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.
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.
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
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.
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 ...
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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: 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.
Meghna Nair is Human Resources Officer at AIFs India country office in Gurgaon.She holds a PGD in Human Resource & Administration from Tata Institute of Social Science -SVE .She has 5+ years of work experience in corporate as well as development sector. Prior to joining AIF in 2021, Meghna has worked with Rentickle.. ...
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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|
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I just built GIGABYTE GA-P35-DS3R Intel Core 2 Duo E6750 Scythe Infinity HSF eVGA 8800GTS 320MB Superclocked 2x1GB Crucial Ballastix (MicronD9GMH)...
Apoptosis inducing factor is involved in initiating a caspase-independent pathway of apoptosis (positive intrinsic regulator of ... Apoptosis inducing factor is a flavoprotein. It also acts as an NADH oxidase. Another AIF function is to regulate the ... Apoptosis Inducing Factor (AIF) is a protein that triggers chromatin condensation and DNA fragmentation in a cell in order to ... Human genes encoding apoptosis inducing factor isozymes include: AIFM1 AIFM2 AIFM3 The apoptotic function of AIFs has been ...
... 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: ...
"Apoptosis-inducing factor CA 2352467 A1". Retrieved 9 August 2015. "Apoptosis-inducing factor CA 2352467 C". Retrieved 9 August ...
There also exists a caspase-independent apoptotic pathway that is mediated by AIF (apoptosis-inducing factor). Amphibian frog ... Database of proteins involved in apoptosis Apoptosis Video Apoptosis Video (WEHI on YouTube ) The Mechanisms of Apoptosis ... Later studies linked this phenomenon to the release of AIF (apoptosis-inducing factor) from the mitochondria and its ... The study of apoptosis brought on by Bunyaviridae was initiated in 1996, when it was observed that apoptosis was induced by the ...
"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". Fortin A, MacLaurin JG, Arbour N, et al. (July 2004). "The proapoptotic ... 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 ...
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 ...
"FOXO proteins regulate tumor necrosis factor-related apoptosis inducing ligand expression. Implications for PTEN mutation in ... November 2007). "The BH3-only protein Puma plays an essential role in cytokine deprivation induced apoptosis of mast cells". ... 2018) demonstrated that FOXO3a activation in vascular smooth muscle cells induces prominent apoptosis and extracellular matrix ... "Phosphorylation of forkhead transcription factors by erythropoietin and stem cell factor prevents acetylation and their ...
"Cowchock syndrome is associated with a mutation in apoptosis-inducing factor". American Journal of Human Genetics. 91 (6): 1095 ...
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: ...
"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 ...
October 2005). "Transcriptional factor FOXL2 interacts with DP103 and induces apoptosis". Biochemical and Biophysical Research ... and increased numbers of secondary follicles as a result of the inability to induce apoptosis. TNF-related apoptosis-inducing ... tumor necrosis factor alpha (TNF alpha) and receptors Fas ligand and receptors TNF-related apoptosis-inducing ligand (TRAIL; ... 2015). "Tumor necrosis factor alpha inhibits ovulation and induces granulosa cell death in rat ovaries". Reproductive Medicine ...
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 ... TNF-Related Apoptosis-Inducing Ligand). Vitamins & Hormones. Vol. 67. pp. 1-17. doi:10.1016/S0083-6729(04)67001-4. ISBN 978-0- ...
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 ...
... 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 ...
"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. ...
... "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 ...
"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 ...
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 ...
"Involvement of Caspases and Apoptosis-Inducing Factor in Bufotalin-Induced Apoptosis of Hep 3B Cells". Journal of Agricultural ... Bufotalin induces apoptosis in vitro in human hepatocellular carcinoma Hep 3B cells and might involve caspases and apoptosis ... Waiwut, P; Inujima, A; Inoue, H; Saiki, I; Sakurai, H (January 2012). "Bufotalin sensitizes death receptor-induced apoptosis ... inducing factor (AIF). The use of bufotalin as a cancer treating compound is still in the experimental phase. It also arrests ...
"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 ...
... 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 ...
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 ...
... 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 ...
This direct contact results in secretion of apoptosis-inducing factors and in death of a cancer cell. Taken together, immune ... In contrast, the transcript level of regulatory factors (Foxp3, Il5, and Il13) was increased. Situation is a bit different when ...
"Atractylenolide II induces G1 cell-cycle arrest and apoptosis in B16 melanoma cells". Journal of Ethnopharmacology. 136 (1): ... In order for the cell to continue through the G1-pm, there must be a high amount of growth factors and a steady rate of protein ... G1 phase and the other subphases of the cell cycle may be affected by limiting growth factors such as nutrient supply, ... The first restriction point is growth-factor dependent and determines whether the cell moves into the G0 phase, while the ...
... is an apoptosis inducing protein that is able to regulate the function of tumor suppressor. More specifically, P14ARF is ... 440 transcription factors were identified within the promoter region. To highlight some of relevance and importance to PANO1: ... It is curious that PANO1, an apoptosis inducer, and SLC25A22, an apoptosis inhibiter, overlap one another. The structure of ... PANO1 is also known as Proapoptotic Nucleolar Protein 1, PANO, and Pre-mRNA-splicing Factor CW22-like. PANO1 is located on ...
October 2005). "The contribution of apoptosis-inducing factor, caspase-activated DNase, and inhibitor of caspase-activated ... "The 40-kDa subunit of DNA fragmentation factor induces DNA fragmentation and chromatin condensation during apoptosis". ... Besides, Caspase 3 induces DNA breaks in the promoter of the factor p21 and this strand breakup is related to p21 gene ... The factor that seems to induce more cell differentiation is caspase-3 protease. This was identified as the penultimate stage ...
... an apoptosis suppressor limited to terminally differentiated cells, is induced in human breast cancer and confers chemo- and ... determines the intracellular localization of the novel nuclear protein Nop30 and its interaction with the splicing factor ... "Apoptosis repressor with caspase domain inhibits cardiomyocyte apoptosis by reducing K+ currents". Am. J. Physiol., Cell ... Koseki T, Inohara N, Chen S, Núñez G (Jun 1998). "ARC, an inhibitor of apoptosis expressed in skeletal muscle and heart that ...
Perlman R, Schiemann WP, Brooks MW, Lodish HF, Weinberg RA (2001). "TGF-beta-induced apoptosis is mediated by the adapter ... It interacts with a wide variety of proteins, such as apoptosis antigen Fas, centromere protein C, and transcription factor ... Only when Daxx was bound to Pml were apoptosis rates higher, suggesting that associated cytoplasmic Daxx has the role of an ... The omnipresence of Daxx in the cell nucleus suggests that the protein may also function as a transcription factor. Although it ...
Guo X, Li T, Wang Y, Shao L, Zhang Y, Ma D, Han W (September 2009). "CMTM5 induces apoptosis of pancreatic cancer cells and has ... Li M, Luo F, Tian X, Yin S, Zhou L, Zheng S (2020). "Chemokine-Like Factor-Like MARVEL Transmembrane Domain-Containing Family ... "CMTM5 inhibits renal cancer cell growth through inducing cell-cycle arrest and apoptosis". Oncology Letters. 14 (2): 1536-1542 ... These proteins are: chemokine-like factor (i.e. CLF, the founding member of the family) and CEF-like marvel transmembrane ...
Granzymes usually cause apoptosis of the infected cell through initiation of the caspase cascade. However, apoptosis can also ... It is a pore-forming peptide, as it can puncture a microbial cell wall, allowing for other death-inducing enzymes to enter the ... The path to transcription has not been elucidated: transcription factors, promoter regions, and pathogen-associated molecular ... Granulysin has also been shown to slow the progression of cancers and destroy transformed cells through apoptosis. Patients ...
Accordingly, gene expression by degradation of transcription factors, such as p53, c-jun, c-Fos, NF-κB, c-Myc, HIF-1α, MATα2, ... Zhang H, Yang B, Pomerantz RJ, Zhang C, Arunachalam SC, Gao L (Jul 2003). "The cytidine deaminase CEM15 induces hypermutation ... signal transduction and apoptosis. Subsequently, a compromised proteasome complex assembly and function lead to reduced ... a cellular factor linked to the G2/M phase transition of the mammalian cell cycle". Proceedings of the National Academy of ...
Lei K, Davis RJ (2003). "JNK phosphorylation of Bim-related members of the Bcl2 family induces Bax-dependent apoptosis". Proc. ... Bcl-2-modifying factor is a protein that in humans is encoded by the BMF gene. The protein encoded by this gene belongs to the ... 2007). "Functional role and oncogene-regulated expression of the BH3-only factor Bmf in mammary epithelial anoikis and ... "Entrez Gene: BMF Bcl2 modifying factor". Day, Catherine L; Puthalakath Hamsa; Skea Gretchen; Strasser Andreas; Barsukov Igor; ...
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 ...
Rauch JN, Gestwicki JE (January 2014). "Binding of human nucleotide exchange factors to heat shock protein 70 (Hsp70) generates ... October 2016). "ARD1-mediated Hsp70 acetylation balances stress-induced protein refolding and degradation". Nature ... and inhibition of apoptosis in ovarian, bladder urothelial, and breast cancers. Patients with chronic hepatitis B or hepatitis ... Rauch JN, Gestwicki JE (January 2014). "Binding of human nucleotide exchange factors to heat shock protein 70 (Hsp70) generates ...
As a result, an IFN-stimulated gene factor 3 (ISGF3) complex forms-this contains STAT1, STAT2 and a third transcription factor ... Type I IFNs can induce expression of genes with either ISRE or GAS elements, but gene induction by type II IFN can occur only ... They also limit viral spread by increasing p53 activity, which kills virus-infected cells by promoting apoptosis. The effect of ... They described these observations in a 1959 publication, naming the responsible factor viral inhibitory factor (VIF). It took ...
Matarrese P, Conti L, Varano B, Gauzzi MC, Belardelli F, Gessani S, Malorni W (January 2000). "The HIV-1 vpr protein induces ... Arthur WT, Ellerbroek SM, Der CJ, Burridge K, Wennerberg K (November 2002). "XPLN, a guanine nucleotide exchange factor for ... Cerniglia GJ, Bernhard EJ, Prendergast GC (May 2001). "RhoB is required to mediate apoptosis in neoplastically transformed ... Gampel A, Parker PJ, Mellor H (September 1999). "Regulation of epidermal growth factor receptor traffic by the small GTPase ...
van Dijk TB, van Den Akker E, Amelsvoort MP, Mano H, Löwenberg B, von Lindern M (November 2000). "Stem cell factor induces ... "Interaction of c-Abl and p73alpha and their collaboration to induce apoptosis". Nature. 399 (6738): 809-13. Bibcode:1999Natur. ... Wen ST, Van Etten RA (October 1997). "The PAG gene product, a stress-induced protein with antioxidant properties, is an Abl SH3 ... Splice variants of an insulin and growth factor receptor-binding protein with PH and SH2 domains". J. Biol. Chem. 272 (5): 2659 ...
1997). "FLAME-1, a novel FADD-like anti-apoptotic molecule that regulates Fas/TNFR1-induced apoptosis". J. Biol. Chem. 272 (30 ... Zheng, L; Schickling O; Peter M E; Lenardo M J (August 2001). "The death effector domain-associated factor plays distinct ... "Caspase-2 induces apoptosis by releasing proapoptotic proteins from mitochondria". J. Biol. Chem. United States. 277 (16): ... a novel FADD-like anti-apoptotic molecule that regulates Fas/TNFR1-induced apoptosis". J. Biol. Chem. UNITED STATES. 272 (30): ...
TGFB1-induced anti-apoptotic factor 1 is a protein that in humans is encoded by the TIAF1 gene. TIAF1 has been shown to ... "A novel protein MAJN binds to Jak3 and inhibits apoptosis induced by IL-2 deprival". Biochemical and Biophysical Research ... "Entrez Gene: TIAF1 TGFB1-induced anti-apoptotic factor 1". Ji H, Zhai Q, Zhu J, Yan M, Sun L, Liu X, Zheng Z (April 2000). " ... and characterization of a novel transforming growth factor-beta1-induced TIAF1 protein that inhibits tumor necrosis factor ...
The acidic pH is actually essential for replication of the bacteria by inducing major virulence genes of the virB operon and ... The smooth LPS also inhibits host cell apoptosis by O-polysaccharides through a TNF-alpha-independent mechanism, which allows ... Lapaque, N., Moriyon, I., Moreno, E., Gorvel, J.P. "Brucella lipopolysaccharide acts as a virulence factor." Curr. Opin. ... and aids in the correct synthesis and activation of certain virulence factors. In addition, the B. suis gene for nickel ...
The expression profiles of these transcription factors are driven by the transcription factors that peak in the prior phase, ... Thus there is a net increase in cell number as the number of cells that die by apoptosis or senescence remains the same. The ... Among other things, this induces the now fertilized oocyte to return from its previously dormant, G0, state back into the cell ... One screen of single-gene knockouts identified 48 transcription factors (about 20% of all non-essential transcription factors) ...
"Tumor necrosis factor-related apoptosis-inducing ligand activates a lysosomal pathway of apoptosis that is regulated by Bcl-2 ... "Galectin-9 induces apoptosis through the calcium-calpain-caspase-1 pathway". Journal of Immunology. 170 (7): 3631-6. doi: ... "A modified version of galectin-9 induces cell cycle arrest and apoptosis of Burkitt and Hodgkin lymphoma cells". British ... Zhang ZY, Dong JH, Chen YW, Wang XQ, Li CH, Wang J, Wang GQ, Li HL, Wang XD (2012). "Galectin-9 acts as a prognostic factor ...
The three PGJ2 cyclopentenone prostaglandins induce apoptosis in rodent cultured neuron cells by a mechanism that involves ... PGD2, PGJ2, Δ12-PGJ2, and 15-deoxy-Δ12,14-PGJ2 activate the transcription factor, PPARγ, with 15-deoxy-Δ12,14-PGJ2 being the ... induces neuronal apoptosis". NeuroReport. 12 (4): 839-43. doi:10.1097/00001756-200103260-00043. PMID 11277593. S2CID 84937311. ... This PG directly binds with and activates PPARγ thereby inducing the transcription of genes containing the PPARγ response ...
In the brain, B. burgdorferi may induce astrocytes to undergo astrogliosis (proliferation followed by apoptosis), which may ... The authors argued that the factors influencing tick density and human risk between sites are still poorly understood, and that ... Borrelia burgdorferi lipoproteins induce both proliferation and apoptosis in rhesus monkey astrocytes". European Journal of ... The spirochetes may also induce host cells to secrete quinolinic acid, which stimulates the NMDA receptor on nerve cells, which ...
NMDA induces a calcium flux that allows for synaptic plasticity which is crucial for AHN. Researchers injected both ... 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 ...
... proto-oncogene, bHLH transcription factor is a protein that in humans is encoded by the MYC gene which is a member of the ... Ruf IK, Rhyne PW, Yang H, Borza CM, Hutt-Fletcher LM, Cleveland JL, Sample JT (2001). "EBV regulates c-MYC, apoptosis, and ... Chettab K, Zibara K, Belaiba SR, McGregor JL (January 2002). "Acute hyperglycaemia induces changes in the transcription levels ... Hu HM, Arcinas M, Boxer LM (March 2002). "A Myc-associated zinc finger protein-related factor binding site is required for the ...
IL-25 has been shown to induce the production of IL-4, IL-5 and IL-13. Evidence is the expression of IL-17RB on Th2 cells, not ... Furuta S, Jeng YM, Zhou L, Huang L, Kuhn I, Bissell MJ, Lee WH (April 2011). "IL-25 causes apoptosis of IL-25R-expressing ... Growth Factor Reviews. 14 (2): 155-74. doi:10.1016/S1359-6101(03)00002-9. PMID 12651226. Rickel EA, Siegel LA, Yoon BR, Rottman ... This cytokine can induce NF-κB activation, and stimulate the production of IL-8 (named also CXCL8), which is the major ...
Activated CD8+ T cells induce keratinocyte apoptosis through various mechanisms such as secretion of tumor necrosis factor (TNF ... Oral LP may also be caused by genetic factor which influence the immune function. A separate study performed in China found an ... Siponen M, Kauppila JH, Soini Y, Salo T (November 2012). "TLR4 and TLR9 are induced in oral lichen planus". Journal of Oral ... Farhi D, Dupin N (2010). "Pathophysiology, etiologic factors, and clinical management of oral lichen planus, part I: facts and ...
... and DR4 induce FADD-dependent apoptosis and activate the NF-kappaB pathway". Immunity. 7 (6): 821-30. doi:10.1016/S1074-7613(00 ... Distinct domains for nuclear factor-kappaB activation and association with tumor necrosis factor signaling proteins". J. Biol. ... Distinct domains for nuclear factor-kappaB activation and association with tumor necrosis factor signaling proteins". J. Biol. ... "Critical roles of TRAF2 and TRAF5 in tumor necrosis factor-induced NF-kappa B activation and protection from cell death". J. ...
"RAP46 is a negative regulator of glucocorticoid receptor action and hormone-induced apoptosis". The Journal of Biological ... "Coactivator TIF1beta interacts with transcription factor C/EBPbeta and glucocorticoid receptor to induce alpha1-acid ... However activated GR can complex with these other transcription factors and prevent them from binding their target genes and ... Schulz M, Eggert M, Baniahmad A, Dostert A, Heinzel T, Renkawitz R (July 2002). "RU486-induced glucocorticoid receptor agonism ...
Accordingly, gene expression by degradation of transcription factors, such as p53, c-jun, c-Fos, NF-κB, c-Myc, HIF-1α, MATα2, ... Zhang H, Yang B, Pomerantz RJ, Zhang C, Arunachalam SC, Gao L (Jul 2003). "The cytidine deaminase CEM15 induces hypermutation ... signal transduction and apoptosis. Subsequently, a compromised proteasome complex assembly and function lead to reduced ...
It can stimulate transcription factor c‑myc (activation of gene expression) and Ras pathway (suppression of apoptosis). In the ... IL-3 also induces various effector functions in both immature and mature cells that more precisely modulate the body's defense ... Sometimes also called colony-stimulating factor, multi-CSF, mast cell growth factor, MULTI-CSF, MCGF; MGC79398, MGC79399: the ... It induces proliferation and differentiation in both early pluripotent stem cells and committed progenitors. It also has many ...
Mensah-Osman, E.; Al-Katib, A.; Dandashi, M.; Mohammad, R. (2003). "XK469, a topo IIbeta inhibitor, induces apoptosis in ... There are genetic factors, with first-degree relatives of Waldenström macroglobulinemia patients shown to have a highly ... "FGFR3 is overexpressed Waldenstrom macroglobulinemia and its inhibition by Dovitinib induces apoptosis, and overcomes stroma- ... An additional predictive factor is elevated serum lactate dehydrogenase (LDH). Of cancers involving the lymphocytes, 1% of ...
S30-3 Functional analysis of apoptosis-inducing factor in the human fungal pathogen Candida albicans WK Tsang1, WP Fong2 1 ... Functional analysis of apoptosis-inducing factor in the human fungal pathogen Candida albicans ... 1. We have cloned and expressed the three putative Candida albicans apoptosis-inducing factor (AIF) sequences (orf19.1438, ...
... the role of these kinases in neuronal cell death using an established model of trophic factor deprivation induced apoptosis in ... BCL-2 family proteins are known to be central regulators of apoptosis and we have determined that the pro-apoptotic family ... Puma is transcriptionally up-regulated in trophic factor deprived neurons and that Puma induction is required for apoptosis in ... AKT is known to regulate a number of downstream pathways, however we have determined that PI3K-AKT inactivation induces Puma ...
Human tumor necrosis factor-related apoptosis-inducing ligand receptor 4 (TRAIL-R4) ELISA Kit from Cusabio. Cat#: CSB-E04749h. ... Human tumor necrosis factor-related apoptosis-inducing ligand receptor 4 (TRAIL-R4) ELISA Kit , CSB-E04749h. (No reviews yet) ... Rat tumor necrosis factor-related apoptosis inducing ligand, TRAIL ELISA Kit , CSB-E13904r , CusabioRat tumor necrosis factor- ... Rat tumor necrosis factor-related apoptosis inducing ligand, TRAIL ELISA Kit , CSB-E13904r , CusabioRat tumor necrosis factor- ...
... as it induces apoptosis of tumor cells but not normal cells, and thus has great therapeutic potential for cancer treatment. ... TRAIL binds to two cell-death-inducing (DR4 and DR5) and two decoy (DcR1, and DcR2) receptors. Here, we compare the expression ... Loss of TRAIL expression is an early event during oral carcinogenesis and may be involved in dysregulation of apoptosis and ... There was no significant association between TRAIL-R expression and OSSC histology grade, nodal status or apoptosis rates of ...
An Apoptosis-inducing Gene Therapy for Pancreatic Cancer with a Combination of 55-kDa Tumor Necrosis Factor (TNF) Receptor Gene ... An Apoptosis-inducing Gene Therapy for Pancreatic Cancer with a Combination of 55-kDa Tumor Necrosis Factor (TNF) Receptor Gene ... In fact, the mutein TNF 471 induced higher splenic natural killer cell activity in nude mice inoculated with clone 10 than did ... Intratumoral injection of recombinant human tumor necrosis factor (TNF) for inoperable pancreatic cancer has shown some ...
Nerve Growth Factor Protects the Ischemic Heart via Attenuation of the Endoplasmic Reticulum Stress Induced Apoptosis by ... Nerve Growth Factor Protects the Ischemic Heart via Attenuation of the Endoplasmic Reticulum Stress Induced Apoptosis by ... Keywords: ischemia/reperfusion injury, nerve growth factor, endoplasmic reticulum, apoptosis. Introduction. Nerve growth factor ... Nerve Growth Factor Protects the Ischemic Heart via Attenuation of the Endoplasmic Reticulum Stress Induced Apoptosis by ...
In tumor cells, loss of CD317 markedly enhanced their susceptibility to serum deprivation-induced apoptosis with no effect on ... Furthermore, overexpression of CD317 in HEK293T cells inhibits serum deprivation-induced apoptosis as well as the release and ... knockdown in serum-deprived tumor cells impaired mitochondria function and subsequently promoted apoptosis-inducing factor (AIF ... and subjected these CD317-manipulated cells to serum deprivation to study the role of CD317 on stress-induced apoptosis and the ...
Role of apoptosis-inducing factor (Aif) in the T cell lineage.. Authors: Prabhu, Savit B. Khalsa, Jasneet K. Banerjee, Hridesh ... Role of apoptosis-inducing factor (Aif) in the T cell lineage. Indian Journal of Medical Research. 2013 Nov; 138(5): 577-590. ... we have observed and reported a variety of non-redundant roles for apoptosis inducing factor (Aif), a mitochondrial ... and decreased sensitivity to neglect-induced death (NID). Thus, Aif seems to have pro-apoptotic and anti-apoptotic roles in the ...
Taken together, these findings indicate that xanthohumol-induced cell death might involve intrinsic and extrinsic apoptotic ... We investigate induction of apoptosis by xanthohumol on Ca Ski cervical cancer cell line. Xanthohumol is a prenylated chalcone ... E. Norberg, S. Orrenius, and B. Zhivotovsky, "Mitochondrial regulation of cell death: processing of apoptosis-inducing factor ( ... induced apoptotic cell death in HeLa cells via the expression of the tumor necrosis factor-related apoptosis-inducing ligand ( ...
... hepatic leukemia factor (Hlf), and thyrotroph embryonic factor (Tef). MTX also increased protein expression of PER2 and ... Under treatment with MTX, expression of core circadian clock genes, circadian transcriptional factor proline and acidic amino ... resulting in apoptosis induction. MTX is important in modulating circadian environments to understand a new aspect of ... From: Methotrexate upregulates circadian transcriptional factors PAR bZIP to induce apoptosis on rheumatoid arthritis synovial ...
Macrophage migration inhibitory factor inhibits neutrophil apoptosis by inducing cytokine release from mononuclear cells.. J ... Macrophage migration inhibitory factor inhibits neutrophil apoptosis by inducing cytokine release from mononuclear cells. ... Here, we show that both MIF and MIF‐2/D‐DT inhibit neutrophil apoptosis. This is not a direct effect, but involves the ... Individually, CXCL8 and MIF (or MIF‐2) did not significantly inhibit neutrophil apoptosis, but in combination they elicited a ...
The regulatory roles of apoptosis-inducing factor in the formation and regression processes of ocular neovascularization. Am J ... The regulatory roles of apoptosis-inducing factor in the formation and regression processes of ocular neovascularization ... The regulatory roles of apoptosis-inducing factor in the formation and regression processes of ocular neovascularization. Am J ... such as apoptosis-inducing factor (AIF) and cytochrome c. In this study, we investigated the regulatory role of cellular ...
Z-VAD-fmk prevented FL-induced apoptosis but was less effective against DOX and PTX. Thus, by inducing Hsp70, GA protected ... a potent inhibitor of apoptosis) and G1 arrest without significant apoptosis. GA blocked caspase activation and apoptosis and ... Here we investigated effects of GA and 17-AAG in apoptosis-prone cells such as HL60 and U937. In these cells, doxorubicin (DOX ... We next compared cytoprotection by GA-induced Hsp70, caspase inhibitors (Z-VAD-fmk) and cell-cycle arrest. Whereas cell-cycle ...
Trail, tumor necrosis factor-α-related apoptosis-inducing ligand; Bim/Puma, Bcl-2 interacting mediator of cell death/p53- ... that trigger apoptosis by binding to cell surface receptors. In the intrinsic pathway, several adverse factors act upon ... Immune Cell Apoptosis Prevention as Potential Therapy for Severe Infections Janie Parrino*, Richard S. Hotchkiss†, and Mike ... The extrinsic pathway is mediated by a variety of death receptor ligands, including tumor necrosis factor (TNF) and Fas ligand ...
... ... Macrophage Migration Inhibitory Factor Limits Activation-Induced Apoptosis of Platelets via CXCR7-Dependent Akt Signaling. ...
Brain-derived neurotrophic factor (BDNF) and cyclic AMP response element-binding protein (CREB) are crucial for neurogenesis ... EGCG induced activation of the PI3K/Akt pathway as evidenced by increased Akt, phospho-Akt, GSK-3β, phospho-GSK-3β, and mTORc1 ... In this study, we aimed to assess the protective effects of EGCG against sevoflurane-induced neurotoxicity in neonatal mice. ... The study indicates that EGCG was able to effectively inhibit sevoflurane-induced neurodegeneration and improve learning and ...
In addition, both cytochrome c and apoptosis-inducing factor (AIF) were upregulated and released from mitochondria to the ... Apoptosis induced by WC-Co nanoparticles and fine particles involves both extrinsic and intrinsic apoptosis pathways. ... In this study, apoptosis and related signaling induced by WC-Co nanoparticles were investigated in JB6 cells and rat lung ... Apoptosis induced by tungsten carbide-cobalt nanoparticles in JB6 cells involves ROS generation through both extrinsic and ...
Therefore, a clear understanding of how tumor hypoxia induces genomic instability is crucial for the improvement of cancer ... Therefore, a clear understanding of how tumour hypoxia induces genomic instability is crucial for the improvement of cancer ... The enhanced tumor aggressiveness stems at least partially from hypoxia-induced genomic instability. ... The enhanced tumour aggressiveness stems at least partially from hypoxia-induced genomic instability. ...
Impact factor: 0, 5-year impact factor: 0. Url: Not available.. Keywords: Animals , Apoptosis Drug Effects , Apoptosis Inducing ... Characterization of an Apoptosis-Inducing Factor Peptide Targeting Human Cyclophilin A to Inhibit Apoptosis Inducing Factor- ... Characterization of an Apoptosis-Inducing Factor Peptide Targeting Human Cyclophilin A to Inhibit Apoptosis Inducing Factor- ... Characterization of an Apoptosis-Inducing Factor Peptide Targeting Human Cyclophilin A to Inhibit Apoptosis Inducing Factor- ...
... induces cell death through the apoptosis-inducing factor in human breast cancer cells ... Ascorbate (vitamin C) induces cell death through the apoptosis-inducing factor in human breast cancer cells ... In this study, we demonstrate that ascorbate induces cell death through the apoptosis-inducing factor (AIF) in the human breast ... ascorbate (vitamin C); apoptosis-inducing factor; caspase; cell death; Ca2+. Citation. ONCOLOGY REPORTS, v.18, no.4, pp.811 - ...
Flow cytometry analysis revealed TRAIL-induced apoptosis of cancer cells. We designed recombinant L. lactis bacteria, which ... capable of inducing effective elimination of human colon cancer cells in vivo. ... Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) selectively eliminates tumor cells. However, the short ... construct was synthesized and cloned in lactococcal plasmid secretion vector pNZ8124 under the control of the nisin-induced ...
... tumour necrosis factor-alpha (TNF-alpha), and TNF-related apoptosis-inducing ligand. Currently, granulysin is accepted as the ... lacked any risk factor. Among participants without risk factors, C difficile infection prevalence was 6.9%. The most commonly ... Risk factors and familial clustering for fever 7-10 days after the first dose of measles vaccinesExternal. Klein NP, Lewis E, ... Drug induced exfoliative dermatitis: state of the artExternal. Yacoub MR, Berti A, Campochiaro C, Tombetti E, Ramirez GA, Nico ...
Tumor necrosis factor-alpha (TNF-alpha) can induce programmed cellular death (apoptosis) in liver cells. Several studies have ... Genetic factors. Although the evidence to prove a genetic predilection to alcoholism is adequate, the role of genetic factors ... The genetic factor that most clearly affects susceptibility is male or female sex. For a given level of ethanol intake, women ... Other factors that correlate with poor prognosis include older age, impaired renal function, encephalopathy, and a rise in the ...
Human dendritic cells induce tumor-specific apoptosis by soluble factors. Joo HG, Fleming TP, Tanaka Y, Dunn TJ, Linehan DC, ...
However, perturbations of the system due to senescence or environmental factors induce alterations of the physiological balance ... Perier, C.; Bové, J.; Dehay, B.; Jackson-Lewis, V.; Rabinovitch, P.S.; Przedborski, S.; Vila, M. Apoptosis-inducing factor ... Antioxidants inhibit the human cortical neuron apoptosis induced by hydrogen peroxide, tumor necrosis factor alpha, dopamine ... Apoptosis inhibition; motor performances enhancement (low striatal dopamine decline). MMP stabilization and apoptosis ...
apoptosis-inducing factor, mitochondrion-associated, 1. AIFM1. 35. AKT1. v-akt murine thymoma viral oncogene homolog 1. AKT1. ... nuclear factor, erythroid 2-like 2. NFE2L2. 82. NFKB1. nuclear factor of kappa light polypeptide gene enhancer in B-cells 1. ... eukaryotic translation elongation factor 1 alpha 1. EEF1A1. 266. EEF1E1. eukaryotic translation elongation factor 1 epsilon 1. ... platelet-derived growth factor receptor, alpha polypeptide. PDGFRA. 51. PDGFRB. platelet-derived growth factor receptor, beta ...
apoptosis inducing factor mitochondria associated 1. ISO. RGD. PMID:14526224. RGD:10047409. NCBI chrNW_004936479:1,441,508... ... activating transcription factor 4. ISO. RGD. PMID:20444431. RGD:13464322. NCBI chrNW_004936492:2,114,478...2,115,969 Ensembl ...
2004) Tumor necrosis factor-like weak inducer of apoptosis-induced neurodegeneration. J Neurosci 24:8237-8244. ... 2002) Hypoxia-induced vascular endothelial growth factor expression causes vascular leakage in the brain. Brain 125:2549-2557. ... Toxic factors from the core of the lesion may pose an additional risk for cells in the penumbra. One such factor is spreading ... OGD induced HMGB1 release from neurons (Fig. 1C). The mild OGD for 4.5 h only induced a slight increase in LDH release from ...
Antibodies to the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptors show significant activity in vitro ... Interferon gamma enhances the effectiveness of tumor necrosis factor-related apoptosis-inducing ligand receptor agonists in a ... Cytokine and Growth Factor Therapy. Future studies will seek to combine T-cell-based vaccination protocols with other ... IL-15 as a mediator of CD4+ help for CD8+ T cell longevity and avoidance of TRAIL-mediated apoptosis. Proc Natl Acad Sci U S A ...
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a transmembrane cytokine that is a promising anticancer ... Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a transmembrane cytokine that is a promising anticancer ... Genistein enhances TRAIL-induced apoptosis in A549 cells. To investigate the effects of genistein co-treatment on TRAIL-induced ... Gen, genistein; TRAIL, tumor necrosis factor-related apoptosis-inducing ligand; CQ, chloroquine. ...
  • Our data suggest that AIF-related apoptosis plays an important role in neovascularization and that mitochondria-regulated apoptosis could offer a new target for the treatment of pathological angiogenesis. (
  • Hsp70 blocks several steps of the apoptotic cascade: upstream from mitochondria, release of cytochrome C and apoptosis-inducing factor (AIF), nuclear import of AIF, activation of procaspases-9 and -3, and even downstream of active caspase-3. (
  • Ascorbate treatment caused the nuclear translocation of AIF, which is retained in the mitochondria in healthy cells, but caspase cleavage is not induced. (
  • Furthermore, cells that had been treated with human AIF-specific siRNA resisted cell death induced by ascorbate, implying that the translocation of AIF from mitochondria to the nucleus is responsible for ascorbate-mediated cell death. (
  • In the intrinsic pathway, several adverse factors act upon mitochondria to cause loss of the mitochondrial membrane potential, resulting in leakage into the cytosol of cytochrome C (Cyto C), which together with apoptotic protease activating factor 1 forms the apoptosome that activates caspase-9. (
  • In addition, both cytochrome c and apoptosis-inducing factor (AIF) were upregulated and released from mitochondria to the cytoplasm. (
  • Phosphorylated AKT inhibits the apoptosis induced by DRAM-mediated mitophagy in hepatocellular carcinoma by preventing the translocation of DRAM to mitochondria. (
  • However, overexpression of AIFM3, like AIF, induced cytochrome c release from the mitochondria, cleavage of caspase 3, and ultimately apoptosis, indicating AIFM3 induces apoptosis through caspase activation. (
  • Hypoxia also increases intracellular Ca(superscript 2+) concentration, tumor necrosis factor-α, lipid peroxidation, prostaglandin E2 production, activity of caspase-3 and -9, and release of cytochrome c from mitochondria, apoptosis inducible factor, and endonuclease G. However, it has been shown that downregulation of iNOS can limit cell injury caused by hypoxia. (
  • A flavoprotein that functions as a powerful antioxidant in the MITOCHONDRIA and promotes APOPTOSIS when released from the mitochondria. (
  • Human tumor necrosis factor-related apoptosis-inducing ligand receptor 4 (TRAIL-R4) ELISA Kit is Available at Gentaur Genprice with the fastest delivery. (
  • CusabioHuman tumor necrosis factor-related apoptosis-inducing ligand receptor 3, TRAIL-R3. (
  • CusabioHuman soluble tumor necrosis factor-related apoptosis inducing ligand, sTRAIL ELISA KIT. (
  • CusabioMouse soluble tumor necrosis factor-related apoptosis inducing ligand, sTRAIL ELISA KIT. (
  • The extrinsic pathway is mediated by a variety of death receptor ligands, including tumor necrosis factor (TNF) and Fas ligand (FaSL), that trigger apoptosis by binding to cell surface receptors. (
  • granulysin, soluble Fas ligand, perforin/granzyme, tumour necrosis factor-alpha (TNF-alpha), and TNF-related apoptosis-inducing ligand. (
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a transmembrane cytokine that is a promising anticancer agent as it selectively induces apoptosis in various types of tumor cells. (
  • Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a transmembrane cytokine that is a promising anticancer agent in cancer research ( 1 ). (
  • Tumor necrosis factor related apoptosis inducing ligand (TRAIL) is not only a key inducer of apoptosis but also a trigger for necroptosis. (
  • Finally, alpha-TOS cooperated with tumor necrosis factor-related apoptosis-inducing ligand in suppression of tumor growth in vivo. (
  • 2014). The initiation of necroptosis can be stimulated by the same death ligands that activate extrinsic apoptotic signaling pathway, such as tumor necrosis factor (TNF) alpha, Fas ligand (FasL), and TRAIL (TNF-related apoptosis-inducing ligand) or toll like receptors 3 and 4 ligands (Holler N et al. (
  • The BV score uses computational integration of the levels of 3 host proteins, including tumor necrosis factor-related apoptosis-inducing ligand, interferon gamma-induced protein 10, and C-reactive protein. (
  • Association between endometriosis and polymorphisms in tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), TRAIL receptor and osteoprotegerin genes and their serum levels. (
  • Fas ligand is a transmembrane protein part of the tumor necrosis factor (TNF) family. (
  • Fas ligand binds to the receptor and forms the death-inducing signalling complex, including the Fas-associated death domain, death-domain associated protein, and caspase-10. (
  • CD317 overexpression inhibits serum deprivation-induced apoptosis in AIF-related manner. (
  • Macrophage migration inhibitory factor inhibits neutrophil apoptosis by inducing cytokine release from mononuclear cells. (
  • Synthetic microRNA designed to target gliomas-associated antigen 1 transcription factor inhibits division and induces late apoptosis in pancreatic tumor cells. (
  • Rochat-Steiner V, Becker K, Micheau O, Schneider P, Burns K, Tschopp J: FIST/HIPK3: a Fas/FADD-interacting serine/threonine kinase that induces FADD phosphorylation and inhibits fas-mediated Jun NH(2)-terminal kinase activation. (
  • Conclusions This study represents the first to demonstrate the importance of DUOXA1 in skeletal muscle myoblasts and that DUOXA1 overexpression in muscle stem cells induces apoptosis and inhibits differentiation through DUOX1 and ASK1. (
  • 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. (
  • 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. (
  • When the activation of PI3K/Akt pathway is blocked by LY294002, the NGF induced suppression of the apoptosis-related proteins expression was reversed. (
  • Taken together, these findings indicate that xanthohumol-induced cell death might involve intrinsic and extrinsic apoptotic pathways, as well as downregulation of XIAP, upregulation of p53 proteins, and S phase cell cycle arrest in Ca Ski cervical cancer cells. (
  • Treated cardiomyocytes exhibited decreased mRNA and protein expression of peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1α) and transcription factors PPARα and ERRα, which regulate mitochondrial fatty acid metabolism, whereas genes that encode for glycolysis-related proteins were significantly upregulated. (
  • Supports regulation of cell growth and transcription factors and normal production of apoptosis-inducing proteins. (
  • We show that in mammalian cells, the Sir2 homolog SIRT1 appears to control the cellular response to stress by regulating the FOXO family of Forkhead transcription factors, a family of proteins that function as sensors of the insulin signaling pathway and as regulators of organismal longevity. (
  • Thus, one way in which members of the Sir2 family of proteins may increase organismal longevity is by tipping FOXO-dependent responses away from apoptosis and toward stress resistance. (
  • Previous studies on Bartonella henselae (B. henselae for short), the bacterium responsible for cat-scratch disease, have shown that it can directly "inject" proteins that inhibit programmed cell death (apoptosis) into the endothelial cells. (
  • Aside from its anticoagulant action, heparin binds to various growth factors, cytokines, and extracellular proteins and consequently is able to affect migration of cancer cells and angiogenesis in tumors. (
  • The three categories of changes examined include (a) immune-related molecules, (b) neurotrophins, growth factors and structural proteins, and (c) molecules associated with metabolism, signaling and regulation. (
  • A number of molecularly targeted agents were reported to modulate angiogenesis, growth factor receptors, cell cycle, and inflammation in cervical cancer signaling pathways. (
  • Both death receptor and mitochondrial apoptosis pathways were also reported to be activated by xanthohumol. (
  • PDF] Protective effects of a green tea polyphenol, epigallocatechin-3-gallate, against sevoflurane-induced neuronal apoptosis involve regulation of CREB/BDNF/TrkB and PI3K/Akt/mTOR signalling pathways in neonatal mice. (
  • Evidence is provided to support the possible involvement of extracellular signal-regulated kinase 1/2 (ERK1/2) and phosphatidylinositol-3 kinase/ protein kinase B (PI3K/AKT) pathways in EGCG-mediated protection against corticosterone-induced neuron injuries. (
  • Apoptosis induced by tungsten carbide-cobalt nanoparticle s in JB6 cells involves ROS generation through both extrinsic and intrinsic apoptosis pathways. (
  • Apoptosis induced by WC-Co nanoparticle s and fine particles involves both extrinsic and intrinsic apoptosis pathways. (
  • 2 NBP improves lipopolysaccharide-induced depressive-like behavior in rats through the involvement of the Nrf2 and NF-κB pathways. (
  • The present study provides a summary of published findings on CNT bioactivity, such as the potential of CNT, especially of multi-wall carbon nanotubes (MWCNT), to activate signaling pathways modulating transcription factor activity, induce apoptosis, induce DNA damage, and initiate biological responses. (
  • Interestingly, Wnt7a induced an alternate senescence pathway, which was independent of β-catenin, and distinct from that of classical oncogene-induced senescence mediated by the well-known p16 INK4a and p19 ARF pathways. (
  • I also have shown that the changes in cancer risk are associated with persistent alterations in the pathways that mediate cell proliferation and apoptosis. (
  • TRAIL has the ability to selectively induce apoptosis in a wide range of tumor cells but does not induce toxicity in most normal cells ( 2 ). (
  • GA blocked caspase activation and apoptosis and delayed cell death caused by DOX. (
  • Inhibitors of apoptosis (IAPs) can prevent caspase activation under certain conditions. (
  • Initiator caspase activation is more sophisticated - by special protein complexes: apoptosomes, PIDDosomes, DISC ( death-inducing signalling complexes ) [ 7 , 8 ]. (
  • Caspase-3 is triggered by the intrinsic and extrinsic apoptosis cascades. (
  • TNF-α binds specific receptors on the cell surface that transduce death signals via the extrinsic pathway of apoptosis, in other words by activating caspase 8. (
  • Xanthohumol (Figure 1 ), a prenylated chalcone isolated from the female hop plant, Humulus lupulus , was reported to have in vitro antiproliferative and apoptosis-inducing properties on prostate, ovarian, breast, and endometrium cancer cell lines [ 5 ]. (
  • Averting apoptosis in AIF-deficient mice decreased apoptosis of leukocytes and endothelial cells compared to wild-type mice and resulted in the persistence of these cells at angiogenic sites in vitro and in vivo. (
  • The in vitro experiments suggested that EGCG and its metabolites could reach the brain parenchyma through the blood-brain barrier and induce neuritogenesis suggest that metabolites of E GCG may play an important role in reducing neurodegenerative diseases. (
  • SIRT1 and the FOXO transcription factor FOXO3 formed a complex in cells in response to oxidative stress, and SIRT1 deacetylated FOXO3 in vitro and within cells. (
  • Details] Millimeter wave induced reversible externalization of phosphatidylserine molecules in cells exposed in vitro [med. (
  • In support of the hypothesis, 7 supernatants from RRMS B cells induced death of rat OL in vitro, while 3 of 4 control samples did not. (
  • 7 A number of studies have shown that NBP can improve post-stroke symptoms through various mechanisms, including inflammation, collateral circulation, mitochondrial function, apoptosis, and oxidative stress. (
  • 8 NBP ameliorates experimental autoimmune encephalomyelitis by suppressing PGAM5-induced necroptosis and inflammation in microglia. (
  • Caspases play an essential role in the apoptosis, necrosis and inflammation processes. (
  • Classically, necrosis and apoptosis have been described as separated and opposite entities by the fact that the hallmark of necrosis is the generation of inflammation caused by the uncontrolled release of the cellular debris in the micro-environment, while apoptosis, as well as the other forms of Programmed Cell Death, avoid inflammation by means of integrated biochemical steps. (
  • A further study demonstrated the pathogenic role of anti-NS1 antibodies on endothelial dysfunction by inducing cell death and inflammation. (
  • e.g. inflammation, genotoxicity, and This chapter focuses on issues as- ellers, growth factors, growth factor epigenetic alterations) and can have sociated with the understanding and receptors, signal transducers, and both genetic and epigenetic origins. (
  • These pro- has been implicated as contributing apoptosis, inflammation, and several liferating cel s replace dead cel s to the cancer phenotype, through pleiotropic responses. (
  • Sitting at 200mg per serving, the extract is designed to help neutralize stress-induced free radicals and inflammation. (
  • NGF pretreatment also induced phosphorylation of Akt. (
  • Importantly, the interaction of TIPRL with eukaryotic initiation factor 2α (eIF2α) led to eIF2α phosphorylation and activation of the eIF2α-ATF4 pathway, thereby inducing autophagy. (
  • Details] Mobile phone base station-emitted radiation does not induce phosphorylation of Hsp27 [med. (
  • The enhanced tumor aggressiveness stems at least partially from hypoxia-induced genomic instability. (
  • Rodent isoform of resistin RELMα, also known as hypoxia induced mitogenic factor (HIMF), attenuates adenosine triphosphate (ATP)-linked OCR, fatty acid oxidation (FAO) and partially increases glycolytic oxidation as compensatory mechanism in NRCMs. (
  • Therefore, iNOS inhibition may be a novel mechanism for protection from hypoxia-induced injury and cell death. (
  • Chung J, Yoon S, Datta K, Bachelder RE, Mercurio AM. Hypoxia-induced vascular endothelial growth factor transcription and protection from apoptosis are dependent on alpha6beta1 integrin in breast carcinoma cells. (
  • Inhibition of DNA synthesis, induction of cell cycle arrest in S phase, apoptosis, and cell differentiation were previously reported to be mediated by xanthohumol on MDA-MB-435 human mammary adenocarcinoma cells [ 7 ]. (
  • Previous studies indicate that genistein exerts anticancer properties that include the inhibition of tumor cell proliferation, enhanced tumor cell differentiation triggering cell cycle arrest, and the induction of apoptosis in some cell types ( 9 - 11 ). (
  • We show that apoptosis of a variety of brain cells after pneumococcal infection arises from inhibition of PtdCho biosynthesis, the first such activity described for a bacterium. (
  • Apoptosis inhibitors did not prevent the bacterial-dependent inhibition of PtdCho biosynthesis. (
  • Short-term effects of NO included cellular growth inhibition involving a p53/p21 mediated cell cycle arrest, accompanied by the secretion of cytokines and growth factors. (
  • Overexpression of DUOXA1 is usually associated with elevated Balaglitazone levels of H2O2 and inhibition of differentiation through increased apoptosis in a DUOX1-dependent manner. (
  • We investigate induction of apoptosis by xanthohumol on Ca Ski cervical cancer cell line. (
  • L-amino acid oxidase from snake venom: Biotransformation and induction of apoptosis in human colon cancer. (
  • Unlike AIF, AIFM3 does not translocate to the nucleus upon induction of apoptosis. (
  • More than 15 years ago, cholesterol decrement was first shown to inhibit tumor cell growth, metastasis of tumor cells, and induction of apoptosis (7). (
  • Although the underlying mechanisms of the hypoxia induce injury and cell death are still not fully understood, it has been shown that hypoxia induces nitric oxide (NO) overproduction and inducible nitric oxide synthase (iNOS) overexpression that play important roles in producing injury including increases in polymorphonuclear neutrophils (PMN) infiltration to injured tissues and leukotriene B4 (LTB4) generation. (
  • Here, we showed that genistein, a major isoflavone compound that exerts its anticancer properties by inhibiting tumor cell proliferation, can induce TRAIL-mediated apoptotic cell death in TRAIL‑resistant human adenocarcinoma A549 cells. (
  • In contrast to apoptosis, necrosis is a pathological form of cell death caused by acute damage, rupture of the membrane, release of the cytoplasm content, and the inflammatory process induced thereby [ 1 , 2 ]. (
  • 2014). In contrast to apoptosis, necroptosis represents a form of cell death that is optimally induced when caspases are inhibited (Holler N et al. (
  • In these cells, doxorubicin (DOX) caused rapid apoptsis, whereas GA-induced heat-shock protein-70 (Hsp70) (a potent inhibitor of apoptosis) and G1 arrest without significant apoptosis. (
  • We investigated the relationship of VEGF as an angiogenic growth factor and endostatin as an angiogenic inhibitor in patients with pre-eclampsia. (
  • Western blot analysis showed activation of proapoptotic factors including Fas, Fas-associated protein with death domain (FADD), caspase 3, 8 and 9, BID and BAX. (
  • The activation of the death receptor recruits Fas-associated death domain protein (FADD) and eventually procaspase-8 to form the death-inducing signaling complex (DISC), leading to the activation of the caspase cascade (caspase-8, -9, -10 and -3) ( 4 , 5 ). (
  • Caspase-8 activity is regulated by CASP8 and FADD-like apoptosis regulator. (
  • Chinnaiyan AM, O'Rourke K, Tewari M, Dixit VM: FADD, a novel death domain-containing protein, interacts with the death domain of Fas and initiates apoptosis. (
  • In addition, xanthohumol modulated the alkaline phosphatase isoenzymes that were expressed in malignant tissues [ 8 ] and was able to inhibit production of inflammatory factors, DNA synthesis and angiogenesis in MCF-7 cells, and breast cancer xenografts in mice [ 9 ]. (
  • In this study, we investigated the regulatory role of cellular apoptosis in angiogenesis using two models of ocular neovascularization: laser injury choroidal neovascularization and VEGF-induced corneal neovascularization in AIF-deficient mice. (
  • In this study, we aimed to assess the protective effects of EGCG against sevoflurane-induced neurotoxicity in neonatal mice. (
  • Blocking the interaction between the apoptosis-inducing factor (AIF) and cyclophilin A (CypA) by the AIF fragment AIF(370-394) is protective against glutamate-induced neuronal cell death and brain injury in mice. (
  • Various murine studies have reported that both spontaneous and carcinogen-induced tumors occur more frequently in mice that lack various elements of innate and adaptive immunity. (
  • 4 Furthermore, stroke has systemic effects that result in a spike in inflammatory cytokines during the initial activation phase, which is followed by severe immunosuppression linked to atrophy of the spleen and thymus in MCAO-induced stroke models in mice. (
  • Wnt7a-null mice under de novo conditions and in both the strains display E-cadherin-to-N-cadherin switch, reduced expression of cellular senescence markers and reduced expression of senescence-associated secretory phenotype, indicating a genetic predisposition of these mice to increased carcinogen-induced lung tumorigenesis. (
  • Lastly, I investigated the effects of maternal exposure to obesity-inducing high fat diet or adipose-tissue derived adipokine leptin during pregnancy on offspring's risk of endometrial carcinogenesis in Pten+/- and wild type mice. (
  • HPV affects body cells by integrating with the host's genome and inducing cellular dysregulation, such as increased DNA synthesis, cell proliferation, and cellular response to growth and differentiation factors, which eventually lead to the development of cervical cancer [ 1 ]. (
  • Promotes healthy cell proliferation and apoptosis. (
  • This effect was associated with reduced levels of estrogen receptor alpha, cell proliferation, and increased apoptosis. (
  • For the present study, a terpenoid constituent from G. biloba , bilobalide, was screened for protective effects on the ischaemic heart and the involvement of the PAFR [PAF (platelet-activating factor) receptor] and the enzyme that degrades PAF, PAF-AH (PAF acetylhydrolase) during hypoxia. (
  • All of the 4 modules are highly interactive with other biomolecules including growth factors, cell-surface receptor molecules and extracellular matrix components. (
  • Exogenous epidermal growth factor ( EGF ) causes apoptosis in EGF receptor (EGFR)-overexpressing cell lines . (
  • Genetic contribution of tumor necrosis factor (TNF)-alpha gene promoter (-1031, -863 and -857) and TNF receptor 2 gene polymorphisms in endometriosis susceptibility. (
  • Tumor necrosis factor (TNF)-TNF receptor gene polymorphisms and their serum levels in Korean women with endometriosis. (
  • Purification and molecular cloning of the APO-1 cell surface antigen, a member of the tumor necrosis factor/nerve growth factor receptor superfamily. (
  • Here,we evaluated TILs and MxA expression in human epidermal growth factor receptor 2 (HER2)-positive breast cancers. (
  • The prognostic significance of TILs has been determined in breast cancers, particularly human epidermal growth factor receptor 2 (HER2)-positive breast cancers and triple-negative breast cancers [ 1 ]. (
  • This article focuses on the use of targeted therapies in cervical cancer, specifically evaluating antiangiogenesis and endothelial growth factor receptor-related treatments. (
  • Elevated lavels of soluble tumour necrosis factor receptor 1, thrombomodulin and soluble endothelial cell adhesion molecules in patients with dengue haemorrhagic fever. (
  • Epidermal growth factor receptor (EGFR) being the most promising marker has potentially offered new methods to prognosticate and plays an essential role in early diagnosis and treatment apart from tumor, node and metastasis staging which has been used till now. (
  • Representative graphs ( left panel ) and statistical analysis ( Right panel ) of cell apoptosis determined by flow cytometric evaluation in HEK293T cells. (
  • In brief, 36 h post transfection,cells were cultured in the indicated conditions for another 48 h and stained with 7-AAD to detect cell apoptosis. (
  • Increased dengue virus-infected endothelial cell apoptosis caused by antibodies against nonstructural protein 1. (
  • Interference of STAT 5b expression by siRNA targeting enhanced the chemo-sensitivity of gastric cancer cells to gefitinib by promoting mitochondrial pathway-mediated cell apoptosis. (
  • Highlights from studies analyzing cytokine-induced changes in early gene expression in mixed CNS glial cultures focus on comparison of potential damaging effects of pro-inflammatory cytokines versus protective effects of downregulatory cytokines. (
  • In humans, neurons of the hippocampus undergo apoptosis as a result of meningitis. (
  • Previously, we reported that the prevention of mitochondrial apoptosis contributed to cellular survival via the prevention of the release of proapoptotic factors, such as apoptosis-inducing factor (AIF) and cytochrome c. (
  • The molecular mechanisms underlying PARP-1-dependent cell death involve release of mitochondrial apoptosis-inducing factor (AIF) and its translocation to the nucleus, which results in chromatinolysis. (
  • Historically, it has been regarded as a drug-induced immune reaction initiated by cytotoxic lymphocytes via a human leukocyte antigen (HLA)-restricted pathway. (
  • We further show that a common regulator of apoptosis apoptosis signal-regulating kinase 1 (ASK1) is usually a downstream target of Balaglitazone DUOXA1-mediated H2O2 production and that knockdown of either DUOX1 or ASK1 rescues the DUOXA1 overexpression phenotype. (
  • 2001. Apoptosis and asbestos-induced disease: is there a connection? (
  • Polymorphisms for interleukin-4 (IL-4) -590 promoter, IL-4 intron3, and tumor necrosis factor alpha -308 promoter: non-association with endometriosis. (
  • Tumor necrosis factor-alpha promotor polymorphisms and endometriosis. (
  • The tumor necrosis factor-alpha promoter -1031C polymorphism is associated with decreased risk of endometriosis in a Japanese population. (
  • Association between susceptibility of endometriosis and the gene polymorphism of tumor necrosis factor]. (
  • Association of tumor necrosis factor-{alpha} gene polymorphisms with advanced stage endometriosis. (
  • Association of the tumor necrosis factor-alpha -1031T/C and its combination with interleukin-6 -634C/G gene polymorphisms with susceptibility to endometriosis]. (
  • The first evidence raised from the observation that Tumor Necrosis Factor-α (TNF-α) is able to induce both apoptosis and necrosis, especially in the presence of caspase-inhibitors. (
  • Autophagy is a lysosomal-dependent degradation process induced during starvation, hypoxic conditions, growth factor deprivation, or endoplasmic reticulum stress in addition to other stressors ( 15 ). (
  • during tumorigenesis or oncogenesis processes it functions as a mechanism for tumor suppression ( 21 - 23 ) whereas when a tumor is formed, autophagy provides a cell survival advantage to resist cell death induced by cancer therapy ( 24 ). (
  • In two different mouse strains (C57Bl/6J and FVB/NJ), we show that the loss of Wnt7a is a major contributing factor for increased lung tumorigenesis owing to reduced cellular senescence, and not reduced apoptosis, or autophagy. (
  • This is the very first report of a vascular endothelial growth factor (VEGF for short)-like protein produced by bacteria. (
  • ABSTRACT We evaluated the prognostic value of serum endostatin and vascular endothelial growth factor (VEGF) for diagnosis of pre-eclampsia. (
  • Vascular endothelial growth factor (VEGF) plays a crucial role in physiological vasculogenesis and vascular permeability and has been implicated in the pathogenesis of pre-eclampsia. (
  • Vascular endothelial growth factor (VEGF) and fibroblast growth factor-2 (FGF-2) are the main factors promoting angiogenesis [ 7 , 8 ]. (
  • 21 Hsp90 is a major repressor of the heat-shock transcription factor 1 (HSF1). (
  • Adenovirus E2 promoter can be divided into early and late promoters, used to regulate the E2 transcription unit, the late E2 promoter region contains Y-box, the binding site of transcription factor YB-1 (Y-box binding protein-1). (
  • Drug induced exfoliative dermatitis (ED) are a group of rare and severe drug hypersensitivity reactions (DHR) involving skin and usually occurring from days to several weeks after drug exposure. (
  • Electromagnetic field exposure induces caspase 3 activation, a protein involved in apoptosis as well as other cellular processes. (
  • Details] Repetitive exposure to a 60-Hz time-varying magnetic field induces DNA double-strand breaks and apoptosis in human cells [med. (
  • Increase in X-ray-induced mutations by exposure to magnetic field (60 Hz, 5 mT) in NF-kappaB-inhibited cells [med. (
  • To identify the genes that give B. henselae this ability, the researchers began inducing random mutations in the DNA of the bacteria and seeing whether the mutated bacteria could still make the endothelial cells multiply. (
  • Roflumilast promoted hippocampal neurons viability, and reduced apoptosis possibly via modulation of MEK/ERK signaling pathway, and could recover sevoflurane-induced deactivation of MEk/ERk pathway. (
  • Phosphatidylcholine (PtdCho) is an essential component of mammalian cell membranes and PtdCho deficiency, either due to chemicals or altered nutrition, leads to apoptosis, especially in hippocampal neurons. (
  • 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. (
  • 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. (
  • Reduced creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH) activity and cTnI levels, as well as decreased myocardial apoptosis ratio were observed in the NGF group. (
  • 7 For example, K562 leukemia cells are apoptosis reluctant, because they express the Bcr-Abl antiapoptotic kinase, which in turn induces heat-shock protein-70 (Hsp70). (
  • Mechanistically, Wnt7a induced cellular senescence via inactivation of S-phase kinase-associated protein 2, an important alternate regulator of cellular senescence. (
  • DUOXA1 knockdown (using a DUOXA1 shRNA construct) resulted in enhanced differentiation compared to cells subjected to a control shRNA and subjecting DUOXA1 overexpressing cells to siRNAs targeting DUOX1 or apoptosis signal-regulating kinase 1 (ASK1) rescued the PRKCA phenotype. (
  • 3 Proinflammatory factors are released, leading to the death of brain neurons and glial cells. (
  • In peripheral mature T cells, Aif deficiency leads to an increased susceptibility of T cell blasts to activation induced cell death (AICD), possibly mediated by its antioxidant function, and decreased sensitivity to neglect-induced death (NID). (
  • Association of tumor necrosis factors-beta gene polymorphism with endometriosis in women in Guangdong Province]. (
  • Genetic variation in tumour necrosis factor and lymphotoxin is not associated with endometriosis in an Australian sample. (
  • These terms describe cases whereby necrosis is not accidental, but rather regulated and programmed, being therefore distinct from both apoptosis and accidental necrosis. (
  • However, when caspase 8 is blocked by synthetic or viral inhibitors, or by drastic depletion of energy (ATP depletion), there is a shift from apoptosis toward necrosis, mediated by the RIP kinases , RIPK1 and RIPK3 . (
  • Thus, these events are not passive, like in the traditional necrosis, but rather induced by an intracellular, dedicated signaling system, represented by the RIP kinases, RIPK1 and RIPK3. (
  • We next compared cytoprotection by GA-induced Hsp70, caspase inhibitors (Z-VAD-fmk) and cell-cycle arrest. (
  • Whereas cell-cycle arrest protected HL60 cells from paclitaxel (PTX) but not from FL and DOX, Z-VAD-fmk prevented FL-induced apoptosis but was less effective against DOX and PTX. (
  • DNA-damage, cell cycle arrest and apoptosis induced in BEAS-2B cells by 2-hydroxymetyl methacrylate (HEMA). (
  • SIRT1 had a dual effect on FOXO3 function: SIRT1 increased FOXO3's ability to induce cell cycle arrest and resistance to oxidative stress but inhibited FOXO3's ability to induce cell death. (
  • During tumor-associated angiogenesis, the balance of angiogenesis stimulators and inhibitors is tipped in favor of angiogenesis by hypoxia-inducible factor-1 gene expression [ 2 ]. (
  • Protective effect of electrolyzed reduced water on the paraquat-induced oxidative damage of human lymphocyte DNA. (
  • In addition, apoptosis induced by xanthohumol also involves endoplasmic reticulum stress and unfolded protein response. (
  • As of now, at lease 14 caspases have been described from mammals: 8 caspases are involved in apoptosis, 5 activate anti-inflammatory cytokines, and one acts in keratinocyte differentiation. (
  • Widespread pathologic damage may occur via indirect cellular responses with the secretion of chemokines, proinflammatory cytokines, nitrous oxide, and other neurotoxic factors. (
  • 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. (
  • In this study, apoptosis and related signaling induced by WC-Co nanoparticle s were investigated in JB6 cells and rat lung macrophages. (
  • The increased cellularity was due to increased macrophages and connective tissue growth factor (CTGF)-immunoreactive fibroblasts in the peritendon. (
  • The chemokine‐like inflammatory cytokine macrophage migration inhibitory factor (MIF) is a pivotal driver of acute and chronic inflammatory conditions, cardiovascular disease, autoimmunity, and cancer. (
  • We suggest that the ability to inhibit neutrophil apoptosis contributes to the proinflammatory role ascribed to MIF, and propose that blocking the interaction between MIF and CXCR2 could be an important anti‐inflammatory strategy in the early inflammatory response. (
  • HMGB1 is a ubiquitous and abundant nuclear protein that is released from necrotic and inflammatory cells and induces an inflammatory response ( Lotze and Tracey, 2005 ). (
  • Identification of Genes Involved in EGF-induced Apoptosis Using CRISPR/Cas9 Knockout Screening: Implications for Novel Therapeutic Targets in EGFR-Overexpressing Cancers. (
  • The CRISPR -based knockout screen revealed 266 genes possibly responsible for EGF -induced apoptosis . (
  • The E2F family of transcription factors regulates the expression of a number of genes whose products are involved in cell cycle control, DNA replication and apoptosis. (
  • We show here that E2F-1 binds in vivo the promoters of ASPP1 and ASPP2 genes, two activators of p53-mediated apoptosis, E2F-1, E2F-2 and E2F-3 all activate the isolated ASPP1 and ASPP2 promoters. (
  • The identification of ASPP1 and ASPP2 genes as transcriptional targets of E2F provides another mechanism by which E2F cooperates with p53 to induce apoptosis. (
  • expression of early (myogenin) and late (myosin heavy chain) markers of differentiation and elevated levels of apoptosis compared to control cells infected with an empty adenoviral vector Balaglitazone (pCMV5-GFP). (
  • Mediates cellular responses to the cytokine KITLG/SCF and other growth factors. (
  • Drozd K, Wysokinski D, Krupa R, Wozniak K. Bisphenol A-glycid methacrylate induces a broad spectrum of DNA damage in human lymphocytes. (
  • ABSTRACT Hyperhomocysteinaemia is considered as an important independent risk factor for atherosclerosis and thrombotic disease. (
  • Binds to the GAS element and activates PRL-induced transcription. (
  • While exploring the mechanisms of T cell death involved at various stages during the life of a T cell, we have observed and reported a variety of non-redundant roles for apoptosis inducing factor (Aif), a mitochondrial flavoprotein. (
  • Apoptosis, also known as programmed cell death, plays major roles in development and normal tissue turnover in addition to tumor formation. (
  • The role of apoptosis in the formation and regression of neovascularization is largely hypothesized, although the detailed mechanism remains unclear. (
  • Adamus, G.(2003).Autoantibody-induced apoptosis as a possible mechanism of autoimmune retinopathy. (
  • We aimed to determine the mechanism of EGF -induced apoptosis using a genome -wide clustered regularly interspaced short palindromic repeat ( CRISPR )-based knockout screen. (