amount of data are available about tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) as an anticancer agent ( 1 ), some studies have suggested a potential role of endogenous TRAIL in type 1 diabetes ( 2 - 4 ). (diabetesjournals.org)
  • In addition, normal primary islet cells are resistant to TRAIL-induced cytotoxicity ( 5 , 6 ), and adenovirus-mediated TRAIL gene delivery into pancreatic islets resulted in prolonged normoglycemia in streptozotocin (STZ)-induced diabetic rats compared with animals grafted with mock-infected islets ( 6 ). (diabetesjournals.org)
  • Moreover, we have analyzed the in vivo effect of treatment with recombinant TRAIL in the type 1 diabetes mouse model induced by multiple low doses of STZ. (diabetesjournals.org)
  • We investigated the role of tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) and its death (TRAIL-R1, TRAIL-R2) and decoy (TRAIL-R3, TRAIL-R4) receptors in periventricular white matter injury (PWMI). (springer.com)
  • TRAIL-induced death of human adult oligodendrocytes is mediated by JNK pathway. (springer.com)
  • Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) in central nervous system inflammation. (springer.com)
  • TRAIL-R2: A novel apoptosis-mediating receptor for TRAIL. (springer.com)
  • TRAIL induces death of human oligodendrocytes isolated from adult brain. (springer.com)
  • As compared with treatment with Apo-2L/tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) or LAQ824 alone, pretreatment with LAQ824 increased the assembly of Fas-associated death domain and caspase-8, but not of c-FLIP, into the Apo-2L/TRAIL-induced death-inducing signaling complex. (unboundmedicine.com)
  • Partial inhibition of apoptosis due to LAQ824 or Apo-2L/TRAIL exerted by Bcl-2 overexpression was reversed by cotreatment with LAQ824 and Apo-2L/TRAIL. (unboundmedicine.com)
  • Significantly, cotreatment with LAQ824 increased Apo-2L/TRAIL-induced apoptosis of primary acute myelogenous leukemia blast samples isolated from 10 patients with acute myelogenous leukemia. (unboundmedicine.com)
  • Taken together, these findings indicate that LAQ824 may have promising activity in augmenting Apo-2L/TRAIL-induced death-inducing signaling complex and apoptosis of human acute leukemia cells. (unboundmedicine.com)
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is considered to induce apoptosis in a variety of cancer cells but not normal cells. (unboundmedicine.com)
  • In the present study, we examined whether chemotherapeutic agents enhance TRAIL-induced apoptosis in the sarcoma cell lines MG-63 and SaOS-2. (unboundmedicine.com)
  • Pretreatment with sub-toxic or slightly toxic concentrations of chemotherapeutic agents (cis-diammine dichloroplatinum, CDDP and doxorubicin, DXR) sensitized both cell lines to TRAIL-induced apoptosis, as assessed by the propidium iodide or Annexin V-Cy5 staining method. (unboundmedicine.com)
  • CDDP down-regulated c-FLIP, tending to lower the activation threshold required for TRAIL-induced caspase-8 activation. (unboundmedicine.com)
  • The CDDP-pretreated cells indeed demonstrated more increased TRAIL-mediated caspase-8 activation, loss of mitochondrial membrane potential (DeltaPsi(m)), and apoptosis than untreated cells. (unboundmedicine.com)
  • Both the increased caspase activation and mitochondrial dysfunction induced by combination of CDDP and TRAIL would contribute to enhanced apoptotic cell death. (unboundmedicine.com)
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) has been reported to specifically kill malignant cells but to be relatively nontoxic to normal cells. (aacrjournals.org)
  • Furthermore, coculture of cancer cells expressing TRAIL with those expressing green fluorescent protein (GFP) resulted in apoptosis of both cells, whereas coculture of Bax-expressing cells with GFP-expressing cells resulted in the cell death of the Bax-expressing cells only, which suggested that the transfer of the TRAIL gene resulted in bystander effects. (aacrjournals.org)
  • 1 ). In fact, the presence of TRAIL in normal tissues suggests that normal cells contain mechanisms that protect them from apoptosis induction by TRAIL . (aacrjournals.org)
  • Tumor necrosis factor-related apoptosis‑inducing ligand (TRAIL) is under clinical development as a cancer therapeutic as it has been shown to induce apoptosis in numerous types of cancer cells without significant toxicity towards normal cells. (spandidos-publications.com)
  • In the present study, celecoxib (CXB), a non-steroidal anti‑inflammatory drug, was administered in combination with TRAIL to induce cell apoptosis and the doses of the two drugs were simultaneously reduced. (spandidos-publications.com)
  • The results revealed that CXB sensitized TRAIL-resistant MG-63 OS cells to TRAIL‑induced apoptosis through downregulation of cellular B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein, caspase-8 and caspase-3. (spandidos-publications.com)
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising antitumor agent since it is capable of killing tumor cells via receptor-mediated apoptosis ( 5 , 6 ). (spandidos-publications.com)
  • For example, TRAIL resistance may occur at the receptor level, due to deregulated expression, or at the death-induced signaling complex (DISC) level, mediated by proteins counteracting DISC formation ( 10 - 12 ). (spandidos-publications.com)
  • In addition, an inability to activate mitochondria during apoptosis, due to high expression levels of antiapoptotic proteins, may result in TRAIL resistance ( 13 , 14 ). (spandidos-publications.com)
  • The aim of the present study was to evaluate the potency of CXB in combination with TRAIL in inhibiting OS cancer cell growth and proliferation, and to reveal the underlying molecular mechanisms involved in TRAIL-induced apoptosis. (spandidos-publications.com)
  • In this report, we show for the first time that apigenin markedly induces the expression of death receptor 5 (DR5) and synergistically acts with exogenous soluble recombinant human tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) to induce apoptosis in malignant tumor cells. (aacrjournals.org)
  • TRAIL is a promising candidate for cancer therapeutics due to its ability to selectively induce apoptosis in cancer cells. (aacrjournals.org)
  • The combined use of apigenin and TRAIL at suboptimal concentrations induces Bcl-2-interacting domain cleavage and the activation of caspases-8, -10, -9, and -3. (aacrjournals.org)
  • Furthermore, human recombinant DR5/Fc chimera protein and caspase inhibitors dramatically inhibit apoptosis induced by the combination of apigenin and TRAIL. (aacrjournals.org)
  • Moreover, apigenin does not sensitize normal human peripheral blood mononuclear cells to TRAIL-induced apoptosis. (aacrjournals.org)
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis in various types of malignant tumor cells through its interaction with the death domain-containing receptor, death receptor 5 (DR5), which is also called TRAIL-R2 ( 15 - 18 ). (aacrjournals.org)
  • However, some tumor cells are resistant to TRAIL-induced apoptosis ( 22 ). (aacrjournals.org)
  • Thus, the expression of DR5 may contribute to the tumor-selective induction of apoptosis mediated by TRAIL. (aacrjournals.org)
  • In this study, we show for the first time that apigenin up-regulates DR5 expression and synergistically enhances TRAIL-induced apoptosis in various types of malignant tumor cells, but not in normal human peripheral blood mononuclear cells (PBMC). (aacrjournals.org)
  • Apo2L/TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) is a member of the tumor necrosis factor gene family known to induce apoptosis in a number of cancer cell lines and may have broad-spectrum activity against human malignancies. (aspetjournals.org)
  • Apo2 ligand, also called tumor necrosis factor (TNF)-related apoptosis-inducing ligand (Apo2L/TRAIL), is a member of the TNF gene superfamily. (aspetjournals.org)
  • DR4 and DR5 signal apoptosis, whereas DcR1, DcR2, and OPG can act as decoys that inhibit Apo2L/TRAIL activity. (aspetjournals.org)
  • This optimized preparation of Apo2L/TRAIL selectively induces apoptosis of cancer cells while sparing normal cells. (aspetjournals.org)
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in conjunction with microtubule-targeting agents may be a promising novel anticancer treatment strategy. (aacrjournals.org)
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a potent cancer cell-specific apoptosis-inducing agent with little to no effect on normal tissues and, along with derivative agents, is being tested in early phase clinical trials ( 6 ), 5 with promising early results ( 7 ). (aacrjournals.org)
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is one of the most promising candidates for new cancer therapeutics. (aacrjournals.org)
  • The combination of baicalein and TRAIL effectively induced apoptosis in TRAIL-resistant colon cancer SW480 cells. (aacrjournals.org)
  • Suppression of this up-regulation with small interfering RNA (siRNA) efficiently reduced the apoptosis induced by TRAIL and baicalein, suggesting that the sensitization was mediated through DR5 induction. (aacrjournals.org)
  • Of note, the combination of TRAIL and baicalein hardly induced apoptosis in normal human cells, such as blood cells and hepatocytes. (aacrjournals.org)
  • Interestingly, baicalein induced reactive oxygen species (ROS) and a ROS scavenger prevented DR5 expression and TRAIL sensitization in PC3 but not SW480 cells. (aacrjournals.org)
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL/Apo2L) selectively induces apoptosis in various cancer cells in vitro and in vivo , with little or no toxicity in normal cells ( 9 - 12 ). (aacrjournals.org)
  • Background Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL), also called Apo-2 ligand, is a member of the TNF family that has been reported to induce apoptosis in a variety of transformed cell lines, as well as in normal human hepatocytes in vitro . (bmj.com)
  • Among the family members, TRAIL displays highest homology to CD95 ligand, receptor of which may not only mediate apoptosis of T cells, but also mediate the proliferation of normal human fibroblasts. (bmj.com)
  • These data suggest that TRAIL can enhance collagen production by fibroblasts that are resistant to TRAIL-induced apoptosis. (bmj.com)
  • Almost all hepatic cancer cells have resistance to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. (medscimonit.com)
  • This study investigated the role of c-FLIPL and RIP-1 in hepatic cancer cell resistance to TRAIL-induced apoptosis. (medscimonit.com)
  • Single TRAIL treatment showed no significant impact on cell proliferation and apoptosis. (medscimonit.com)
  • TRAIL mediates apoptosis resistance through upregulating RIP-1 expression, enhancing NF-kB transcriptional activity, and weakening caspase activity. (medscimonit.com)
  • Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family with a promising toxicity profile and synergistic activity with chemotherapeutic agents. (aacrjournals.org)
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) was identified as an unique death ligand in respect to its ubiquitous receptor expression and the lack of cytotoxic effects in normal tissue ( 4 , 5 ). (aacrjournals.org)
  • Regulation of TRAIL-induced apoptosis was further attributed to cellular FLICE inhibitory protein (FLIP), which can efficiently block caspase-8 cleavage ( 10 ) due to a structural similarity to caspase-8. (aacrjournals.org)
  • The newly discovered member of the tumor necrosis factor superfamily, Apo2L/tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), has been identified as an apoptosis-inducing agent in sensitive tumor cells but not in the majority of normal cells, and hence it is of potential therapeutic application. (aacrjournals.org)
  • However, many tumor cells are resistant to Apo2L/TRAIL-mediated apoptosis. (aacrjournals.org)
  • This study examined whether an Adriamycin-resistant multiple myeloma (MM) cell line (8226/Dox40) can be sensitized by Adriamycin (ADR) to Apo2L/TRAIL-mediated apoptosis. (aacrjournals.org)
  • Treatment with the combination of Apo2L/TRAIL and subtoxic concentrations of ADR resulted in synergistic cytotoxicity and apoptosis for both the parental 8226/S and the 8226/Dox40 tumor cells. (aacrjournals.org)
  • Combination treatment with Apo2L/TRAIL and ADR resulted in significant mitochondrial membrane depolarization and activation of caspase-9 and caspase-3 and apoptosis. (aacrjournals.org)
  • Because ADR is shown to sensitize ADR-resistant tumor cells to Apo2L/TRAIL, these findings reveal that ADR can still signal ADR-resistant tumor cells, resulting in the modification of the Apo2L/TRAIL-mediated signaling pathway and apoptosis. (aacrjournals.org)
  • Combination index revealed that the combined treatment of DAPT and TRAIL synergistically enhanced apoptosis compared with treatment with either drug alone. (selleckchem.com)
  • TRAIL combined with the clinically evaluated γ-secretase inhibitor 3-[(1r, 4s)-4-(4-chlorophenylsulfonyl)-4-(2, 5-difluorophenyl) cyclohexyl] propanoic acid (MK-0752) also significantly enhanced TRAIL-induced cell death compared with either drug alone. (selleckchem.com)
  • DAPT/TRAIL apoptotic synergy was dependent on the extrinsic apoptotic pathway and was associated with a decrease in BH3 interacting-domain death agonist and x-linked inhibitor of apoptosis. (selleckchem.com)
  • We analyzed the sensitivity to soluble Fas-ligand (FasL) and tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), 2 members of the TNF superfamily in peripheral blood leukocytes (PBL) from patients with SzS. (uzh.ch)
  • Our data on primary SzS lymphocytes reveal frequent resistance to apoptosis induced by FasL and TRAIL, which may contribute to their accumulation in patients with SzS and be relevant at a therapeutic level. (uzh.ch)
  • Apo2L/TRAIL [Apo2 ligand/tumor necrosis factor (TNF)-related apoptosis-inducing ligand], a member of the TNF cytokine superfamily, induces cell death by apoptosis in a number of human cancer cells and is a potential agent for cancer therapy. (aspetjournals.org)
  • Contrary to other members of the TNF family with antitumor activity, induction of apoptosis by Apo2L/TRAIL is independent of NF-κB activation. (aspetjournals.org)
  • Upon binding of Apo2L/TRAIL, DR4 and DR5 can each recruit and activate apoptosis-initiating proteases (caspase 8 and 10), through the death domain-containing adaptor molecule Fas-associated death domain. (aspetjournals.org)
  • In this article, we demonstrate that the synthetic cannabinoid R -(+)-(2,3-dihydro-5-methyl-3-[(4-morpholinyl)methyl]pyrol[1,2,3-de]-1,4-benzoxazin-6-yl)-(1-naphthalenyl) methanone mesylate (WIN 55,212-2) sensitizes human hepatocellular carcinoma (HCC) cells to apoptosis mediated by tumor necrosis-related apoptosis inducing ligand (TRAIL). (aspetjournals.org)
  • The apoptotic mechanism induced by treatment with WIN/TRAIL combination involved the loss of the mitochondrial transmembrane potential and led to the activation of caspases. (aspetjournals.org)
  • In HCC cells, WIN treatment induced the up-regulation of TRAIL death receptor DR5, an effect that seemed to be related to the increase in the level of p8 and CHOP, two factors implicated in cellular stress response and apoptosis. (aspetjournals.org)
  • This relationship was suggested by the observation that the down-regulation of p8 or CHOP by specific small interfering RNAs attenuated both WIN-mediated DR5 up-regulation and the cytotoxicity induced by WIN/TRAIL cotreatment. (aspetjournals.org)
  • The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), a member of the tumor necrosis factor family, is a potent apoptosis-inducing cytokine. (aspetjournals.org)
  • Thus, it is important to find therapeutic agents capable of sensitizing resistant cancer cells to TRAIL-induced apoptosis. (aspetjournals.org)
  • BACKGROUND: The tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) death receptor, DR5, mediates proapoptotic signals and is implicated in the pathogenesis of many neoplasms including nonsmall-cell lung cancer (NSCLC). (garvan.org.au)
  • Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family of cytokines and has been shown to induce cell death in many types of tumor and transformed cells but not in normal cells. (pubmedcentralcanada.ca)
  • However, safety issues are a concern because certain preparations of recombinant TRAIL protein were reported to induce toxicity in normal human hepatocytes in culture. (pubmedcentralcanada.ca)
  • It was not known whether exogenous or overexpression of TRAIL in a syngeneic system could induce tumor cell death while leaving normal tissue cells unharmed. (pubmedcentralcanada.ca)
  • Thus, the tumor selectivity of TRAIL-induced apoptosis remains to be further characterized. (pubmedcentralcanada.ca)
  • This approach may be used further to identify important molecules that regulate the sensitivity of tumor cells to TRAIL-induced cell death in vivo . (pubmedcentralcanada.ca)
  • These include Fas receptor-mediated apoptosis ( 1 ), perforin-granzyme-mediated cytotoxicity ( 2 ), and tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis ( 3 , 4 ). (pubmedcentralcanada.ca)
  • Unlike TNF and Fas ligand (FasL), which can cause life-threatening toxic effects when used systemically ( 7 , 8 ), recombinant TRAIL protein has been shown to induce cell death in many types of tumor and transformed cells, but not in normal cells, in culture and xenograft animal models ( 5 , 6 , 9 , 10 ). (pubmedcentralcanada.ca)
  • In addition, initial xenograft studies using recombinant human soluble forms of the TRAIL protein showed TRAIL-induced apoptosis of human cancer cells transplanted into immunodeficient mice without toxicity to the normal tissues of the mice bearing these xenograft tumors ( 9 , 10 ). (pubmedcentralcanada.ca)
  • These studies do not directly address the tumor selectivity of TRAIL-induced apoptosis due to the fact that the human and mouse forms of TRAIL share only 65% amino acid sequence identity and thus may behave differently in vivo and also because human TRAIL does not kill mouse cells with the same efficacy as human cells ( 5 , 6 ). (pubmedcentralcanada.ca)
  • Results: The TF signaling complexes were shown to prevent apoptosis induced by serum starvation and TRAIL in cancer cells by reduced activation of caspase-8 in a PI3k/AKT-dependent manner. (diva-portal.org)
  • Background Dulanermin is a recombinant soluble human Apo2 ligand/tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) that activates apoptotic pathways by binding to proapoptotic death receptor (DR) 4 and DR5. (springermedizin.de)
  • Zhu L, Wang X, Li XM (2012) Mechanism of TRAIL induced tumor cell apoptosis and application of TRAIL based on tumor therapy. (springermedizin.de)
  • TRAIL plays an important role in host immunosurveillance against tumor progression, as it induces apoptosis of tumor cells but not normal cells, and thus has great therapeutic potential for cancer treatment. (biomedcentral.com)
  • TRAIL binds to two cell-death-inducing (DR4 and DR5) and two decoy (DcR1, and DcR2) receptors. (biomedcentral.com)
  • There was no significant association between TRAIL-R expression and OSSC histology grade, nodal status or apoptosis rates of tumor cells and TIL. (biomedcentral.com)
  • Loss of TRAIL expression is an early event during oral carcinogenesis and may be involved in dysregulation of apoptosis and contribute to the molecular carcinogenesis of OSCC. (biomedcentral.com)
  • Furthermore, PHA665752 treatment upregulated DR5 expression via generation of reactive oxygen species in PTC cell lines, and synergistically potentiated death receptor-induced apoptosis with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). (springer.com)
  • The various receptors for tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) are located on chromosome 8p21.2 , a region frequently deleted in ovarian cancer. (aacrjournals.org)
  • Lack of expression of TRAIL receptor 1 (death receptor 4, DR4) correlates with resistance to TRAIL-induced apoptosis in ovarian cancer cells. (aacrjournals.org)
  • A considerable amount of effort has been put into the mutational analysis of receptors for apoptosis-inducing proteins, including those for tumor necrosis factor (TNF)-related apotosis inducing ligand (TRAIL), but definite mutations are rare. (aacrjournals.org)
  • Therefore, we sought to clarify the role of Cav-1 in regulating tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis after isoflurane exposure in colon cancer cell lines. (asahq.org)
  • Global Markets Direct's, 'Tumor Necrosis Factor Receptor Superfamily Member 10A (Death Receptor 4 or TNF Related Apoptosis Inducing Ligand Receptor 1 or TRAIL Receptor 1 or DR4 or CD261 or TNFRSF10A) - Pipeline Review, H2 2017', provides in depth analysis on Tumor Necrosis Factor Receptor Superfamily Member 10A (Death Receptor 4 or TNF Related Apoptosis Inducing Ligand Receptor 1 or TRAIL Receptor 1 or DR4 or CD261 or TNFRSF10A) targeted pipeline therapeutics. (globalmarketsdirect.com)
  • Additionally, the report provides an overview of key players involved in Tumor Necrosis Factor Receptor Superfamily Member 10A (Death Receptor 4 or TNF Related Apoptosis Inducing Ligand Receptor 1 or TRAIL Receptor 1 or DR4 or CD261 or TNFRSF10A) targeted therapeutics development and features dormant and discontinued projects. (globalmarketsdirect.com)
  • The report analyses the pipeline products from therapy areas Oncology, Central Nervous System, Hematological Disorders and Immunology under development targeting Tumor Necrosis Factor Receptor Superfamily Member 10A (Death Receptor 4 or TNF Related Apoptosis Inducing Ligand Receptor 1 or TRAIL Receptor 1 or DR4 or CD261 or TNFRSF10A). (globalmarketsdirect.com)
  • MBS019114 is a ready-to-use microwell, strip plate Sandwich ELISA (enzyme-linked immunosorbent assay) Kit for analyzing the presence of the Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand 3 (TRAIL-R3) ELISA Kit target analytes in biological samples. (mybiosource.com)
  • TNF-related apoptosis-inducing ligand (TRAIL) receptor agonists are attractive anti-tumor agents because of their capability to induce apoptosis in cancer cells by activating death receptors (DR) 4 and 5 with little toxicity against normal cells. (biomedcentral.com)
  • Previously, we reported that basal B subtype TNBC cell lines were effectively killed by glutathione-S-transferase (GST)-tagged tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL), while cell lines representative of the other subtypes of breast cancer remained comparatively resistant [ 9 ]. (biomedcentral.com)
  • Chicken tumor necrosis factor-related apoptosis-inducing ligand 3(TRAIL-R3)ELISA Kit is an ELISA kit which is manufactured by highest quality antibodies and plates to provide you with excellent and reproducible results in your work. (antibody-antibodies.com)
  • We previously reported that low ratio of osteoprotegerin (OPG) to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) was associated with Disease Activity Score in 28 joints (DAS28) remission at 6 months in patients with early rheumatoid arthritis (RA). (biomedcentral.com)
  • The cytokine tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) was initially described for its ability to trigger cell death in a somewhat tumor-selective manner. (biomedcentral.com)
  • However, we found that TRAIL induces apoptosis only in a subset of RA FLSs and induces proliferation in surviving cells [ 7 ]. (biomedcentral.com)
  • Tumor necrosis factor-related apoptosis-inclucing ligand (TRAIL) is a potential anticancer drug that selectively induces apoptosis in a variety of cancer cells by interacting with death receptors DR4 and DR5. (nuigalway.ie)
  • TRAIL can also bind to decoy receptors (DcR1, DcR2, and osteoprotegerin receptor) that cannot induce apoptosis. (nuigalway.ie)
  • Even wild-type TRAIL-insensitive ovarian cancer cell lines could be brought into apoptosis. (nuigalway.ie)
  • In addition, our results demonstrate that there is no requirement for anti body-mediated cross-linking or membrane-bound TRAIL to induce apoptosis through DRS. (nuigalway.ie)
  • TRAIL has been shown to induce apoptosis in various tumor cell lines, whereas most primary cells seem to be resistant. (ox.ac.uk)
  • These studies demonstrate activation-induced sensitization of thymocytes to TRAIL-mediated apoptosis and expression of the apoptosis-inducing TRAIL receptors. (ox.ac.uk)
  • However, with the use of several model systems, our subsequent experiments rule out the possibility that TRAIL plays a major role in antigen-induced deletion of thymocytes. (ox.ac.uk)
  • Thus, susceptibility to TRAIL-induced apoptosis is controlled differently by central and peripheral T cells. (ox.ac.uk)
  • Should the Canine Tumor Necrosis Factor Related Apoptosis Inducing Ligand (TRAIL) ELISA Kit is proven to show malperformance, you will receive a refund or a free replacement. (signetlabs.com)
  • Description: A sandwich quantitative ELISA assay kit for detection of Canine Tumor Necrosis Factor Related Apoptosis Inducing Ligand (TRAIL) in samples from tissue homogenates, cell lysates or other biological fluids. (signetlabs.com)
  • Lack of tumor necrosis factor-related apoptosis-inducing ligand but presence of its receptors in the human brain. (springer.com)
  • The protein encoded by this gene is a cytokine that belongs to the tumor necrosis factor (TNF) ligand family. (mybiosource.com)
  • Repression of tumor necrosis factor-related apoptosis-inducing ligand " by Nadarajah Vigneswaran, Darryl C. Baucum et al. (tmc.edu)
  • Tumor necrosis factor-related apoptosis-inducing ligand in T cell development: sensitivity of human thymocytes. (ox.ac.uk)
  • Apoptosis-inducing factor, mitochondria-associated 3 is a protein that in humans is encoded by the AIFM3 gene. (wikipedia.org)
  • The protein may also be known as CD27BP, Siva-1, Siva-2, apoptosis regulatory protein Siva, and CD27-binding (Siva) protein. (biocompare.com)
  • 1) a transient decrease of phosphorylated extracelluar signal-requlated kinase (ERK), 2) translocation of apoptosis inducing factor (AIF) from mitochondria to cytosol concurrent with a decreased membrane potential, and 3) downregulation of bcl-2 protein. (curehunter.com)
  • Recent findings suggest that apoptotic protein apoptosis-inducing factor (AIF) may also play an important non-apoptotic function inside mitochondria. (scielo.org.ar)
  • Induction of apoptosis results in the translocation of this protein to the nucleus where it effects chromosome condensation and fragmentation. (antibodies-online.com)
  • In this study, we further investigated the mechanisms of NaF on proliferation and apoptosis in the primary cultured mouse osteoblasts, which were exposed to different concentration of NaF (10(-6)-5 × 10(-4) M). We examined the effect of NaF on proliferation, cell cycle, apoptosis, oxidative stress, and the protein level of insulin-like growth factor-I (IGF-I) in osteoblasts. (fluoridealert.org)
  • On the other hand, we found that NaF increased oxidative stress and decreased protein expression of IGF-I. Our study herein suggested that NaF caused proliferation suppression, and apoptosis may contribute to decrease IGF-I expression and increased oxidative stress damage by NaF in the primary mouse osteoblasts. (fluoridealert.org)
  • Second, TFF1 interferes with caspase-9 and caspase-3 activation through an NF-κB-induced increase in the expression of XIAP (X-linked inhibitor of apoptosis protein). (arvojournals.org)
  • The levels of apoptosis-related protein were detected by Western blot analysis. (medscimonit.com)
  • Moreover, WIN induced a significant decrease in the levels of some survival factors (survivin, c-inhibitor of apoptosis protein 2, and Bcl-2) and in particular in that of the active phosphorylated form of AKT. (aspetjournals.org)
  • Second, induction of ATF3 is mediated in part by the NF-kappaB and Jun N-terminal kinase/stress-activated protein kinase signaling pathways, two stress-induced pathways implicated in both type 1 and type 2 diabetes. (garvan.org.au)
  • Increased expression of nerve growth factor (NGF) has been found in the myocardium suffered from ischemia and reperfusion (I/R). The pro-survival activity of NGF on ischemic heart has been supposed to be mediated by phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway. (medsci.org)
  • Myocardial apoptosis rate was measured by TUNEL staining, and expression of glucose-related protein 78 (GRP78), CCAAT/enhancer-binding protein homologous protein (CHOP), caspase-12, total- and phospho-(Ser473)-Akt were assessed by Western blot analyses. (medsci.org)
  • However, TGF-β1 induced caspase-dependent cleavage of BAD at its N terminus to generate a 15-kDa truncated protein. (asm.org)
  • Overexpression of the 15-kDa truncated BAD protein enhanced TGF-β1-induced apoptosis, whereas a mutant BAD resistant to caspase 3 cleavage blocked TGF-β1-induced apoptosis. (asm.org)
  • Recently, it has been shown that Daxx, a Fas-receptor-associated protein that mediates the activation of JNK and programmed cell death induced by Fas, physically interacts with TβRII and is involved in mediating TGF-β-induced apoptosis ( 35 , 46 ). (asm.org)
  • Another report has shown that ARTS, a protein product of the human septin H5/PNUTL2/CDCrel2b gene, acts to enhance cell death induced by TGF-β ( 27 ). (asm.org)
  • BAD is cleaved by a caspase(s) at its N terminus to generate a 15-kDa truncated protein after IL-3 deprivation-induced apoptosis in murine myeloid precursor 32Dcl3 cells ( 13 ). (asm.org)
  • The 15-kDa truncated BAD is a more potent inducer of apoptosis than the wild-type (WT) protein, whereas a mutant BAD resistant to caspase 3 cleavage is a weaker apoptosis inducer ( 13 ). (asm.org)
  • DEVD-CHO protects cells from Fas induced apoptosis but does not prevent fodrin proteolysis, indicating that cleavage of this protein can be uncoupled from apoptotic cell, death. (harvard.edu)
  • This protein preferentially induces apoptosis in transformed and tumor cells, but does not appear to kill normal cells although it is expressed at a significant level in most normal tissues. (mybiosource.com)
  • Approximately 60-70% of breast cancers are estrogen receptor (ER) or progesterone receptor (PR) positive, and 15-30% of cases have gene amplification and overexpression of the human epidermal growth factor receptor 2 (HER2) protein [ 2 ]. (biomedcentral.com)
  • These patients usually have high levels of rheumatoid factor (RF) and high titers of anti-citrullinated protein antibodies (ACPA), very high disease activity and/or early radiographic joint damage [ 2 ]. (biomedcentral.com)
  • Our previous work demonstrated that ectopic expression of interferon regulatory factor 4 binding protein (IBP) was correlated with the malignant behaviour of human breast cancer cells. (biomedcentral.com)
  • This protein inhibits apoptosis. (wikibooks.org)
  • Another important protein is apoptosis-inducing factor (AIF), a flavoprotein that can stimulate a caspase-independent cell-death pathway required for early embryonic morphogenesis. (archives-ouvertes.fr)
  • PERK phosphorylates the eukaryotic initiation factor 2 α (eIF2α) and itself at its cytoplasmic kinase domain, which leads to reduction of global protein biosynthesis, one of the feedback loops to reduce protein stress in the ER. (biologists.org)
  • Activation of IRE1 initiates the non-conventional splicing of the transcription factor X-box-binding protein 1 (XBP1), which is responsible for the activation of a larger number of ER-stress responsive genes, including chaperones of the ER. (biologists.org)
  • This gene encodes a protein that reduces cell growth by stimulating apoptosis. (genecards.org)
  • BLCAP (BLCAP Apoptosis Inducing Factor) is a Protein Coding gene. (genecards.org)
  • Tissue factor (TF) is a transmembrane protein that acts as a receptor for activated coagulation factor VII (FVIIa), initiating the coagulation cascade. (biomedcentral.com)
  • Tissue factor (TF) is a transmembrane protein that belongs to the class II cytokine receptor superfamily that shares a significant degree of homology with the interferon gamma receptor [ 1 ]. (biomedcentral.com)
  • p38 is a member of the mitogen-activated protein (MAP) kinase superfamily activated by stress signals and implicated in cellular processes involving inflammation and apoptosis. (elsevier.com)
  • Kummer, JL, Rao, PK & Heidenreich, KA 1997, ' Apoptosis induced by withdrawal of trophic factors is mediated by p38 mitogen-activated protein kinase ', Journal of Biological Chemistry , vol. 272, no. 33, pp. 20490-20494. (elsevier.com)
  • Apoptosis is induced either by binding of ligands to specific death receptors on cell surface or by unspecific cellular stress, which promotes cytochrome c release from mitochondria and the formation of the apoptosome. (aacrjournals.org)
  • Isoflurane may induce apoptosis through Bcl-2 family proteins, mitochondrial reactive oxygen species-associated apoptosis, or by causing abnormal calcium release from the endoplasmic reticulum via excessive activation of inositol trisphosphate receptors. (asahq.org)
  • Its activity may be modulated by binding to the decoy receptors TNFRSF10C/TRAILR3, TNFRSF10D/TRAILR4 and TNFRSF11B/OPG that cannot induce apoptosis. (mybiosource.com)
  • Mitochondria play a key part in the regulation of apoptosis (cell death). (nih.gov)
  • it is normally confined to mitochondria but translocates to the nucleus when apoptosis is induced. (nih.gov)
  • It induces purified mitochondria to release the apoptogenic proteins cytochrome c and caspase-9. (nih.gov)
  • Your search returned 112 apoptosis inducing factor mitochondria associated 1 ELISA ELISA Kit across 13 suppliers. (biocompare.com)
  • A flavoprotein that functions as a powerful antioxidant in the MITOCHONDRIA and promotes APOPTOSIS when released from the mitochondria. (curehunter.com)
  • Thimerosal-induced apoptosis was associated with depolarization of mitochondrial membrane, generation of reactive oxygen species, and release of cytochrome c and apoptosis-inducing factor (AIF) from mitochondria to cytosol. (spandidos-publications.com)
  • Here we report that the two agents that cause oxidative stress, MeHg (1 µm) and H2O2 (50 µm), induce translocation of apoptosis‐inducing factor (AIF) from the mitochondria to the nucleus in CGC. (deepdyve.com)
  • ARTS localizes to mitochondria and undergoes a mitochondrion-to-nucleus translocation during TGF-β-induced apoptosis. (asm.org)
  • Deprivation of survival factors induces BAD dephosphorylation by the specific serine/threonine phosphatase PP1α ( 38 ), resulting in dissociation of BAD from 14-3-3 proteins and translocation to the mitochondria, where it interacts with Bcl-X L and Bcl-2 and antagonizes their antiapoptotic functions. (asm.org)
  • Mitochondria play a key role in apoptosis due to their capacity to release potentially lethal proteins. (archives-ouvertes.fr)
  • Their intermembrane space contains several proteins that are liberated through the outer membrane in order to participate in the degradation phase of apoptosis. (nih.gov)
  • Assays of proliferation, apoptosis and tumor growth were performed, along with analysis of the proteins involved. (spandidos-publications.com)
  • In conditions of acute cellular redox, stress cells manipulated to lose the expression of apoptosis-inducing factor (AIF) nucleate SG signature proteins (e.g. (cnrs.fr)
  • TNF induces apoptosis through the recruitment of the death domain-containing adaptor proteins FADD and TRADD to its receptor, which in turn leads to the activation of the initiator caspase, caspase-8. (ahajournals.org)
  • The authors used cell fractionation to detect lipid raft-associated proteins, coimmunoprecipitation to explore the formation of a death-inducing signaling complex (DISC), and a combination of immunofluorescence, immunoblotting, flow cytometry, siRNA-mediated decrease in gene expression, and electrophoretic mobility shift assay to explore the mechanisms of TFF1-protective effects. (arvojournals.org)
  • The epithelial surface of the eye and its specialized glandular infoldings produce the components of tear film, which include water, antimicrobial agents, cytokines, lipids, mucins, and trefoil factor (TFF) family proteins. (arvojournals.org)
  • Endoplasmic reticulum (ER) stress, which is activated initially as a defensive response to eliminate the accumulated unfolded proteins, has shown a critical involvement in the ischemia induced myocardial apoptosis. (medsci.org)
  • GRP78, caspase-12 and CHOP were highly expressed in ischemic myocardium, while NGF significantly inhibited the overexpression of these proteins which were involved in ER stress-induced myocardial apoptosis. (medsci.org)
  • When the activation of PI3K/Akt pathway is blocked by LY294002, the NGF induced suppression of the apoptosis-related proteins expression was reversed. (medsci.org)
  • The Bcl-2 family proteins serve as critical regulators of pathways involved in apoptosis, acting to either inhibit or promote cell death ( 26 , 33 ). (asm.org)
  • In interleukin-3 (IL-3)-dependent lymphoid cells, BAD, a proapoptotic member of the Bcl-2 family of proteins is a key regulator of apoptosis ( 19 ). (asm.org)
  • We report the TF complexes to govern the extrinsic pathway of apoptosis, present data on FVIIa-dependent regulation of apoptosis-related genes, and exclude known surface proteins as transmitters of the anti-apoptotic signals. (diva-portal.org)
  • Melatonin ameliorates metabolic risk factors, modulates apoptotic proteins, and protects the rat heart against diabetes-induced apoptosis. (sciepub.com)
  • 2002). SIVA1 interacts with BCL2 and BCL-XL , abrogates their antiapoptotic functions and modulates the intrinsic apoptosis pathway (Chu et al. (atlasgeneticsoncology.org)
  • These results suggest that HDL prevent the suicide pathway leading to apoptosis of endothelial cells by decreasing the CPP32-like protease activity and that HDL thus play a protective role against the "response-to-injury" hypothesis of atherogenesis. (nih.gov)
  • Death receptor ligation activates the extrinsic apoptosis pathway and results in recruitment of FADD and caspase 8 to the death-inducing signaling complex (DISC), followed by activation of caspase 8 and caspase 3 [ 8 - 12 ]. (hindawi.com)
  • This type of apoptosis differs mechanistically from that brought about by the cell intrinsic pathway, which is mediated by early activation of caspase 9, and leads to loss of mitochondrial membrane potential [ 13 , 14 ]. (hindawi.com)
  • The caspase-dependent pathway is initiated by release of cytochrome c , which associates with APAF1 (apoptosis proteases-activating factor) to activate caspases ( Danial and Korsmeyer, 2004 ). (jneurosci.org)
  • Our objective is to test the hypothesis that, in human luteinized granulosa cells, epidermal growth factor (EGF) works through the MAPK signaling pathway and inhibition of EGF receptor by a specific tyrosine kinase inhibitor, tyrphostin 51, will inhibit the activation of MAPK and induce apoptosis. (sigmaaldrich.com)
  • Blockage of EGF receptor also induced apoptosis as demonstrated by the activation of caspase-3, an executioner protease of the apoptotic pathway, and by an increased percentage of subdiploid apoptotic nuclei. (sigmaaldrich.com)
  • These results support the hypothesis that in human luteinized granulosa cells, EGF works through the MAPK signaling pathway and that its inhibition by tyrphostin 51 inhibits MAPK phosphorylation and induces apoptotic nuclear changes. (sigmaaldrich.com)
  • In this study, we show that thimerosal, at nanomolar concentrations, induces neuronal cell death through the mitochondrial pathway. (spandidos-publications.com)
  • Background: The nuclear factor-κB (NF-κB) pathway activates many of the target genes that are critical to the initiation and establishment of endometriosis. (ebscohost.com)
  • This study was aimed to investigate whether NGF induced heart protection against I/R injury includes a mechanism of attenuation of ER stress-induced myocardial apoptosis by activation of PI3K/Akt pathway. (medsci.org)
  • Resistance to A. fumigatus of mice lacking Bak compared to wild-type mice demonstrates the in vivo relevance of this GT-induced apoptotic pathway involving Bak and suggests a correlation between GT production and virulence. (rupress.org)
  • Treatment of PTC cell lines with PHA665752, an inhibitor of c-Met tyrosine kinase, inhibited cell proliferation and induced apoptosis via the mitochondrial pathway in PTC cell lines. (springer.com)
  • IBP is a novel p53 target gene which suppresses cisplatin-mediated apoptosis of breast cancer cells via negative feedback regulation of the p53 signalling pathway, suggesting IBP may serve as a target for pharmacologic intervention of breast cancer resistant to cisplatin therapy. (biomedcentral.com)
  • Our results demonstrate that IBP is a novel p53 target gene which suppresses cisplatin-mediated apoptosis of breast cancer cells via negative feedback regulation of the p53 signaling pathway. (biomedcentral.com)
  • Since the pathway through apoptosis is very long if one biochemical reaction is not carried out it can eventually lead to cells that do not die and go on creating havoc in the organism. (wikibooks.org)
  • This study shows that in neuroblastoma cell lines overexpressed TF ligated with FVIIa produced upregulation of Bcl-2 expression through the JAK/STAT5 signaling pathway, resulting in resistance to apoptosis. (biomedcentral.com)
  • It binds to coagulation factor VII (FVII) and its active form (FVIIa), thus initiating the coagulation cascade via the extrinsic pathway. (biomedcentral.com)
  • PD98059 did not influence insulins ability to block apoptosis, indicating that the extracellular signal-regulated kinase pathway does not mediate insulin's survival effects. (elsevier.com)
  • These data further support the role of p38 in cellular apoptosis and support the hypothesis that insulin promotes cell survival, at least in part, by inhibiting the p38 pathway. (elsevier.com)
  • Our results demonstrated that hAMSCs and hAMSC-CM efficiently cure heat stress-induced skin injury by inhibiting apoptosis of skin cells and promoting their proliferation through activating PI3K/AKT signaling pathway, suggesting that hAMSCs and hAMSC-CM may provide an alternative therapeutic approach for the treatment of skin injury. (biomedcentral.com)
  • This finding suggests evolutionary multiplication of one gene in this region and subsequent gain or loss of function as mediator or inhibitor of apoptosis, respectively. (aacrjournals.org)
  • We show that GT induces apoptotic cell death by activating the proapoptotic Bcl-2 family member Bak, but not Bax, to elicit the generation of reactive oxygen species, the mitochondrial release of apoptogenic factors, and caspase-3 activation. (rupress.org)
  • Furthermore, high levels of IBP were found to decrease cisplatin-induced growth suppression and apoptotic cell death, which was associated with decreased p53 activity and imbalanced Bcl-2 family member expression. (biomedcentral.com)
  • In a series of studies using, in turn, neuroblastoma cell lines that express only p75, mutant NGF species that bind selectively to either p75 or trkA, and a polyclonal antibody that binds to the NGF-binding domain of p75, we demonstrate that NGF binding to p75 is both necessary and sufficient for the abrogation of apoptosis in neuroblastoma cells treated with antimitotic agents. (jneurosci.org)
  • Intracellular events conducted by the TF/FVIIa complex selectively enhanced PDGF-BB induced chemotaxis which was partly explained by the TF/FVIIa-induced transactivation of the PDGFβ-receptor. (diva-portal.org)
  • This study was designed to investigate the molecular mechanisms responsible for the induction of proinflammatory cytokines gene expression and apoptosis in human monocytic cell line THP-1 stimulated by lipoproteins (LPs) prepared from Mycoplasma genitalium . (hindawi.com)
  • LPs were also found to increase the DNA-binding activity of NF- B, a possible mechanism for the induction of cytokine mRNA expression and the cell apoptosis. (hindawi.com)
  • genitalium -derived LP may be an important etiological factor of certain diseases due to the ability of LP to produce proinflammatory cytokines and induction of apoptosis, which is probably mediated through the activation of NF- B. (hindawi.com)
  • Whether related to hypoxia, loss of nutrients, induction of nonspecific inflammatory reactions, or immune effectors implicated in the development of autoimmune disease or allograft rejection, the final outcome of these processes is destruction of the transplanted islets by apoptosis. (rupress.org)
  • It has been suggested that p75 expression is required for the induction of apoptosis in response to these insults. (jneurosci.org)
  • Induction of apoptosis plays a pivotal role in cellular homeostasis, and in this scenario, the impairment of any of its components may result in accumulation of genetic defects, preceding cancer development ( 2 ). (aacrjournals.org)
  • The cellular processes leading to apoptosis induction are not completely understood, but an important event is the activation of a cascade of cysteine proteases named caspases (2), leading to cleavage of specific substrates involved in cell death. (scielo.br)
  • Therefore, both the induction of DR5 via p8 and CHOP and the down-regulation of survival factors seem to be crucial for the marked synergistic effects induced by the two drugs in HCC cells. (aspetjournals.org)
  • Similar to Bcl-2, a transdominant-negative mutant of the NF-kappaB p65 subunit partially inhibited apoptosis, indicating a direct involvement of the transcription factor in induction of cell death. (rupress.org)
  • Surprisingly, long-term induction of CHOP by metformin is not accompanied by apoptosis even though CHOP is regarded to be a mediator of ER-stress-induced apoptosis. (biologists.org)
  • A molecular explanation of these hypoxia-induced effects includes increased anaerobic glycolysis, induction of angiogenesis and increased expression of drug export pumps, e.g. (biomedcentral.com)
  • The cytoprotective effect of A20 against apoptosis correlates with and is dependent on the abrogation of cytokine-induced NO production. (rupress.org)
  • Cytokine-mediated β cell apoptosis requires the active participation of the β cells. (rupress.org)
  • Islets deficient in ATF3 are partially protected from cytokine- or NO-induced apoptosis. (asm.org)
  • Fourth, ATF3 knockout islets are partially protected from cytokine- or nitric oxide-induced apoptosis. (garvan.org.au)
  • Coculture of IRF4 −/− and IRF4 +/+ CD4 + cells did not increase survival of IRF4 −/− CD4 + cells, indicating that the enhanced rate of IRF4 −/− Th cell apoptosis was neither transferable nor due to lack of a cytokine. (rupress.org)
  • Montelukast inhibited cell proliferation and colony formation and induced the cell death of lung cancer cells. (mdpi.com)
  • Downregulating RIP-1 and/or BAY11-7082 significantly reduced NF-kB transcriptional activity, blocked cells in G0/G1 phase, weakened proliferation, elevated caspase-8 and caspase-3 activities, and promoted cell apoptosis. (medscimonit.com)
  • It has been reported that sodium fluoride suppressed proliferation and induced apoptosis in osteoblasts. (fluoridealert.org)
  • All the tested NaF inhibited proliferation and arrested cell cycle at S phase in osteoblasts, and further demonstrated to induce apoptosis in osteoblasts. (fluoridealert.org)
  • Transcription factors of the interferon regulatory factor (IRF) family contribute to the regulation of cell proliferation and apoptosis. (rupress.org)
  • May regulate cell proliferation and coordinate apoptosis and cell cycle progression via a novel mechanism independent of both p53/TP53 and NF-kappa-B. (genecards.org)
  • We then investigated the biological effects of hAMSCs and hAMSC-CM on the apoptosis and proliferation of heat stress-injured human keratinocytes HaCAT and dermal fibroblasts (DFL) both in vivo and in vitro. (biomedcentral.com)
  • hAMSCs and hAMSC-CM markedly inhibited heat stress-induced apoptosis in HaCAT and DFL cells in vitro through activation of PI3K/AKT signaling and promoted their proliferation by activating GSK3β/β-catenin signaling. (biomedcentral.com)
  • Further investigation showed the down-regulation of B-cell lymphoma 2 (Bcl-2), up-regulation of Bcl-2 homologous antagonist/killer (Bak), and nuclear translocation of apoptosis-inducing factor (AIF) in montelukast-treated lung cancer cells. (mdpi.com)
  • In conclusion, montelukast induced lung cancer cell death via the nuclear translocation of AIF. (mdpi.com)
  • AIFM2 expression was found to be activated by overexpression of p53, which leads to cell cycle arrest or apoptosis. (atlasgeneticsoncology.org)
  • Neurons carrying double mutations for Hq/Apaf1 -/- (apoptosis proteases-activating factor) are impaired in both caspase-dependent and AIF-mediated mitochondrial cell death pathways. (jneurosci.org)
  • Using Hq/Apaf1 -/- mice, we show that reduced AIF confers sustained protection in DNA damage-induced neuronal cell death when caspase activity was inhibited. (jneurosci.org)
  • Reduced levels of AIF also protect hippocampal neurons in vivo against cell death evoked by kainic acid-induced seizure. (jneurosci.org)
  • Cell viability was monitored over time by Trypan blue dye exclusion, and apoptosis was monitored by double staining with Annexin V/propidium iodide, as previously described ( 13 ). (diabetesjournals.org)
  • Cell apoptosis was also detected by Annexin V-FITC-propidium iodide (PI) staining and acridine orange (AO)-ethidium bromide (EB) staining. (hindawi.com)
  • Growth factors may be involved in the control of ovarian cell fate and could contribute to regulation of ovarian cell apoptosis. (sigmaaldrich.com)
  • Apoptosis-inducing factor (AIF) and leukocyte elastase inhibitor/L-DNase II (LEI/LDNaseII), can interact to conduct caspase-independent cell death. (sigmaaldrich.com)
  • Programmed cell death is an important factor in tissue homeostasis. (sigmaaldrich.com)
  • In this work we show that two caspase-independent effectors of cell death, namely apoptosis-inducing factor and leukocyte elastase inhibitor derived DNase II interact and can cooperate to induce cell death. (sigmaaldrich.com)
  • Present studies demonstrate that treatment with the histone deacetylases inhibitor LAQ824, a cinnamic acid hydroxamate, increased the acetylation of histones H3 and H4, as well as induced p21(WAF1) in the human T-cell acute leukemia Jurkat, B lymphoblast SKW 6.4, and acute myelogenous leukemia HL-60 cells. (unboundmedicine.com)
  • This was associated with increased accumulation of the cells in the G(1) phase of the cell cycle, as well as accompanied by the processing and activity of caspase-9 and -3, and apoptosis. (unboundmedicine.com)
  • The intratumoral delivery elicited tumor cell apoptosis and suppressed tumor growth. (aacrjournals.org)
  • Low expression of antioxidants and a predilection to produce nitric oxide (NO) have been shown to underscore β cell apoptosis. (rupress.org)
  • β cell apoptosis can be induced by either specific T lymphocyte-mediated killing or proinflammatory cytokines. (rupress.org)
  • NO-mediated toxicity is the predominant mechanism responsible for β cell dysfunction and apoptosis induced by soluble mediators. (rupress.org)
  • Thimerosal, in a concentration- and time-dependent manner, decreased cell viability as assessed by calcein-ethidium staining and caused apoptosis detected by Hoechst 33258 dye. (spandidos-publications.com)
  • Apigenin induces growth inhibition, cell cycle arrest, and apoptosis in various types of human malignant tumor cells including breast cancer ( 7 ), prostate cancer ( 8 ), colon cancer ( 9 ), and leukemic cells ( 10 ). (aacrjournals.org)
  • We also previously reported that apigenin induces cell cycle arrest ( 11 ) and p21/WAF1 up-regulation in a tumor suppressor p53-independent manner ( 12 ). (aacrjournals.org)
  • Cell apoptosis was tested by flow cytometry. (medscimonit.com)
  • RIP-1 or c-FLIPL siRNA markedly induced cell apoptosis and enhanced caspase-8 and caspase-3 activities. (medscimonit.com)
  • Downregulation of RIP1 and c-FLIPL can relieve caspase-8 suppression, activate caspase-3, and promote cell apoptosis. (medscimonit.com)
  • Moreover, quinolinic acid-induced internucleosomal DNA fragmentation and striatal cell death were significantly reduced by the intrastriatal administration of NFκB SN50, a cell-permeable recombinant peptide that blocks NFκB nuclear translocation. (aspetjournals.org)
  • Apoptosis is mediated by cysteine-dependent, aspartate-directed proteases of the caspase family that proteolyse strategic intracellular substrates to induce cell suicide. (ebscohost.com)
  • Small interference RNA knock down of Grx significantly inhibited tumor necrosis factor-α-induced endothelial cell death because of attenuated caspase-3 cleavage concomitant with increased caspase-3 glutathiolation. (ahajournals.org)
  • Once caspase-3 is activated, it proteolyses important structural and regulatory components of the cell, leading to apoptosis. (ahajournals.org)
  • We demonstrated that 4 mM butyrate induces apoptosis in murine peritoneal macrophages in a dose- and time-dependent manner as indicated by studies of cell viability, flow cytometric analysis of annexin-V binding, DNA ladder pattern and the determination of hypodiploid DNA content. (scielo.br)
  • Apoptosis is a process of programmed cell death which is essential in maintaining homeostasis of mammalian tissues. (scielo.br)
  • The mechanisms by which butyrate induces apoptosis in different cell types are not known, but there is evidence that butyrate cell death induced in some cancer cells is triggered via activation of the caspase cascade (14). (scielo.br)
  • TFF1 upregulation on inflammatory conditions may be a protective mechanism that limits conjunctival cell loss by inhibiting apoptosis upstream and downstream of the mitochondrial events. (arvojournals.org)
  • Ocular surface disorders, ranging from ocular irritation to defective wound healing and surface destruction, induce alterations in the tear film, whose defect is the hallmark of dry-eye disorders, and the epithelium, including epithelial cell death. (arvojournals.org)
  • Cell apoptosis was determined by Hoechst staining FC assay. (medscimonit.com)
  • These initiating caspases in turn activate "effector" caspases such as caspase-3, -6 and -7, which result in tumor cell apoptosis. (aspetjournals.org)
  • through induced tumor cell apoptosis, suppressed tumor progression, and improved survival. (aspetjournals.org)
  • In this report, we describe several lines of evidence supporting a role of ATF3 in stress-induced beta-cell apoptosis. (garvan.org.au)
  • First, ATF3 is induced in beta cells by signals relevant to beta-cell destruction: proinflammatory cytokines, nitric oxide, and high concentrations of glucose and palmitate. (garvan.org.au)
  • Taken together, our results suggest ATF3 to be a novel regulator of stress-induced beta-cell apoptosis. (garvan.org.au)
  • Role for the proapoptotic factor BIM in mediating imatinib-induced apoptosis in a c-KIT-dependent gastrointestinal stromal tumor cell line. (harvard.edu)
  • We have previously shown that TGF-β1 rapidly induces apoptosis in the FaO rat hepatoma cell line. (asm.org)
  • Aim: The aim of this thesis was to study different aspects of TF activity, e.g. the importance of procoagulant MP and TF-induced intracellular signaling pathways, with focus on cell migration (chemotaxis) and apoptosis. (diva-portal.org)
  • AIF is one of the crucial factors responsible for mitochondrial apoptosis, however, it can also promote cell survival independently from its role in apoptosis, and therefore can be potentially used as a tool in prevention of the onset of CKD in diabetic patients. (elsevier.com)
  • Conclusions: Our study provides insight into AIF expression pattern during short term diabetes model, confirming possible dual role of AIF, not only in apoptosis but also in cell function and homeostasis, and proving AIF as potential therapeutic target and marker of advancement of CKD. (elsevier.com)
  • Defects in programmed cell death (apoptosis) mechanisms play an important role in tumor pathogenesis by enabling neoplastic cells to escape from cell autonomous or immunologic growth control mechanisms ( 1 ). (aacrjournals.org)
  • Isoflurane, one of the most commonly used volatile anesthetics, has been shown to induce apoptosis in different cell types, where anesthetic exposure leads to neuronal cell death via apoptosis in the developing rodent brain, and prolonged isoflurane has been reported to induce apoptosis in cancer cells. (asahq.org)
  • The cytotoxic activities and cell death mechanism against B16F10-Nex2 cells were determined with synthetic peptide R18H derived from the POU domain of the BRN2 transcription factor. (eurekaselect.com)
  • Objective: To determine the cell death mechanisms and in vivo activity of peptide R18H derived from the POU domain of the BRN2 transcription factor against B16F10-Nex2 cells. (eurekaselect.com)
  • Enhanced CD4 + cell apoptosis was also observed after anti-CD95 mAb treatment, despite normal CD95 expression. (rupress.org)
  • Removal of endogenous cytokines, notably interleukin (IL)-4, led to increased and equally high levels of IRF4 −/− and IRF4 +/+ cell apoptosis, whereas the protective activity of exogenous IL-4 was reduced in IRF4 −/− CD4 + cells despite normal expression of the IL-4 receptor. (rupress.org)
  • Estrogen binding to ERα induces both genomic and nongenomic actions of the ER, which ultimately lead to increased breast cancer cell growth. (biomedcentral.com)
  • These variants do not induce apoptosis in DR4-responsive cell lines but show a large increase in biological activity in DR5-responsive cancer cell lines. (nuigalway.ie)
  • Apoptosis is the programmed death of a cell. (wikibooks.org)
  • This orderly pattern of events is called programmed cell death, also known as apoptosis. (wikibooks.org)
  • Apoptosis was studied in roundworms and in the final stages of its cell death, there discovery of the death-inducing protease CED-3 activation became the cause of the apoptosis. (wikibooks.org)
  • There are 3 different mechanisms for cell apoptosis. (wikibooks.org)
  • Description: A sandwich ELISA for quantitative measurement of Human apoptosis inducing factor,AIF in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. (srbiosystem.com)
  • This apoptosis inducing factor ELISA kit is validated to work with samples from whole blood, serum, plasma and cell culture supernatant. (srbiosystem.com)
  • Description: Quantitativesandwich ELISA kit for measuring Human apoptosis inducing factor, AIF in samples from serum, plasma, tissue homogenates, cell lysates. (srbiosystem.com)
  • Pre-exposure to a novel nutritional mixture containing a series of phytochemicals prevents acetaminophen-induced programmed and unprogrammed cell deaths by enhancing BCL-XL expression and minimizing oxidative stress in the liver. (sciepub.com)
  • In order to identify novel causes of resistance to cisplatin, we explored the role of Apoptosis Inducing Factor (AIF) that mediates caspase independent apoptosis in cisplatin induced cell death in PC. (semanticscholar.org)
  • Apicularen A acetate induces cell death via AIF translocation and disrupts the microtubule network by down-regulating tubulin in HM7 human colon cancer cells. (semanticscholar.org)
  • Enforced expression of TF in a TF-negative neuroblastoma cell line in the presence of FVIIa induced upregulation of Bcl-2, leading to resistance to doxorubicin. (biomedcentral.com)
  • Conversely, inhibition of endogenous TF expression in a TF-overexpressing neuroblastoma cell line using siRNA resulted in down-regulation of Bcl-2 and sensitization to doxorubicin-induced apoptosis. (biomedcentral.com)
  • Unlike the extracellular signal- regulated kinases (p42 and p44 MAP kinases), which are stimulated by insulin in many cell types, p38 activity is inhibited by insulin in postmitotic fetal neurons for which insulin is a potent survival factor (Heidenreich, K. A., and Kummer, J. L. (1996) J. Biol. (elsevier.com)
  • To better understand the relationship between p38 activity and cell survival, we induced apoptosis in two cell lines and examined the ability of insulin or a specific p38 inhibitor (a pyridinyl imidazole compound PD169316) to block p38 activity and cell death. (elsevier.com)
  • Here we report that HDL prevent the apoptosis of human umbilical venous endothelial cells (HUVECs) induced by tumor necrosis factor-alpha (TNF-alpha) via an inhibition of CPP32-like protease activity. (nih.gov)
  • Epidermal growth factor receptor inhibition by tyrphostin 51 induces apoptosis in luteinized granulosa cells. (sigmaaldrich.com)
  • Inhibition of Fibroblast Growth Factor Receptor 3 Induces Differentiation and Apoptosis in t(4;14) Myeloma. (mayo.edu)
  • Of note is the inhibition of the etoposide-induced activation of p53 under hypoxia. (biomedcentral.com)
  • Cluster analysis of data unravels several possible pathways involved in the hypoxia-induced protection against etoposide-induced apoptosis: one of them could be the inhibition of p53 activity under hypoxia since caspase 3 activity parallels Bax and Bak expression profile. (biomedcentral.com)
  • Molecular characterization of mitochondrial apoptosis-inducing factor. (nih.gov)
  • However, the molecular mechanisms of increased apoptosis in insulin-resistant macrophages remain unclear. (harvard.edu)
  • Ceccatelli, S. 2002-11-01 00:00:00 We have previously shown that the neurotoxic compounds colchicine, methylmercury (MeHg) and hydrogen peroxide (H2O2) cause apoptosis in primary cultures of cerebellar granule cells (CGC), characterized by nuclear condensation and high‐molecular weight DNA fragmentation. (deepdyve.com)
  • Nuclear translocation of apoptosis inducing factor is associated with cisplatin induced apoptosis in LNCaP prostate cancer cells. (semanticscholar.org)
  • AIF (apoptosis-inducing factor) is an important caspase-independent death regulator in multiple neuronal injury pathways. (jneurosci.org)
  • We have previously described the differential pathways activated by UV irradiation and benzalkonium chloride (BAK), the most commonly used preservative in ophthalmic solutions, when triggering apoptosis of conjunctival cells. (arvojournals.org)
  • In conclusion, metformin induces distinct ER stress pathways in cardiomyocytes and our results indicate that CHOP is not necessarily a mediator of apoptosis. (biologists.org)
  • The third ER sensor in UPR pathways is the membrane-bound transcription factor ATF6. (biologists.org)
  • To investigate the anti-apoptotic role of tumor necrosis factor-α (TNF-α) and its signaling pathways in cultured human fibroblast-like synoviocytes (FLS) from patients with rheumatoid arthritis. (elsevier.com)
  • Synthetic analogue of rocaglaol displays a potent and selective cytotoxicity in cancer cells: involvement of apoptosis inducing factor and caspase-12. (semanticscholar.org)
  • Our data thus provide additional information regarding regulation of apoptosis in luteinized granulosa cells. (sigmaaldrich.com)
  • These findings demonstrate a novel mechanism of caspase-3 regulation by Grx in tumor necrosis factor-α-induced apoptosis. (ahajournals.org)
  • Apoptosis would seem a logical candidate to participate in macrophage regulation, as it is known to regulate other cells in the immune system such as activated T cells (6,7), B cells (8,9) and granulocytes (10). (scielo.br)
  • Butyrate could be important in the regulation of macrophage apoptosis in situations where these cells are uncontrolled such as in atherosclerotic lesions and in the treatment of some types of leukemia with chemotherapeutic drugs. (scielo.br)
  • Because of the low proliferative potential of tumor cells in patients with Sézary syndrome (SzS), their accumulation has been suggested to be due to defective regulation of apoptosis. (uzh.ch)
  • Regulation of gene expression through HIF-1 (hypoxia-inducible factor-1) but also via other transcription factors plays an important role in this process. (biomedcentral.com)
  • PARP1 [poly(ADP-ribose) polymerase-1] activation is required for AIF translocation in N -methyl- N ′-nitro- N -nitrosoguanidine-induced damage or NMDA-induced excitotoxicity because AIF fails to translocate in PARP1 -/- neurons (Yu et al. (jneurosci.org)
  • In Hq mice, instead of supernumerary cells attributable to failed apoptosis, surprisingly their cerebellum degenerates progressively and Hq neurons are more sensitive to oxidative stress. (jneurosci.org)
  • Furthermore, Hq neurons exhibit a striking resistance specifically to NMDA- and kainic acid-induced excitotoxicity. (jneurosci.org)
  • Excitotoxin-induced destruction of striatal neurons, proposed as a model of Huntington's disease, involves a process having the biochemical stigmata of apoptosis. (aspetjournals.org)
  • They further suggest that NFκB activation contributes to the excitotoxin-induced death of striatal neurons. (aspetjournals.org)
  • Valproic acid induces apoptosis in differentiating hippocampal neurons by the release of tumor necrosis factor-α from activated astrocytes. (semanticscholar.org)
  • Sulindac attenuates valproic acid-induced oxidative stress levels in primary cultured cortical neurons and ameliorates repetitive/stereotypic-like movement disorders in Wistar rats prenatally exposed to valproic acid. (semanticscholar.org)
  • Both were biologically active, inducing apoptosis of both human and murine target cells in vitro with similar specific activities. (nih.gov)
  • Human oligodendrocyte precursor cells in vitro: phenotypic analysis and differential response to growth factors. (springer.com)
  • The in vitro transfer elicited apoptosis, as demonstrated by the quantification of viable or apoptotic cells and by the analysis of activation of pro-caspase-8 and cleavage of poly(ADP-ribose) polymerase. (aacrjournals.org)
  • We show here that wild-type p53 protects cells from caspase-dependent death induced by this therapeutic combination in vitro . (aacrjournals.org)
  • Moreover, purified fodrin is cleaved in vitro by CPP32 (but not by ICE) into fragments of the same size observed in vivo during apoptosis. (harvard.edu)
  • In vitro, activation of IRF4 −/− CD4 + Th cells led to greatly increased apoptosis compared with wild-type cells. (rupress.org)
  • In this pre-clinical in vitro study conducted in estrogen receptor positive (ER+) breast cancer cells, we have characterized the effects of insulin-like growth factor I (IGF-1) on the cytostatic and cytotoxic action of antiestrogen treatment when used as a single agent or in combination with the antiprogestin mifepristone (MIF). (biomedcentral.com)
  • and immunoblot analysis to determine the levels of cleaved poly-ADP ribose polymerase (PARP) and lamin A that result from caspase-dependent apoptosis. (biomedcentral.com)
  • In the search for tumor-specific agents of gene therapy, one promising agent has arisen from among the TNF 4 family of factors. (aacrjournals.org)
  • Here we show that human and rat islets can be induced to rapidly express the antiapoptotic gene A20 after interleukin (IL)-1β activation. (rupress.org)
  • Overexpression of A20 by means of adenovirus-mediated gene transfer protects islets from IL-1β and interferon γ-induced apoptosis. (rupress.org)
  • FoxO1 was shown by chromatin immunoprecipitation and promoter expression analysis to induce inhibitor of κBɛ gene expression and thereby to attenuate the increase of nuclear p65 and nuclear factor-κB activity during endoplasmic reticulum stress, with proapoptotic and anti-inflammatory consequences. (harvard.edu)
  • Activating transcription factor 3 (ATF3) is a stress-inducible gene and encodes a member of the ATF/CREB family of transcription factors. (garvan.org.au)
  • To evaluate the alternations in the apoptosis inducing factor (AIF) gene expression, real-time polymerase chain reaction (real-time -PCR) was performed, and the obtained data were analyzed using REST software. (ac.ir)
  • Glabridin triggers over-expression of apoptosis inducing factor (AIF) gene in Candida albicans', Current Medical Mycology , 4(3), pp. 19-22. (ac.ir)
  • Prevention by nerve growth factor (NGF) of apoptotic death in neural cells has been variously ascribed to binding of NGF to its low-affinity (p75) or high-affinity (trkA) receptor or to a cooperative interaction between the two. (jneurosci.org)
  • This event seemed to be dependent on the transcription factor peroxisome proliferator-activated receptor-γ whose level significantly increased after WIN treatment. (aspetjournals.org)
  • Antioxidative treatment prevents activation of death-receptor- and mitochondrion-dependent apoptosis in the hearts of diabetic rats. (sciepub.com)
  • However, our data indicate that apoptosis induced by butyrate and LPS involves different mechanisms. (scielo.br)
  • Several clinicopathological variables, including stage, cancer invasion and distant metastasis, are used for prognostication for PTC ( 4 , 5 ) However, the factors and mechanisms determining the aggressive behavior of some papillary carcinomas that result in recurrence and metastatic lesions refractory to current modalities of treatment are still not fully known. (springer.com)
  • Despite a significant body of research on the role of TF on tumor growth and metastases in some solid tumors, the mechanisms involved in both TF-mediated signaling control of apoptosis and the cellular response to anticancer treatments has not been studied in any detail thus far. (biomedcentral.com)
  • Butyrate has been shown to induce apoptosis in many different cells of the immune system, including murine thymocytes, splenic T cells, human Jurkat T cells (12) and lymphocytic leukemia cells (13). (scielo.br)
  • Interleukin 1 beta-converting enzyme (ICE)/Ced-3 proteases play a critical role in apoptosis. (harvard.edu)
  • Overexpression of NF-κB p65 by transient transfection protected the cells from the Cd-induced apoptosis. (ebscohost.com)
  • Overexpression of active FoxO1 or FoxO3 failed to induce apoptosis in unchallenged macrophages but exacerbated apoptosis in macrophages with an active endoplasmic reticulum stress response. (harvard.edu)
  • Overexpression of Smad3 dramatically enhanced TGF-β1-induced cleavage of BAD and apoptosis, whereas antisense Smad3 blocked TGF-β1-induced apoptosis and BAD cleavage. (asm.org)
  • These results suggest that TGF-β1 induces apoptosis through the cleavage of BAD in a Smad3-dependent mechanism. (asm.org)
  • Finally, we explain the mechanism behind simvastatin-induced apoptosis in cancer cells and how statins interfere with TF-dependent signaling and coagulation. (diva-portal.org)
  • MEK1 expression reduced the levels of ROS and mitochondrial membrane depolarization induced by the hormonal treatments via a mechanism that involved the phosphorylation and proteasomal turnover of the proapoptotic BH3-only Bcl-2 family member Bim. (biomedcentral.com)
  • Pretreatment of the cells with the antioxidant U83836E or butylated hydroxytoluene preserved the DNA-binding activity and blocked the Cd-induced decease in IκB-α phosphorylation. (ebscohost.com)
  • NGF pretreatment also induced phosphorylation of Akt. (medsci.org)
  • eIF2α phosphorylation promotes the expression of activating transcription factors (ATFs) such as ATF4 and ATF5. (biologists.org)
  • At 1-10 ng·ml -1 concentrations, TNF-α induced phosphorylation of Akt and BAD in a time and concentration-dependent manner. (elsevier.com)
  • To further analyze the contribution of NFκB to excitotoxic neuronal death in vivo , changes in binding activities of NFκB and other transcription factors as well as the consequences of inhibiting NFκB nuclear translocation were measured after the infusion of quinolinic acid (120 nmol) into rat striatum. (aspetjournals.org)
  • Conversely, attenuation of NF-κB activity by pretreatment with SN50, an NF-κB nuclear translocation inhibitor, potentiated apoptosis. (ebscohost.com)
  • A20 inhibits the activation of the transcription factor nuclear factor κB at a level upstream of IκBα degradation. (rupress.org)
  • Baicalein is also known as a selective 12-lipoxygenase (12-LOX) inhibitor ( 1 ), which induces antiproliferation and apoptosis in various cancer cells ( 2 - 4 ). (aacrjournals.org)
  • Beyond family history, the most important risk factors for ovarian cancer include early menarche, late menopause, nulliparity, and in contrast, the use of anovulatory drugs that reduces the risk. (aacrjournals.org)
  • The epidemiologic observation that all factors that limit the number of ovulations over lifetime are protective against ovarian cancer resulted in the so-called incessant ovulation theory decades ago ( 1 ). (aacrjournals.org)
  • Our findings indicate that resveratrol induces apoptosis via HIF-1α/ROS/p53 signaling in prostate cancer cells and may be a useful therapeutic agent against prostate cancer. (medscimonit.com)
  • 24 Given the role of caveolin in anesthetic-induced protection, the potential exists that caveolin status ( i.e. , presence or lack of caveolin expression) may be an important clinical determinant of the response of cancer cells to volatile anesthetics and subsequent postoperative anticancer therapy. (asahq.org)
  • Importantly, small-molecule inhibitors of MEK1 circumvented the prosurvival action of IGF-1 by restoring Bim to levels that more effectively mediated apoptosis in ER + breast cancer cells. (biomedcentral.com)
  • Breast cancer cells overexpressing IBP were resistant to cisplatin-induced growth suppression and apoptosis. (biomedcentral.com)
  • Glabridin can also mediate apoptosis in yeast cells by changing the mitochondrial membrane potential, activation of caspase-like proteases, and DNA cleavage. (ac.ir)
  • in this study, physiological hypoxia was shown to inhibit apoptosis induced in HepG2 cells by etoposide. (biomedcentral.com)
  • In addition to its direct toxic potential, NO induces Fas expression on β cells, priming them to T lymphocyte-mediated killing ( 15 ). (rupress.org)
  • Transcription factors, such as nuclear factor-kappa B (NF-κB), mediate the expression of a number of genes involved in apoptosis. (ebscohost.com)
  • Pyrrolidine Dithiocarbamate Attenuates Nuclear Factor-κB Activation, Cyclooxygenase-2 Expression and Prostaglandin E2 Production in Human Endometriotic Epithelial Cells. (ebscohost.com)
  • NF-κB-dependent MnSOD expression protects adenocarcinoma cells from TNF-α-induced apoptosis. (ebscohost.com)
  • Transfection of control cells with high (J82 cells) or low (MiaPaCa-2 cells) TF expression with siRNATF oligonucleotides caused apoptosis of the J82 but not of the MiaPaCa-2 cells. (lu.se)
  • Recent studies demonstrate that expression of tumor-derived TF also mediates intracellular signaling relevant to tumor growth and apoptosis. (biomedcentral.com)
  • Moreover, specific downregulation of HIF-1α by RNA interference significantly enhanced apoptosis under hypoxia possibly by preventing the hypoxia mediated decrease in Bak expression without altering Bax expression. (biomedcentral.com)
  • we have tested the necessity for and sufficiency of p75 binding of NGF for protection of neuroblastoma cells from antimitotic agent-induced apoptosis. (jneurosci.org)
  • Our data suggest that thimerosal causes apoptosis in neuroblastoma cells by changing the mitochondrial microenvironment. (spandidos-publications.com)
  • Wei K, Liu L, Xie F, Hao X, Luo J, Min S. Nerve Growth Factor Protects the Ischemic Heart via Attenuation of the Endoplasmic Reticulum Stress Induced Apoptosis by Activation of Phosphatidylinositol 3-Kinase. (medsci.org)
  • RESULTS-Insulin-resistant macrophages showed attenuated Akt activation and increased nuclear localization of FoxO1 during endoplasmic reticulum stress induced by free cholesterol loading. (harvard.edu)
  • Recent studies suggested that transcription factor nuclear factor (NF)-κB may be involved in excitotoxicity. (aspetjournals.org)
  • Other transcription factor changes included AP-1, whose binding peaked about 6 hr after quinolinic acid administration, and E2F-1, which was only modestly and transiently elevated. (aspetjournals.org)
  • These results illustrate the complex temporal pattern of transcription factor change attending the apoptotic destruction produced in rat striatum by quinolinic acid. (aspetjournals.org)
  • The present study was designed to examine the involvement of this transcription factor in Cd-induced apoptosis. (ebscohost.com)
  • CONCLUSIONS-Decreased Akt and increased FoxO transcription factor activity during the endoplasmic reticulum stress response leads to increased apoptosis of insulin-resistant macrophages. (harvard.edu)
  • Background: BRN2 transcription factor is associated with the development of malignant melanoma. (eurekaselect.com)
  • Conclusion: Peptide R18H from BRN2 transcription factor induced apoptosis in B16F10-Nex2 and displayed antitumor activity in vivo. (eurekaselect.com)
  • Bcl-2 down-regulates the activity of transcription factor NF-kappaB induced upon apoptosis. (rupress.org)
  • Among the many target genes of the transcription factor NF-kappaB are p53 and c-myc, both of which are involved in apoptosis. (rupress.org)
  • In vivo excitotoxic studies using kainic acid-induced seizure showed that Hq mice had significantly less hippocampal damage than wild-type littermates. (jneurosci.org)
  • The topical application of apigenin in mice decreases the number and size of tumors in the skin induced by chemical carcinogens ( 2 ) or by UV exposure in vivo ( 3 ). (aacrjournals.org)
  • These results suggest that Cd-induced apoptosis involves suppression of NF-κB activity which may be mediated by oxidative stress. (ebscohost.com)
  • Transforming growth factor β (TGF-β) family members regulate a broad spectrum of cellular processes, including cellular growth, differentiation, and apoptosis ( 37 ). (asm.org)
  • The Human Apoptosis Inducing Factor (AIF) ELISA Kit allows for quantitative determination of Apoptosis Inducing Factor in Serum, Plasma, Tissue homogenates and other biological fluids. (fishersci.com)
  • Background: Tissue factor (TF) is a 47 kDa transmembrane glycoprotein known as the main initiator of blood coagulation. (diva-portal.org)
  • Tissue factor (TF) has been implicated in the thrombotic complications seen during vascular rejection of allografts and may contribute to intimal hyperplasia in chronic allograft vasculopathy. (lu.se)
  • For example, the formation of fingers and toes of a fetus is made possible by apoptosis of the tissue between them. (wikibooks.org)
  • Description: A sandwich quantitative ELISA assay kit for detection of Rat Apoptosis Inducing Factor (AIF) in samples from serum, plasma, tissue homogenates or other biological fluids. (srbiosystem.com)
  • To evaluate the role of AIF in BAX-dependent (DNA damage induced) and BAX-independent (excitotoxic) neuronal death, we used Harlequin ( Hq ) mice, which are hypomorphic for AIF. (jneurosci.org)
  • Insulin-resistant macrophages are more susceptible to endoplasmic reticulum stress-associated apoptosis probably contributing to macrophage death and necrotic core formation in atherosclerotic plaques in type 2 diabetes. (harvard.edu)
  • Because tumor necrosis factor-α (TNF-α)-induced inflammation and apoptosis contribute to vascular diseases including atherosclerosis and hypertension, 10-13 we are interested in the role of glutathiolation in TNF-α-induced death signaling. (ahajournals.org)
  • Specifically, we show that Grx plays a key role in caspase-3 cleavage by regulating caspase-3 glutathiolation in response to TNF-α, thereby modulating TNF-α-induced death signaling. (ahajournals.org)
  • ref. 6 ), recruiting Fas-associated death domain and procaspase-8 ( 7 - 9 ) to their intracellular death domains, hereby forming the death-inducing signaling complex and initiating apoptosis. (aacrjournals.org)
  • The present invention discloses artificial death switches (ADSs) based on chemically induced dimerization of the cysteine proteases, caspase-1 (ICE) and caspase-3 (YAMA). (google.com)
  • One of these latent death factors is cytochrome c, which can stimulate the proteolytic activation of caspase zymogens. (archives-ouvertes.fr)
  • Both insulin and PD169316 markedly blocked the increase in p38 activity and apoptosis. (elsevier.com)