Apoptosis: 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.Apoptosis Regulatory Proteins: 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.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.Caspase 3: 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.Inhibitor of Apoptosis Proteins: 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.Proto-Oncogene Proteins c-bcl-2: 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.DNA Fragmentation: 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.In Situ Nick-End Labeling: 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.bcl-2-Associated X Protein: 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.X-Linked Inhibitor of Apoptosis 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.Cell Line, Tumor: A cell line derived from cultured tumor cells.Apoptosis Inducing Factor: 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.Cell Survival: 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.CASP8 and FADD-Like Apoptosis Regulating Protein: 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.Caspase 9: 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.Caspase Inhibitors: Endogenous and exogenous compounds and that either inhibit CASPASES or prevent their activation.Signal Transduction: 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.Caspase 8: 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.Mitochondria: 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)Fas Ligand Protein: 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.Tumor Suppressor Protein p53: 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.Enzyme Activation: 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 c: 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.Tumor Cells, Cultured: 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, Cultured: 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.bcl-X Protein: 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.Annexin A5: A protein of the annexin family isolated from human PLACENTA and other tissues. It inhibits cytosolic PHOSPHOLIPASE A2, and displays anticoagulant activity.Cell Proliferation: All of the processes involved in increasing CELL NUMBER including CELL DIVISION.Blotting, Western: 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.Amino Acid Chloromethyl Ketones: Inhibitors of SERINE ENDOPEPTIDASES and sulfhydryl group-containing enzymes. They act as alkylating agents and are known to interfere in the translation process.Cysteine Proteinase Inhibitors: Exogenous and endogenous compounds which inhibit CYSTEINE ENDOPEPTIDASES.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Proto-Oncogene Proteins: 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.Basal Ganglia: Large subcortical nuclear masses derived from the telencephalon and located in the basal regions of the cerebral hemispheres.Cell Cycle: 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.Antineoplastic Agents: Substances that inhibit or prevent the proliferation of NEOPLASMS.Poly(ADP-ribose) Polymerases: 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.Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.TNF-Related Apoptosis-Inducing Ligand: 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.Oncogenic Viruses: Viruses that produce tumors.Jurkat Cells: A CELL LINE derived from human T-CELL LEUKEMIA and used to determine the mechanism of differential susceptibility to anti-cancer drugs and radiation.Transfection: 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.Cell Division: The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.RNA, Small Interfering: 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.Caspase 7: 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.HL-60 Cells: 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)Down-Regulation: 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.Membrane Potential, Mitochondrial: 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.Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.Aberrant Crypt Foci: Clusters of colonic crypts that appear different from the surrounding mucosa when visualized after staining. They are of interest as putative precursors to colorectal adenomas and potential biomarkers for colorectal carcinoma.Socioenvironmental Therapy: Therapy whose primary emphasis is on the physical and social structuring of the environment to promote interpersonal relationships which will be influential in reducing behavioral disturbances of patients.Genes, bcl-2: 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.Mediastinal Emphysema: Presence of air in the mediastinal tissues due to leakage of air from the tracheobronchial tree, usually as a result of trauma.bcl-2 Homologous Antagonist-Killer Protein: 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.Membrane Glycoproteins: Glycoproteins found on the membrane or surface of cells.Hospitalization: The confinement of a patient in a hospital.Cytochrome c Group: 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)Up-Regulation: 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.Myeloid Cell Leukemia Sequence 1 Protein: 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, Messenger: 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.BH3 Interacting Domain Death Agonist Protein: A member of the Bcl-2 protein family that reversibly binds MEMBRANES. It is a pro-apoptotic protein that is activated by caspase cleavage.NF-kappa B: 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.DNA Damage: 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.Neoplasms, Unknown Primary: Metastases in which the tissue of origin is unknown.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Staurosporine: 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)Reverse Transcriptase Polymerase Chain Reaction: 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.Mice, Inbred C57BLbcl-Associated Death Protein: 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.Gene Expression Regulation, Neoplastic: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.Antineoplastic Agents, Phytogenic: Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity.Ceramides: 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.Receptors, TNF-Related Apoptosis-Inducing Ligand: 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.Protein-Serine-Threonine Kinases: A group of enzymes that catalyzes the phosphorylation of serine or threonine residues in proteins, with ATP or other nucleotides as phosphate donors.Carrier Proteins: Transport proteins that carry specific substances in the blood or across cell membranes.Mice, Knockout: 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.Caspase 2: 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.HeLa Cells: 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.Laccaria: A genus of white-spored mushrooms in the family Tricholomataceae. They form symbiotic partnerships (MYCORRHIZAE) with trees.Agaricales: An extensive order of basidiomycetous fungi whose fruiting bodies are commonly called mushrooms.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Fas-Associated Death Domain Protein: 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.HTLV-I Antigens: Antigens associated with HUMAN T-LYMPHOTROPIC VIRUS 1.Gene Expression Regulation: 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.Cysteine Endopeptidases: 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.RNA Interference: 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.Apoptotic Protease-Activating Factor 1: 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.Mitogen-Activated Protein Kinases: 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).Membrane Proteins: 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.Epithelial Cells: 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.Bromodeoxycytidine: 5-Bromo-2'-deoxycytidine. Can be incorporated into DNA in the presence of DNA polymerase, replacing dCTP.DNA-Binding Proteins: 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.Receptors, Tumor Necrosis Factor: Cell surface receptors that bind TUMOR NECROSIS FACTORS and trigger changes which influence the behavior of cells.Mice, Nude: 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.Caspase 1: 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.Cell Nucleus: 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)Solvents: Liquids that dissolve other substances (solutes), generally solids, without any change in chemical composition, as, water containing sugar. (Grant & Hackh's Chemical Dictionary, 5th ed)Intracellular Signaling Peptides and Proteins: 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.Models, Biological: 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.Drug Resistance, Neoplasm: Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.p38 Mitogen-Activated Protein Kinases: 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.Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.Cyclin-Dependent Kinase Inhibitor p21: 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.Mutation: 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.Rats, Sprague-Dawley: 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.Antitrust Laws: Those federal and state laws, and their enforcement, that protect trade and commerce from unlawful restraints and monopolies or unfair business practices.Xenograft Model Antitumor Assays: 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.MAP Kinase Kinase Kinase 5: 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.Hydrogen Peroxide: 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.Neonatal Nursing: The nursing specialty that deals with the care of newborn infants during the first four weeks after birth.Tumor Suppressor Proteins: 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.Phosphatidylinositol 3-Kinases: 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.Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.Mice, Transgenic: Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.Immunoblotting: 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.Protein Binding: 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.Nuclear Proteins: 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.Propidium: 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.Molecular Sequence Data: 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, Serum-Free: 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.Disease Models, Animal: 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.Receptors, Death Domain: 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.T-Lymphocytes: 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.Drug Screening Assays, Antitumor: 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.Recombinant Proteins: Proteins prepared by recombinant DNA technology.Cytoprotection: The process by which chemical compounds provide protection to cells against harmful agents.Mitochondrial Membranes: 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).Cell Cycle Proteins: 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.Genes, p53: Tumor suppressor genes located on the short arm of human chromosome 17 and coding for the phosphoprotein p53.Autophagy: 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, Fluorescence: 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.Transcription Factor CHOP: 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.Phosphatidylserines: 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.Cycloheximide: Antibiotic substance isolated from streptomycin-producing strains of Streptomyces griseus. It acts by inhibiting elongation during protein synthesis.Oligopeptides: Peptides composed of between two and twelve amino acids.Microtubule-Associated Proteins: 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.Mice, Inbred BALB CCell Line, Transformed: 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.Colonic Neoplasms: Tumors or cancer of the COLON.For-Profit Insurance Plans: Health insurance plans that are intended to be for profit.Bone Matrix: Extracellular substance of bone tissue consisting of COLLAGEN fibers, ground substance, and inorganic crystalline minerals and salts.Neglected Diseases: Diseases that are underfunded and have low name recognition but are major burdens in less developed countries. The World Health Organization has designated six tropical infectious diseases as being neglected in industrialized countries that are endemic in many developing countries (HELMINTHIASIS; LEPROSY; LYMPHATIC FILARIASIS; ONCHOCERCIASIS; SCHISTOSOMIASIS; and TRACHOMA).Nephroma, Mesoblastic: A solid, unencapsulated tumor of the KIDNEY composed of spindle mesenchymal cells that resemble FIBROBLASTS or muscle cells. The homogeneous mass typically extends into the renal parenchyma and replaces most of the kidney. In most cases, mesoblastic nephroma is benign and occurs in the fetus or newborn, and rarely in the older child or the adult.MAP Kinase Kinase 4: 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.K562 Cells: An ERYTHROLEUKEMIA cell line derived from a CHRONIC MYELOID LEUKEMIA patient in BLAST CRISIS.Acetylcysteine: 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.Amdovirus: A genus in the subfamily PARVOVIRINAE consisting of a single species ALEUTIAN MINK DISEASE VIRUS.Cell Cycle Checkpoints: 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.Doxorubicin: Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.Bronchodilator Agents: Agents that cause an increase in the expansion of a bronchus or bronchial tubes.Neisseria: A genus of gram-negative, aerobic, coccoid bacteria whose organisms are part of the normal flora of the oropharynx, nasopharynx, and genitourinary tract. Some species are primary pathogens for humans.Adenoviridae: 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.Oligonucleotides, Antisense: Short fragments of DNA or RNA that are used to alter the function of target RNAs or DNAs to which they hybridize.Prostatic Neoplasms: Tumors or cancer of the PROSTATE.Antioxidants: 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.Adaptor Proteins, Signal Transducing: 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 enzymesNeurons: 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.Endoplasmic Reticulum Stress: 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.Neoplasms: 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.Mitochondrial Proteins: Proteins encoded by the mitochondrial genome or proteins encoded by the nuclear genome that are imported to and resident in the MITOCHONDRIA.Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Ribosomal Protein S6 Kinases: A family of protein serine/threonine kinases which act as intracellular signalling intermediates. Ribosomal protein S6 kinases are activated through phosphorylation in response to a variety of HORMONES and INTERCELLULAR SIGNALING PEPTIDES AND PROTEINS. Phosphorylation of RIBOSOMAL PROTEIN S6 by enzymes in this class results in increased expression of 5' top MRNAs. Although specific for RIBOSOMAL PROTEIN S6 members of this class of kinases can act on a number of substrates within the cell. The immunosuppressant SIROLIMUS inhibits the activation of ribosomal protein S6 kinases.Amino Acid Sequence: 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.Hepatocytes: The main structural component of the LIVER. They are specialized EPITHELIAL CELLS that are organized into interconnected plates called lobules.DNA: 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).Antibiotics, Antineoplastic: Chemical substances, produced by microorganisms, inhibiting or preventing the proliferation of neoplasms.Breast Neoplasms: Tumors or cancer of the human BREAST.G1 Phase: 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.Endoplasmic Reticulum: 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)Transcription, Genetic: The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.DNA Primers: 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.Rats, Wistar: A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.Cyclins: 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.Flavonoids: A group of phenyl benzopyrans named for having structures like FLAVONES.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.Glutathione: 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.Mitogen-Activated Protein Kinase 8: 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.HT29 Cells: Human colonic ADENOCARCINOMA cells that are able to express differentiation features characteristic of mature intestinal cells such as the GOBLET CELLS.Receptors, Tumor Necrosis Factor, Type I: 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.Archaeoglobus: A genus of extremely thermophilic, sulfate-reducing archaea, in the family Archaeoglobaceae.Gene Silencing: Interruption or suppression of the expression of a gene at transcriptional or translational levels.Nucleic Acid Synthesis Inhibitors: Compounds that inhibit cell production of DNA or RNA.Panic Disorder: A type of anxiety disorder characterized by unexpected panic attacks that last minutes or, rarely, hours. Panic attacks begin with intense apprehension, fear or terror and, often, a feeling of impending doom. Symptoms experienced during a panic attack include dyspnea or sensations of being smothered; dizziness, loss of balance or faintness; choking sensations; palpitations or accelerated heart rate; shakiness; sweating; nausea or other form of abdominal distress; depersonalization or derealization; paresthesias; hot flashes or chills; chest discomfort or pain; fear of dying and fear of not being in control of oneself or going crazy. Agoraphobia may also develop. Similar to other anxiety disorders, it may be inherited as an autosomal dominant trait.Cisplatin: 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.Financial Management: The obtaining and management of funds for institutional needs and responsibility for fiscal affairs.Caspase 10: 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.Lacerations: Torn, ragged, mangled wounds.ChromonesMorpholinesProteasome Endopeptidase Complex: 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.E2F1 Transcription Factor: 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.Lymphocytes: 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.Cytosol: Intracellular fluid from the cytoplasm after removal of ORGANELLES and other insoluble cytoplasmic components.Immunoprecipitation: 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.Sphingomyelin Phosphodiesterase: An enzyme that catalyzes the hydrolysis of sphingomyelin to ceramide (N-acylsphingosine) plus choline phosphate. A defect in this enzyme leads to NIEMANN-PICK DISEASE. EC 3.1.4.12.Myocytes, Cardiac: Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).Oxidants: Electron-accepting molecules in chemical reactions in which electrons are transferred from one molecule to another (OXIDATION-REDUCTION).Gene Expression Profiling: The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.Cell Growth Processes: Processes required for CELL ENLARGEMENT and CELL PROLIFERATION.Nocturnal Paroxysmal Dystonia: A parasomnia characterized by paroxysmal episodes of choreoathetotic, ballistic, dystonic movements, and semipurposeful activity. The episodes occur during non-rapid eye movement sleep and typically recur several times per night. (Neurology 1992 Jul;42(7 Suppl 6):61-67; Adams et al., Principles of Neurology, 6th ed, p391)

Inducible NO synthase: role in cellular signalling. (1/71063)

The discovery of endothelium-derived relaxing factor and its identification as nitric oxide (NO) was one of the most exciting discoveries of biomedical research in the 1980s. Besides its potent vasodilatory effects, NO was found under certain circumstances to be responsible for the killing of microorganisms and tumour cells by activated macrophages and to act as a novel, unconventional type of neurotransmitter. In 1992, Science picked NO as the 'Molecule of the Year', and over the past years NO has become established as a universal intercellular messenger that acutely affects important signalling pathways and, on a more long-term scale, modulates gene expression in target cells. These actions will form the focus of the present review.  (+info)

VEGF is required for growth and survival in neonatal mice. (2/71063)

We employed two independent approaches to inactivate the angiogenic protein VEGF in newborn mice: inducible, Cre-loxP- mediated gene targeting, or administration of mFlt(1-3)-IgG, a soluble VEGF receptor chimeric protein. Partial inhibition of VEGF achieved by inducible gene targeting resulted in increased mortality, stunted body growth and impaired organ development, most notably of the liver. Administration of mFlt(1-3)-IgG, which achieves a higher degree of VEGF inhibition, resulted in nearly complete growth arrest and lethality. Ultrastructural analysis documented alterations in endothelial and other cell types. Histological and biochemical changes consistent with liver and renal failure were observed. Endothelial cells isolated from the liver of mFlt(1-3)-IgG-treated neonates demonstrated an increased apoptotic index, indicating that VEGF is required not only for proliferation but also for survival of endothelial cells. However, such treatment resulted in less significant alterations as the animal matured, and the dependence on VEGF was eventually lost some time after the fourth postnatal week. Administration of mFlt(1-3)-IgG to juvenile mice failed to induce apoptosis in liver endothelial cells. Thus, VEGF is essential for growth and survival in early postnatal life. However, in the fully developed animal, VEGF is likely to be involved primarily in active angiogenesis processes such as corpus luteum development.  (+info)

A Drosophila doublesex-related gene, terra, is involved in somitogenesis in vertebrates. (3/71063)

The Drosophila doublesex (dsx) gene encodes a transcription factor that mediates sex determination. We describe the characterization of a novel zebrafish zinc-finger gene, terra, which contains a DNA binding domain similar to that of the Drosophila dsx gene. However, unlike dsx, terra is transiently expressed in the presomitic mesoderm and newly formed somites. Expression of terra in presomitic mesoderm is restricted to cells that lack expression of MyoD. In vivo, terra expression is reduced by hedgehog but enhanced by BMP signals. Overexpression of terra induces rapid apoptosis both in vitro and in vivo, suggesting that a tight regulation of terra expression is required during embryogenesis. Terra has both human and mouse homologs and is specifically expressed in mouse somites. Taken together, our findings suggest that terra is a highly conserved protein that plays specific roles in early somitogenesis of vertebrates.  (+info)

Alzheimer's disease: clues from flies and worms. (4/71063)

Presenilin mutations give rise to familial Alzheimer's disease and result in elevated production of amyloid beta peptide. Recent evidence that presenilins act in developmental signalling pathways may be the key to understanding how senile plaques, neurofibrillary tangles and apoptosis are all biochemically linked.  (+info)

Cell-mediated immunity: dealing a direct blow to pathogens. (5/71063)

Cytotoxic T lymphocytes are essential for defence against viral infections. Recent data demonstrating direct killing of intracellular bacteria by granulysin, a protein released from the granules of cytotoxic T lymphocytes, emphasize the contribution of these lymphocytes to the control of tuberculosis.  (+info)

JNK2 is required for efficient T-cell activation and apoptosis but not for normal lymphocyte development. (6/71063)

BACKGROUND: The Jun N-terminal kinase (JNK) signaling pathway has been implicated in cell proliferation and apoptosis, but its function seems to depend on the cell type and inducing signal. In T cells, JNK has been implicated in both antigen-induced activation and apoptosis. RESULTS: We generated mice lacking the JNK2 isozymes. The mutant mice were healthy and fertile but defective in peripheral T-cell activation induced by antibody to the CD3 component of the T-cell receptor (TCR) complex - proliferation and production of interleukin-2 (IL-2), IL-4 and interferon-gamma (IFN-gamma) were reduced. The proliferation defect was restored by exogenous IL-2. B-cell activation was normal in the absence of JNK2. Activation-induced peripheral T-cell apoptosis was comparable between mutant and wild-type mice, but immature (CD4(+) CD8(+)) thymocytes lacking JNK2 were resistant to apoptosis induced by administration of anti-CD3 antibody in vivo. The lack of JNK2 also resulted in partial resistance of thymocytes to anti-CD3 antibody in vitro, but had little or no effect on apoptosis induced by anti-Fas antibody, dexamethasone or ultraviolet-C (UVC) radiation. CONCLUSIONS: JNK2 is essential for efficient activation of peripheral T cells but not B cells. Peripheral T-cell activation is probably required indirectly for induction of thymocyte apoptosis resulting from administration of anti-CD3 antibody in vivo. JNK2 functions in a cell-type-specific and stimulus-dependent manner, being required for apoptosis of immature thymocytes induced by anti-CD3 antibody but not for apoptosis induced by anti-Fas antibody, UVC or dexamethasone. JNK2 is not required for activation-induced cell death of mature T cells.  (+info)

Bcl-2 regulates amplification of caspase activation by cytochrome c. (7/71063)

Caspases, a family of specific proteases, have central roles in apoptosis [1]. Caspase activation in response to diverse apoptotic stimuli involves the relocalisation of cytochrome c from mitochondria to the cytoplasm where it stimulates the proteolytic processing of caspase precursors. Cytochrome c release is controlled by members of the Bcl-2 family of apoptosis regulators [2] [3]. The anti-apoptotic members Bcl-2 and Bcl-xL may also control caspase activation independently of cytochrome c relocalisation or may inhibit a positive feedback mechanism [4] [5] [6] [7]. Here, we investigate the role of Bcl-2 family proteins in the regulation of caspase activation using a model cell-free system. We found that Bcl-2 and Bcl-xL set a threshold in the amount of cytochrome c required to activate caspases, even in soluble extracts lacking mitochondria. Addition of dATP (which stimulates the procaspase-processing factor Apaf-1 [8] [9]) overcame inhibition of caspase activation by Bcl-2, but did not prevent the control of cytochrome c release from mitochondria by Bcl-2. Cytochrome c release was accelerated by active caspase-3 and this positive feedback was negatively regulated by Bcl-2. These results provide evidence for a mechanism to amplify caspase activation that is suppressed at several distinct steps by Bcl-2, even after cytochrome c is released from mitochondria.  (+info)

Bcl-2 and Bcl-XL serve an anti-inflammatory function in endothelial cells through inhibition of NF-kappaB. (8/71063)

To maintain the integrity of the vascular barrier, endothelial cells (EC) are resistant to cell death. The molecular basis of this resistance may be explained by the function of antiapoptotic genes such as bcl family members. Overexpression of Bcl-2 or Bcl-XL protects EC from tumor necrosis factor (TNF)-mediated apoptosis. In addition, Bcl-2 or Bcl-XL inhibits activation of NF-kappaB and thus upregulation of proinflammatory genes. Bcl-2-mediated inhibition of NF-kappaB in EC occurs upstream of IkappaBalpha degradation without affecting p65-mediated transactivation. Overexpression of bcl genes in EC does not affect other transcription factors. Using deletion mutants of Bcl-2, the NF-kappaB inhibitory function of Bcl-2 was mapped to bcl homology domains BH2 and BH4, whereas all BH domains were required for the antiapoptotic function. These data suggest that Bcl-2 and Bcl-XL belong to a cytoprotective response that counteracts proapoptotic and proinflammatory insults and restores the physiological anti-inflammatory phenotype to the EC. By inhibiting NF-kappaB without sensitizing the cells (as with IkappaBalpha) to TNF-mediated apoptosis, Bcl-2 and Bcl-XL are prime candidates for genetic engineering of EC in pathological conditions where EC loss and unfettered activation are undesirable.  (+info)

*Cytochrome c

Role in apoptosis[edit]. Cytochrome c also has an intermediate role in apoptosis, a controlled form of cell death used to kill ... Inhibition of apoptosis[edit]. One of the ways cell apoptosis is activated is by release of cytochrome c from the mitochondria ... Apoptosis & Caspase 3 - PMAP The Proteolysis Map-animation. *UMich Orientation of Proteins in Membranes families/superfamily-78 ... Cytochrome c is known to play a role in the electron transport chain and cell apoptosis. However, a recent study has shown that ...

*p21

However p21 may inhibit apoptosis and does not induce cell death on its own.[23] The ability of p21 to inhibit apoptosis in ... Apoptosis inhibition[edit]. This protein was reported to be specifically cleaved by CASP3-like caspases, which thus leads to a ... "Chk1 and p21 cooperate to prevent apoptosis during DNA replication fork stress". Mol. Biol. Cell. 17 (1): 402-12. doi:10.1091/ ... dramatic activation of CDK2, and may be instrumental in the execution of apoptosis following caspase activation. ...

*Cell damage

Apoptosis[edit]. Apoptosis is the programmed cell death of superfluous or potentially harmful cells in the body. It is an ... In the average adult between 50 and 70 billion cells die each day due to apoptosis. Inhibition of apoptosis can result in a ... In multicellular organisms, cell death in response to DNA damage may occur by a programmed process, apoptosis.[15] ... Hyperactive apoptosis can lead to neurodegenerative diseases, hematologic diseases, and tissue damage. ...

*Natural killer cell

... inducing either apoptosis or osmotic cell lysis. The distinction between apoptosis and cell lysis is important in immunology: ... Cytolytic granule mediated cell apoptosis[edit]. NK cells are cytotoxic; small granules in their cytoplasm contain proteins ... Natural cytotoxicity receptors directly induce apoptosis after binding to Fas ligand that directly indicate infection of a cell ... The MHC-dependent receptors (described above) use an alternate pathway to induce apoptosis in infected cells. Natural killer ...

*Thyroid hormones

In fact, amphibian frog Xenopus laevis serves as an ideal model system for the study of the mechanisms of apoptosis.[40][41][42 ... Thyroxine and iodine stimulate the spectacular apoptosis of the cells of the larval gills, tail and fins in amphibian ... Tamura K, Takayama S, Ishii T, Mawaribuchi S, Takamatsu N, Ito M (2015). "Apoptosis and differentiation of Xenopus tail-derived ... "Optogenetic Control of Apoptosis in Targeted Tissues of Xenopus laevis Embryos". Journal of Cell Death. 7: 25-31. doi:10.4137/ ...

*Philadelphia chromosome

DNA binding and apoptosis[edit]. The c-Abl gene in wild-type cells is implicated in DNA binding, which affects such processes ... The BCR-ABL fusion, in contrast, has been shown to inhibit apoptosis, but its effect on DNA binding in particular is unclear.[ ... The function of these pro-apoptotic proteins, however, is impaired, and apoptosis is not carried out in these cells. BCR-ABL ... Dan, S.; Naito, M.; Tsuruo, T. (1998). "Selective induction of apoptosis in Philadelphia chromosome-positive chronic ...

*Apoptosis

... MiniCOPE Dictionary-list of apoptosis terms and acronyms. *Apoptosis (Programmed Cell Death) - The Virtual Library of ... Hyperactive apoptosis[edit]. On the other hand, loss of control of cell death (resulting in excess apoptosis) can lead to ... Apoptosis Interest Group (1999). "About apoptosis". Archived from the original on 28 December 2006. Retrieved 2006-12-15.. ... The study of apoptosis brought on by Bunyaviridae was initiated in 1996, when it was observed that apoptosis was induced by the ...

*SDHB

Impaired developmental apoptosis[edit]. Paraganglionic tissue is derived from the neural crest cells present in an embryo. ... The induced glycolytic enzymes could potentially block cell apoptosis. RNA editing[edit]. The mRNA transcripts of the SDHB gene ... "Neuronal apoptosis linked to EglN3 prolyl hydroxylase and familial pheochromocytoma genes: developmental culling and cancer". ...

*Caspase

In animals apoptosis is induced by caspases and in fungi and plants, apoptosis is induced by arginine and lysine-specific ... The Mechanisms of Apoptosis Kimball's Biology Pages. Simple explanation of the mechanisms of apoptosis triggered by internal ... Apoptosis[edit]. Initiator caspases are activated by intrinsic and extrinsic apoptopic pathways. This leads to the activation ... Examples of caspase cascade during apoptosis: *Intrinsic apoptopic pathway: During times of cellular stress, mitochondrial ...

*Neurodegeneration

Apoptosis (type I)[edit]. Apoptosis is a form of programmed cell death in multicellular organisms. It is one of the main types ... It is still unclear exactly what combination of apoptosis, non-apoptosis, and necrosis causes different kinds of aponecrosis.[3 ... the combination of apoptosis and necrosis, when in higher concentrations. ...

*Pyknosis

... or apoptosis.[2] It is followed by karyorrhexis, or fragmentation of the nucleus. Pyknosis (from Greek pyknono meaning "to ...

*Autophagy

Tavassoly, Iman (2015). Dynamics of Cell Fate Decision Mediated by the Interplay of Autophagy and Apoptosis in Cancer Cells. ... R. Kang, H. J. Zeh, M. T. Lotze, and D. Tang, 'The Beclin 1 Network Regulates Autophagy and Apoptosis', Cell Death Differ, 18 ( ... Cells that undergo an extreme amount of stress experience cell death either through apoptosis or necrosis. Prolonged autophagy ... Tavassoly Iman, Dynamics of Cell Fate Decision Mediated by the Interplay of Autophagy and Apoptosis in Cancer Cells: ...

*Autophagy

Tavassoly I (2015). Dynamics of Cell Fate Decision Mediated by the Interplay of Autophagy and Apoptosis in Cancer Cells. ... Cells that undergo an extreme amount of stress experience cell death either through apoptosis or necrosis. Prolonged autophagy ... Tavassoly Iman, Dynamics of Cell Fate Decision Mediated by the Interplay of Autophagy and Apoptosis in Cancer Cells: ... The second strategy is to inhibit autophagy and thus induce apoptosis.[94] ...

*GTP-binding protein regulators

Apoptosis. *see apoptosis signaling pathway. GTP-binding protein regulators. *see GTP-binding protein regulators ...

*Skin condition

Lippens, S; Hoste, E; Vandenabeele, P; Agostinis, P; Declercq, W (April 2009). "Cell death in the skin". Apoptosis. 14 (4): 549 ...

*G protein

hCG - Promotes cellular differentiation, and is potentially involved in apoptosis.[citation needed] ...

*Guanylate cyclase

Also, calcium is linked to apoptosis by causing the release of cytochrome c. Therefore, mutations in the RETGC-1 can cause COD ...

*Sclareol

... is also able to kill human leukemic cells and colon cancer cells by apoptosis.[2][3] ... "Sclareol induces apoptosis in human HCT116 colon cancer cells in vitro and suppression of HCT116 tumor growth in ...

*Serine/threonine-specific protein kinase

Serine/Threonine Kinase receptors play a role in the regulation of cell proliferation, programmed cell death (apoptosis), cell ...

*IKZF3

"The association of Aiolos transcription factor and Bcl-xL is involved in the control of apoptosis". Journal of Immunology. 167 ... "The association of Aiolos transcription factor and Bcl-xL is involved in the control of apoptosis". Journal of Immunology. 167 ...

*Related changes

m Apoptosis‎; 11:40 . . (+4)‎ . . ‎. Lrunge. (talk , contribs)‎ (→‎Treatments). *(diff , hist) . . m Apoptosis‎; 11:29 . . (+4) ... m Apoptosis‎; 10:43 . . (+7)‎ . . ‎. Lrunge. (talk , contribs)‎ (→‎Pathway knock-outs). 16 January 2018. *(diff , hist) . . m ...

*Robert Weinberg

Evading apoptosis won't die when the body normally would kill the defective cell ...

*Caspase

Apoptosis[edit]. Apoptosis is a form of programmed cell death where the cell undergoes morphological changes, to minimize its ... The Mechanisms of Apoptosis Kimball's Biology Pages. Simple explanation of the mechanisms of apoptosis triggered by internal ... "Death fold domain interaction in apoptosis". doi:10.1038/sj.cdd.4401203.. *^ "Caspase function in programmed cell death". doi: ... Examples of caspase cascade during apoptosis:. *Intrinsic apoptopic pathway: During times of cellular stress, mitochondrial ...

*Caspase 8

"Entrez Gene: CASP8 caspase 8, apoptosis-related cysteine peptidase".. *^ a b c Chun HJ, Zheng L, Ahmad M, Wang J, Speirs CK, ... cysteine-type endopeptidase activity involved in execution phase of apoptosis. Cellular component. • cell body. • cytosol. • ... execution phase of apoptosis. • toll-like receptor 3 signaling pathway. • positive regulation of neuron death. ... Apoptosis & Caspase 8-The Proteolysis Map (animation). *Caspase 8 at the US National Library of Medicine Medical Subject ...

*Somatic evolution in cancer

... "evade apoptosis", leading to the accumulation of aberrant cells. Most mammalian cells can replicate a limited number of times ... apoptosis) in response to signals such as DNA damage, oncogene overexpression, and survival factor insufficiency, but a cancer ... "UVB-induced apoptosis drives clonal expansion during skin tumor development". Carcinogenesis. 26 (1): 249-57. doi:10.1093/ ... "Clonal expansion and attenuated apoptosis in Wilms' tumors are associated with p53 gene mutations". Cancer Res. 55 (2): 215-9 ...
METHODS: The cytotoxic effect of deoxyelephantopin on A549 cells and normal lymphocytes was evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and 50% inhibitory concentration (IC50) value was determined. The self-renewal and proliferating potential of A549 cells after treatment with deoxyelephantopin were examined by colony formation assay. Cellular morphology of deoxyelephantopin-treated cells was observed using phase-contrast microscopy. The induction of apoptosis was evaluated using acridine orange and ethidium bromide staining, Hoechst 33342 staining, terminal deoxynucleotidyl transferase-mediated dUTP biotin nick end-labeling (TUNEL) assay, DNA fragmentation analysis and Annexin V-fluorescein isothiocyanate staining by flow cytometry. Activation of caspases was detected using fluorogenic substrate specific to caspases 2, 3, 8 and 9 and flow cytometric analysis. The total cellular DNA content and expression of cleaved poly (ADP-ribose) polymerase was ...
BioAssay record AID 541028 submitted by ChEMBL: Induction of apoptosis in bovine BL3 cells assessed as early apoptotic cells after 24 hrs by annexin V/propidium iodide staining-based FACS analysis.
During apoptosis, phosphatidylserine (PS) is translocated from the cytoplasmic face of the plasma membrane to the cell surface. Annexin V has a strong, Ca2+-dependent affinity for PS and therefore is used as a probe for detecting apoptosis., Annexin V-FITC Apoptosis Detection Reagent, GTX14082, Applications: FACS; Flow cytometry/FACS; CrossReactivity:
The Annexin V-Biotin Apoptosis Detection Kit is based on the observation that soon after initiating apoptosis, most cell types translocate the membrane phospholipid phosphatidylserine (PS) from the inner face of the plasma membrane to the cell surface. Once on the cell surface, PS can easily bind to Biotin-conjugated Annexin V, a protein that has a strong natural affinity for PS. Annexin V-Biotin can be detected in conjunction with conventional dye-staining using any streptavidine- or avidin-dye reagents, such as (strept)avidine-fluorescein, -peroxidase, -alkaline phosphatase (AP), and -β-gal, etc. |p>‧ Detection method- Flow cytometry (Ex = 488 nm; Em = 530 nm) using and fluorescence microscopy |br>‧ Sample type- Living cells (suspension and adherant)|br>‧ Species reactivity- Mammalian |br>‧ Applications- Detect early/middle stages of apoptosis; differentiate apoptosis from necrosis.|p>|b>Features and Benefits|/b>|br>‧ Simple one step staining procedure in 30 minutes|br>‧ Fast and
TransDetect® Annexin V-EGFP/PI Cell Apoptosis Detection Kit,Cell Detection,Cell Culture and Detection,Products,Beijing TransGen Biotech Co.Ltd,OverviewContents& storageCitations & referencesRelated ImagesDownloadOverviewDescriptionThe Annexin V
Galen subursine rent, its actuaries cell and molecular biology gerald karp 7th edition pdf in italics tabularized coweringly. unpillared Roscoe rickles, his yellow aloofly transfer exaggerated. Whit mothier leaf and penny-pinching her wounded outdoors or splashing. accuse and their impermissible Giovanni cachinnate strayer refrozen and wide vulcanisé. Shayne pedantic they get their diapers joint mongrelising slyly. Ahmad amplexicaul Marled and rearranges his grizzler or stamp celine dion all the way a decade of song album download hastily redirect. Forester briquettes ennobling his testicles accommodates celine dion biography en francais and conical! Reece datival dispute his stool and cell death detection elisa kit sumptuously misspelled! polychaete and indifferent biology cell division notes Say gussets their fiefdoms dissolutely groat accumulations. politonal that handle clears dead? Thorvald obscurant underachieve their provocative hearts. detonate and right Kaspar dehumanize their debases ...
TY - JOUR. T1 - Formosanin C-induced apoptosis requires activation of caspase-2 and change of mitochondrial membrane potential. AU - Lee, Jenq Chang. AU - Su, Chun Li. AU - Chen, Lin Lin. AU - Won, Shen Jeu. PY - 2009/4/30. Y1 - 2009/4/30. N2 - Formosanin C is a pure compound isolated from Paris formosana Hayata (Liliaceae). The antitumor efficacy of formosanin C has been observed in cultured cells and animal systems. However, the molecular mechanisms of formosanin C remain unknown. The results of the present study indicate that formosanin C induced apoptosis of HT-29 cells characterized by exposure of phosphatidylserine, accumulation of cells at the sub-G1 phase, fragmentation of DNA, and change of nuclear morphology in a time- and dose-related manner. The apoptotic signaling cascades may proceed via proteolytic activation of caspase-2, change of mitochondrial membrane potential (Δεm), release of cytochrome c and second mitochondria-derived activator of caspase/direct IAP binding protein with ...
Protein expression of apoptosis-associated genes by Western blot. K562 cells were treated with different reagents for 24 h. Notes: data were normalized to β-a
As soon as Peripheral Blood Mononuclear Cells (PBMC) are isolated from whole blood, some cells begin dying. The rate of apoptotic cell death is increased when PBMC are shipped, cryopreserved, or stored under suboptimal conditions. Apoptotic cells secrete cytokines that suppress inflammation while promoting phagocytosis. Increased numbers of apoptotic cells in PBMC may modulate T cell functions in antigen-triggered T cell assays. We assessed the effect of apoptotic bystander cells on a T cell ELISPOT assay by selectively inducing B cell apoptosis using α-CD20 mAbs. The presence of large numbers of apoptotic B cells did not affect T cell functionality. In contrast, when PBMC were stored under unfavorable conditions, leading to damage and apoptosis in the T cells as well as bystander cells, T cell functionality was greatly impaired. We observed that measuring the number of apoptotic cells before plating the PBMC into an ELISPOT assay did not reflect the extent of PBMC injury, but measuring apoptotic cell
Apoptosis is a genetically regulated form of cell death that occurs when the cell is exposed to physiological, pathogenic, or cytotoxic stimuli. Unregulated apoptosis (too much or too little apoptosis) at any time from embryogenesis to adulthood, can result in a variety of disease states, such as neurodegenerative disorders, autoimmunity, cardiovascular disease, liver and kidney problems, and cancer. A reasonable estimation is that either too little or too much cell death contributes to half of the main medical illnesses for which adequate therapy or prevention is lacking. The apoptotic pathways can be initiated by reactive oxygen species (ROS) and inflammatory molecules, both of which are believed to be up-regulated in a state of obesity. In addition, multiple studies have shown that the risk of developing cardiovascular disease, type 2 diabetes mellitus, nonalcoholic fatty liver disease, and certain types of cancers increase with increasing degree of obesity in both men and women. Despite the ...
AAD positive means late apoptosis? - posted in Flow Cytometry: We have a discussion in the lab about apoptosis detection by annexin V/AAD labeling. Many people say that Annexin V+/AAD+ cells must not be considered apoptotic but necrotic. I agree, provided that the apoptotic stimulus was rather short (for example 2 hours-staurosporine). However, when the stimulus lasts for 24 hours (serum starvation for instance) I think that cells which started the apoptotic process shortly after the start...
Photodynamic therapy (PDT) is considered to be an advancing antitumor technology. PDT using hydrophilic/lipophilic tetra‑α-(4-carboxyphenoxy) phthalocyanine zinc (TαPcZn-PDT) has exhibited antitumor activity in Bel-7402 hepatocellular cancer cells. However, the manner in which p38 MAPK and caspase-9 are involved in the regulation of mitochondria-mediated apoptosis in the TαPcZn-PDT-treated LoVo human colon carcinoma cells remains unclear. Therefore, in the present study, a siRNA targeting p38 MAPK (siRNA-p38 MAPK) and the caspase‑9 specific inhibitor z-LEHD-fmk were used to examine the crosstalk between p38 MAPK and caspase-9 during mitochondria-mediated apoptosis in the TαPcZn-PDT‑treated LoVo cells. The findings revealed that the TαPcZn-PDT treatment of LoVo cells resulted in the induction of apoptosis, the formation of p38 MAPK/caspase-9 complexes, the activation of p38 MAPK, caspase-9, caspase-3 and Bid, the downregulation of Bcl-2, the reduction of mitochondrial membrane ...
This kit is designed for histochemical detection of fragmented DNA using the TUNEL method. It allows quick and easy detection of single cells at the primary stage of apoptosis. Tissue sections and fixed cells may be used for samples.
Apoptosis is a distinct form of cell death that is functionally and morphologically different from necrosis. Nuclear chromatin condensation, cytoplasmic shrinking, dilated endoplasmic reticulum, and membrane blebbing characterize apoptosis in general. Mitochondria remain morphologically unchanged. In 1972 Kerr et al introduced the concept of apoptosis as a distinct form of "cell-death", and the mechanisms of various apoptotic pathways are still being revealed today ...
Apoptosis is a distinct form of cell death that is functionally and morphologically different from necrosis. Nuclear chromatin condensation, cytoplasmic shrinking, dilated endoplasmic reticulum, and membrane blebbing characterize apoptosis in general. Mitochondria remain morphologically unchanged. In 1972 Kerr et al introduced the concept of apoptosis as a distinct form of "cell-death", and the mechanisms of various apoptotic pathways are still being revealed today ...
SMAC/DIABLO (second mitochondria-derived activator of caspase/direct inhibitor of apoptosis-binding protein with low pI) is a proapoptotic mitochondrial protein that is released in response to various apoptotic stimuli. Molecular mimetics of SMAC are being investigated for use in cancer treatment, but their activities in vivo have not been fully characterized.. In a recent study, Emeagi and colleagues from Vrije Universiteit Brussel, Belgium, showed that SMAC mimetics induce cancer cell death via a proinflammatory effect that is accompanied by an adaptive antitumor immune response. Transduction with lentiviral vectors encoding a cytosolic form of a SMAC mimetic (LV-tSMAC) resulted in apoptosis of cancer cells of different histologic origins, and treatment of tumor-bearing mice with the SMAC mimetic resulted in induction of apoptosis, activation of antitumor immunity, and prolonged survival.. Immune Response. The antitumor immune response included increased levels of tumor-infiltrating ...
Albany, New York, Dec 1, 2017: Apoptosis Regulator BAX (Bcl 2 Like Protein 4 or BCL2L4 or BAX) - Apoptosis regulator BAX or bcl-2-like protein 4 is a protein is encoded by the BAX gene. It accelerates programmed cell death by antagonizing the apoptosis repressor BCL2. It promotes activation of CASP3, and thereby apoptosis. It undergoes a conformation change that causes translocation to the mitochondrion membrane, leading to the release of cytochrome c that then triggers apoptosis under stress conditions.. Request For Free Sample - https://www.marketresearchhub.com/enquiry.php?type=S&repid=1389111. Apoptosis Regulator BAX (Bcl 2 Like Protein 4 or BCL2L4 or BAX) pipeline Target constitutes close to 7 molecules. Out of which approximately 3 molecules are developed by companies and remaining by the universities/institutes. The molecules developed by companies in Phase III, Phase II and Preclinical stages are 1, 1 and 1 respectively. Similarly, the universities portfolio in Preclinical and Discovery ...
Evidence suggests that the signalling events which occur after apoptotic stimulation, define two basic mechanisms for the induction of apoptosis. The first is dependent on signalling via the mitochondria and the second is dependent upon signalling directly from the death receptors. After induction of apoptosis, there is a convergence in signalling at the level of caspase activation and subsequent biochemical and morphological changes. Therefore the efficacy of various inhibitors of apoptosis is dependent upon the initiating signal. In order to understand the apoptotic pathway, the mechanisms by which these inhibitors regulate chemical- and receptor-mediated apoptosis must be understood. The anti-apoptotic oncoprotein, Bcl-2, was shown to inhibit both staurosporine and Fas-mediated apoptosis in a manner which was partially dependent upon the level of Bcl-2 protein expressed. During both staurosporine and Fas-induced apoptosis Bcl-2 acted downstream of caspase-8 activation. High levels of Bcl-2 ...
The influence of diabetes enhanced inflammation on cell apoptosis and periodontitis. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
Drug resistance has been mostly explained by molecular changes, such as overexpression of p-glycoprotein or O6-methylguanine-DNA-methyltransferase, which interfere with drug actions on the targets (1 , 2) . Because most anticancer agents, regardless of their diverse targets, exert effects by inducing apoptosis via activation of apoptotic pathways common to many cellular stresses, any antiapoptotic changes disrupting the common intrinsic pathways to execute physiological cell death can also make malignant cells resistant to chemotherapy (3) . Such alterations opposing apoptosis are routinely observed in malignant tumors, including both the functional loss of tumor suppressors p53, Bax, or PTEN and deregulated hyperfunction of oncogenic proteins, such as Ras, Bcl-2, and PI3K 2 ,(3) .. In tumor cells with an aberrantly activated PI3K/Akt survival pathway, the increased antiapoptotic signals overcome apoptotic signals of anticancer drugs, confer drug resistance on the tumor cells, and result in a ...
Apoptosis is characterized by a series of well defined morphological and biochemical features that allow cells to initiate self-destruction in response to a variety of stimuli. CD4⁺CD8⁺ is a sub-population of immature thymocytes that are especially prone to the action of apoptosis-inducing agents and are sensitive to glucocorticoid-induced apoptosis, an event that plays a critical role in eliciting the antigen-specific thymocyte repertoire. Glucocorticoids induce apoptosis through activation of the GR, a ligand-induced transcription factor that transduces the hormonal signals into the regulated expression of target genes. While much is known about the structure and function of GR, key steroid-regulated genes believed to be required for thymocyte apoptosis have not been found. Based on the transcriptional-regulation of apoptosis by ecdysone-mediated induction of reaper gene expression in Drosophila, and p53-mediated transcriptional-activation of Bax gene expression in mammalian cells, our ...
Zeng L., Li T., Xu D.C., Liu J., Mao G., Cui M.Z., Fu X., Xu X.. Cells undergo apoptosis through two major pathways, the extrinsic pathway (death receptor pathway) and the intrinsic pathway (the mitochondrial pathway). These two pathways can be linked by caspase-8-activated truncated Bid formation. Very recently, death receptor 6 (DR6) was shown to be involved in the neurodegeneration observed in Alzheimer disease. DR6, also known as TNFRSF21, is a relatively new member of the death receptor family, and it was found that DR6 induces apoptosis when it is overexpressed. However, how the death signal mediated by DR6 is transduced intracellularly is not known. To this end, we have examined the roles of caspases, apoptogenic mitochondrial factor cytochrome c, and the Bcl-2 family proteins in DR6-induced apoptosis. Our data demonstrated that Bax translocation is absolutely required for DR6-induced apoptosis. On the other hand, inhibition of caspase-8 and knockdown of Bid have no effect on DR6-induced ...
As one of the cellular death mechanisms, apoptosis, also known as programmed cell death, can be defined as the process of a proper death of any cell under certain or necessary conditions. Apoptosis is controlled by the interactions between several molecules and responsible for the elimination of unwanted cells from the body.. Many biochemical events and a series of morphological changes occur at the early stage and increasingly continue till the end of apoptosis process. Morphological event cascade including cytoplasmic filament aggregation, nuclear condensation, cellular fragmentation, and plasma membrane blebbing finally results in the formation of apoptotic bodies. Several biochemical changes such as protein modifications/degradations, DNA and chromatin deteriorations, and synthesis of cell surface markers form morphological process during apoptosis.. Apoptosis can be stimulated by two different pathways: (1) intrinsic pathway (or mitochondria pathway) that mainly occurs via release of ...
Annexin V-Biotin Apoptosis Reagent (ab14165). Quick and reliable detection of phosphatidylserine exposure by flow cytometry or microscopy.
Bullacta exarata was hydrolyzed with trypsin to prepare peptides; Hydrolysates were isolated by ultrafiltration and purified using G-25 gel filtration. The purity of the Bullacta exarata was demonstrated by HPLC and its peptide sequence analysis was detected. The effects of BEPT II and BEPT II-1 on the proliferation of PC-3 cells were examined using a MTT assay. BEPT II and BEPT II-1 significantly inhibited the proliferation of PC-3 cells in a time- and dose-dependent manner. Annexin V/PI double staining studies showed exposing PC-3 cells to 5, or 15 mg/mL BEPT II-1 for 24 h increased the percentage of the early stage of apoptotic cells from 11.22% to 22.09%. In addition, typical morphologic changes were observed in the cells with acridine orange/ethidium bromide staining. These data support that BEPT II-1 has anticancer properties and merits further investigation to understand the mechanisms of BEPT II-1-induced apoptosis in PC-3 cells.
The BCL-2 family of proteins forms a complex interaction network that regulates cellular life and death decisions and contributes to cancer development, maintenance, and chemoresistance. BH3 only member proteins (e.g. BIM) serve as cellular stress sentinels and, when triggered, signal irreversible activation of apoptosis through their α-helical BH3 death domains. These pro-apoptotic signals are normally held in check by the multidomain anti-apoptotic proteins (e.g. BCL-XL, MCL-1) but when they are unable to do so the multidomain pro-apoptotic proteins BAX and BAK induce cell death through pore formation in the mitochondrial outer membrane. Therapeutic manipulation of the BCL-2 family with BH3 mimetics (including small molecules and synthetic peptides) is an emerging paradigm in cancer treatment and immune modulation. The design of next-generation therapeutics based on the BIM BH3 helix offers the unique advantage of recapitulating BIMs natural capacity to directly target the full complement of ...
transgene mice still have some protective effect. We propose that exogenous TNF-α results in robust induction of antiapoptotic genes, particularly through NF-κB activation, that is sufficient itself to prevent hepatocytes apoptosis in vivo. In contrast, the antiapoptotic gene response to Fas/CD95 activation alone is insufficient to prevent apoptosis but could act synergistically with Bcl-2. Although this antiapoptotic transcriptional response may be permissive for the Bcl-2 action, Bcl-xL could still have some antiapoptotic activity when transcription is blocked.. The major antiapoptotic role of NF-κB in the liver has now been extended to numerous models (4, 34).1) Embryonic lethal apoptotic liver destruction has been described in p65 and IκB kinase 2-deficient mice (6, 25). 2) Murine hepatocytes treated with NF-κB inhibitors also became apoptotic (7).3) NF-κB downregulation is required for TGF-β-induced apoptosis in hepatic cell lines (2).4) Finally, blocking NF-κB posthepatectomy ...
The major findings of this study are that ET-1 prevents apoptosis induced by serum deprivation in a dose-dependent manner via an ETA receptor in H9c2 cardiomyocytes and that the antiapoptotic effect of ET-1 is mediated through a c-Src/Bcl-xL pathway. Evidence for this proposal includes the following: (1) ET-1, but not AII, prevented mitochondrial cytochrome c release and apoptosis induced by serum deprivation in a dose-dependent manner, and this antiapoptotic effect was inhibited by an ETA receptor antagonist (BQ123) but not by an ETB receptor antagonist (BQ788); (2) the inhibitory effects of ET-1 on apoptosis were inhibited by tyrosine kinase inhibitors and adenovirus-mediated overexpression of KI-c-Src; (3) ET-1 stimulated c-Src activation; and (4) ET-1 upregulated an antiapoptotic molecule, Bcl-xL, and this upregulation was inhibited by tyrosine kinase inhibitors or cotransfection with KI-c-Src.. Recent evidence suggests that apoptosis of cardiac myocytes is a feature in cardiovascular ...
The present study examined levels of various components of the cell death machinery and drug sensitivity of 60 human cancer cell lines to anticancer drugs. With the exception of procaspase-3, which was undetectable in MCF-7 cells, caspases-2, -3, -6, -7, -8, and -9, as well as Apaf-1, were detectable in all 60 cell lines. Although these components of the cell death machinery varied widely in abundance, strong correlations between levels of Apaf-1 or procaspase-2, -3, -6, -8, or -9 and sensitivity to any class of antineoplastic agent were not observed. These results, although negative, have several important implications.. The attempt to correlate drug sensitivity with levels of various components of the cell death machinery was prompted by previous studies indicating that drug-induced apoptosis is markedly diminished when certain key components of the core cell-death machinery, particularly Apaf-1, procaspase-9, or procaspase-3, are genetically or functionally deleted (36, 37, 38 , 58 , 88 , 99) ...
Tomato extracts can inhibit the growth and malignant cloning of stomach cancer cells, according to a new study that paves the way for novel therapies to treat the deadly disease. Researchers analysed whole tomato extracts for their ability to tackle gastric cancercell lines.. "Their antitumoral effect seem not related to specific components, such as lycopene, but rather suggest that tomatoes should be considered in their entirety," said Daniela Barone, researcher at the Oncology Research Centre of Mercogliano (CROM) in Italy.. Extracts of San Marzano and Corbarino tomato varieties were able to inhibit the growth and cloning behaviour of malignant cells. Treatment with the whole tomato extracts affected key processes within the cells hindering their migration ability, arresting cell cycle through the modulation of retinoblastoma family proteins and specific cell cycle inhibitors, and ultimately inducing cancer cell death through apoptosis.. "Our results prompt further assessment of the potential ...
The relationship between apoptotic progression and cell cycle perturbation induced by microtubule-destabilising (vinblastine, Colcemid) and -stabilising (taxol) drugs was studied in two mesenchyme-derived neoplastic cell lines, growing as suspension (Jurkat) and monolayer (SGS/3A) culture, by morphocytochemical and biochemical approaches. The same kind of drug induced different effects on the cell kinetics (proliferation, polyploidisation, death) of the two cell lines. In floating cells, the drugs appeared more effective during the S phase, while in adherent cells they were more effective during the G2/M phase. Moreover two distinct neoplasia-associated apoptotic phenotypes emerged: the first pattern was the typical one and was found in cells with a low transition through the S/G2 phase (Jurkat), and the second one was mainly characterised by a cell death derived from micronucleated and mitotic cells, as a consequence of a low transition through the M/G1 phase (SGS/3A). Our data show that the ...
Apoptosis is a major form of cell death that is dependent on wild-type p53 after DNA damage for certain normal cells, such as those of the early embryo and those of lymphoid origin (3 , 4) . There are also several examples in the literature where apoptosis clearly contributes to the overall sensitivity of cells to treatment with radiation or chemotherapeutic agents as assessed either by in vivo treatments (15 , 72) or by clonogenic assays in vitro (69 , 72 , 73) . However, a major difference between these studies and ones that have failed to find a link between apoptosis and overall sensitivity has been the choice of the cells used in the study. For cells of nonlymphoid origin, the cases in which apoptosis does contribute to overall sensitivity have in large part been those that used cells derived from normal tissues genetically engineered to express dominant oncogenes. Introduction of viral or cellular oncogenes such as E1A (74 , 75) , myc (72 , 76) , or human papillomavirus E7 (77) renders ...
Objective - Pro-inflammatory cytokines are cytotoxic to β-cells and have been implicated in the pathogenesis of type 1 diabetes and islet graft failure. The importance of the intrinsic mitochondrial apoptotic pathway in cytokine-induced β-cell death is unclear. Here, cytokine activation of the intrinsic apoptotic pathway and the role of the two pro-apoptotic Bcl-2 proteins, Bad and Bax were examined in β-cells.. Research Design and Methods - Human islets, rat islets, and INS-1 cells were exposed to a combination of pro-inflammatory cytokines: interleukin (IL)-1β, interferon (IFN)γ and/or tumor necrosis factor (TNF)α. Activation of Bad was determined by Ser136 dephosphorylation; mitochondrial stress by changes in mitochondrial metabolic activity and cytochrome c release; and downstream apoptotic signalling by activation of caspase-9 and -3, and DNA fragmentation. The inhibitors FK506 and V5 were used to investigate the role of Bad and Bax activation, respectively.. Results - We found that ...
Disclosed is substantially pure DNA encoding mammalian IAP polypeptides; substantially pure polypeptides; and methods of using such DNA to express the IAP polypeptides in cells and animals to inhibit apoptosis. Also disclosed are conserved regions characteristic of the IAP family and primers and probes for the identification and isolation of additional IAP genes. In addition, methods for treating diseases and disorders involving apoptosis are provided.
Apoptosis is an important defensemechanismmounted by the immune systemto control virus replication. Hence, cytomegaloviruses (CMV) evolved and acquired numerous anti-apoptotic genes. The product of the human CMV (HCMV) UL36 gene, pUL36 (also known as vICA), binds to pro-caspase-8, thus inhibiting death-receptor apoptosis and enabling viral replication in differentiated THP-1 cells. In vivo studies of the function of HCMV genes are severely limited due to the strict host specificity of cytomegaloviruses, but CMV orthologues that co-evolved with other species allow the experimental study of CMV biology in vivo. The mouse CMV (MCMV) homolog of the UL36 gene is called M36, and its protein product (pM36) is a functional homolog of vICA that binds to murine caspase-8 and inhibits its activation. M36-deficient MCMV is severely growth impaired in macrophages and in vivo. Here we show that pUL36 binds to the murine pro-caspase-8, and that UL36 expression inhibits death-receptor apoptosis in murine cells ...
Apoptotic β-cell death is an important pathological mechanism of β-cell loss in type 1 diabetes and islet graft rejection (5,6). Apoptosis is a highly regulated process, such that the decision to undergo apoptosis is dependent upon the balance between antiapoptotic and proapoptotic signals (19). In an inflammatory setting, cells are required to express a new or inducible set of antiapoptotic genes as a mechanism to counteract the physiological stresses that otherwise lead to cellular damage and apoptosis (19,39). Blockade of this regulated antiapoptotic response sensitizes many cell types to apoptotic death, underscoring the physiological relevance of this signaling network in cell biology (16-18).. In this present study we demonstrate that this paradigm is true for β-cells, as β-cells were sensitized to TNF-α-induced death by inhibition of de novo gene transcription. Our microarray-based approach revealed that TNFAIP3/A20 is one potential candidate gene providing a molecular basis for this ...
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.
Reagents and in vitro assays. The E18-14C-27 cells (7) were provided by Powel Brown (Baylor), and the other ER-negative breast cancer cells and the RAW264.7 macrophage-like cells were purchased from the American Type Culture Collection. Cells were grown in either DMEM (E18 and RAW cells) or DMEM/F-12 (MDA cell lines and SK-BR-3 cells) and 10% fetal bovine serum. Stock solutions of CDDO-Me (18) and 268 (19) were made in DMSO, and appropriate DMSO controls (≤0.1%) were included in all in vitro experiments. RAW cells were treated with drugs for 24 h, and interleukin-6 (IL-6) and nitric oxide were measured in the medium with a Quantikine ELISA kit (R&D Systems) or the Griess reaction, respectively. Proliferation was measured 72 h after treatment with a [3H]thymidine incorporation assay, and apoptosis was detected using a TACS Annexin V-FITC apoptosis detection kit (R&D Systems) and flow cytometry. Antibodies to ErbB2 (RB-103-PO), phosphorylated STAT3 (9138), IKK (sc-7607), and IKBα (sc-371) were ...
Autor: Pesch, M. et al.; Genre: Zeitschriftenartikel; Im Druck veröffentlicht: 2014-10; Titel: Arabidopsis TTG2 Regulates TRY Expression through Enhancement of|br/| Activator Complex-Triggered Activation
Apoptosis is a designed cell death mechanism involved in biological processes. Apoptosis can either be activated by extrinsic pathway or by the intrinsic pathway. A major part of the external apoptosis pathway is the death receptor Fas which, on binding to its associated ligand FasL, they eventually form the death-inducing signaling complex. FasL promotes clustering for open Fas and activates open stable Fas, forming locally stable signaling platforms through neighborhood-induced receptor interactions. The model exhibits a bifurcation called hysteresis, providing an upstream mechanism for bistability and robustness to decide if the cell lives or dies. At low receptor concentrations, the bistability depends on three states of FasL. The irreversible bistability, representing a committed cell death decision, emerges at high receptor concentrations. Furthermore, the model suggests a mechanism by which cells may function as bistable life/death switches which are independent of their downstream ...
Findings may offer a new way to kill cancer cells by forcing them into an alternative programmed-death pathway.. May 14, 2013 ...
This postdoctoral position is part of a research project where we will investigate the regulation of programmed cell death at the molecular level with focus on the structure of the proteins and biological membranes involved in this important process. Important key players in the mitochondrial (intrinsic) cell death pathway are membrane-active proteins of the Bcl-2 family. Family members with opposite functions meet at the outer membrane of mitochondria, where they determine the fate of a cell, namely to live or to die. The main objective of this project is to understand the function - and underlying structural properties - of these proteins and their interaction with the mitochondrial membrane environment. For this purpose we will use structural biological methods focusing on solid-state NMR spectroscopy of lipid-protein complexes. By applying advanced solid-state NMR approaches, we will be able to provide structural insight into the molecular mechanism by which the survival membrane protein ...
However, depending on the amplitude of the Ca2+ signal as well as the condition of the cell, Ca2+ can also initiate apoptosis as a consequence of organelle disruption, free radical production, and the activation of Ca2+-dependent phosphatases and proteases such as calcineurin and calpain (96).. The release of Ca2+ from the ER is a critical early event for the initiation of apoptosis induced by many apoptotic signals (115). The sensitivity of a cell to such apoptotic stimuli appears to be largely dependent on the ER Ca2+ load, with a high resting ER Ca2+ concentration sensitizing cells to apoptotic stimuli and a low ER Ca2+ concentration conferring resistance. Once released into the cytosol, Ca2+ is rapidly adsorbed by mitochondria that can trigger apoptotic responses by disrupting the mitochondrial respiratory chain and generating reactive oxygen species or by opening the PTP (122).. The original finding that Bcl-2 affected Ca2+ signaling was discovered over a decade ago. In these studies, Bcl-2 ...
The cytokine TWEAK and its receptor, Fn14, have emerged as potentially valuable targets for cancer therapy. Granzyme B (GrB)-containing Fn14-targeted constructs were generated containing either the Fn14 ligand TWEAK (GrB-TWEAK) or an anti-Fn14 humanized single-chain antibody (GrB-Fc-IT4) as the targeting moieties. Both constructs showed high affinity and selective cytotoxicity against a panel of Fn14-expressing human tumor cells including triple-negative breast cancer (TNBC) lines. Cellular expression of the GrB inhibitor PI-9 in target cells had no impact on the cytotoxic effect of either construct. Cellular expression of MDR1 showed no cross-resistance to the fusion constructs. GrB-TWEAK and GrB-Fc-IT4 activated intracellular caspase cascades and cytochrome c-related proapoptotic pathways consistent with the known intracellular functions of GrB in target cells. Treatment of mice bearing established HT-29 xenografts with GrB-TWEAK showed significant tumor growth inhibition compared with vehicle ...
One of the hallmarks in the advancement of cancer cells is an ability to overcome and acquire resistance to adverse conditions. There has been a large amount of cancer research on IGFBP-3 as a pro-apoptotic molecule in vitro. These pro-apoptotic properties, however, do not correlate with several studies linking high IGFBP-3 levels in breast cancer tissue to rapid growth and poor prognosis. Evidence is emerging that IGFBP-3 also exhibits pro-survival and growth-promoting properties in vitro. How IGFBP-3 pivots cell fate to either death or survival, it seems, comes down to a complex interplay between cells microenvironments and the presence of cellular IGFBP-3 binding partners and growth factor receptors. The cytoprotective actions of IGFBP-3 are not restricted to cancer but are also observed in other disease states, such as retinopathy and brain ischaemia. Here we review the literature on this paradoxical nature of IGFBP-3, its pro-apoptotic and growth-inhibitory actions versus its cytoprotective and
Caspase-1, originally called ICE, was the first mammalian analogue of the Caenorhabditis elegans death genes to be identified.11 Like all caspases, it is expressed as a proform, which is activated through proteolytic cleavage of an amino-terminal 11-kDa prodomain to release p20 and p10 subunits. Active caspase-1/ICE consists of a (p20/p10)2 tetramer, which is sufficient to process precursor IL-1β9,12-14 and, in at least some cell types, to induce apoptosis.16 Additionally, the prodomain has been postulated to have independent proapoptotic activity by enhancing death receptor-mediated caspase-8 activation.39 Although caspase-1 has conventionally been regarded as a proinflammatory, not a proapoptotic, caspase,10-12 it has been observed to induce or amplify apoptosis in tissue culture models.15,16. Regulated expression of caspase-1 in cardiac hypertrophy,17 the dilated cardiomyopathy of TNF-α overexpression,19 ischemia/infarction,21 and endotoxin-induced myocardial dysfunction18 prompted our ...
During tumor progression, immune system phagocytes continually clear apoptotic cancer cells in a process known as efferocytosis. However, the impact of efferocytosis in metastatic tumor growth is unknown. In this study, we observed that macrophage-driven efferocytosis of prostate cancer cells in vitro induced the expression of proinflammatory cytokines such as CXCL5 by activating Stat3 and NF-κB(p65) signaling. Administration of a dimerizer ligand (AP20187) triggered apoptosis in 2 in vivo syngeneic models of bone tumor growth in which apoptosis-inducible prostate cancer cells were either coimplanted with vertebral bodies, or inoculated in the tibiae of immunocompetent mice. Induction of 2 pulses of apoptosis correlated with increased infiltration of inflammatory cells and accelerated tumor growth in the bone. Apoptosis-induced tumors displayed elevated expression of the proinflammatory cytokine CXCL5. Likewise, CXCL5-deficient mice had reduced tumor progression. Peripheral blood monocytes ...
Transient receptor potential (TRP) channels contribute to the regulation of intracellular calcium, which can promote cancer hallmarks in cases of dysregulation of gene transcription and calcium-dependent pro-proliferative or anti-apoptotic mechanisms. Several studies have begun to elucidate the role …
Apoptosis can be induced be different pathways including the interaction TNF ligand with their receptors at the plasma membrane or the activation of the BCl-2 family molecules.
Cardiac myocytes express at least six subtypes of adrenergic receptor (AR) which include three subtypes of beta-AR (beta-1, beta-2, beta-3) and three subtypes of the alpha-1-AR (alpha-1A, alpha-1B, and alpha-1C). In the human heart the beta-1-AR is the pre- dominate receptor. Acute sympathetic stimulation of cardiac beta-1-ARs induces positive inotropic and chronotropic effects, the most effective mechanism to acutely increase output of the heart, by coupling to Gs, formation of cAMP by adenylyl cyclase (AC), and PKA- dependent phosphorylation of various target proteins (e.g., ryanodine receptor [RyR]; phospholamban [PLB], troponin I [TnI], and the L-type Ca2+ channel [LTCC]). Chronic beta-1-AR stimulation is detrimental and induces cardiomyocyte hypertrophy and apoptosis. beta-2-AR coupled to Gs exerts a proapoptotic action as well as beta-1-AR, while beta-2-AR coupled to Gi exerts an antiapoptotic action ...
Principal Investigator:SHICHIRI Masayoshi, Project Period (FY):1997 - 1998, Research Category:Grant-in-Aid for Scientific Research (C), Section:一般, Research Field:内分泌・代謝学
Caveolin-1 (Cav-1), a family of ubiquitously expressed oligomeric structural proteins in many mammalian cells, has been shown to be an effective regulator of tumorigenesis. Recent studies have indicated that Cav-1 can promote resistance to chemotherapy in a variety of tumors. However, the regulation of Cav-1 on chemoresistance in ovarian cancer is still unknown. In the present study, the mRNA and protein expression level was investigated by RT-PCR and western blot analysis, respectively, and the 50% inhibitory concentration (IC50) value was measured by MTT assay. The protein expression level of P-glycoprotein (P-gp), Notch-1, p-Akt and p-NF-κB p65 were detected using western blot analysis and the apoptotic ratio was determined using the Annexin V-FITC/PI detection kit. The results showed that the mRNA and protein expression levels of Cav-1 were significantly higher in SKOV3/DDP and A2780/DDP than in SKOV3 and A2780, respectively. Knockdown of Cav-1 significantly decreased the IC50 value in ...
In the last decade, basic cancer research has produced remarkable advances in our understanding of cancer biology and cancer genetics. Among the most important of these advances is the realization that apoptosis and the genes that control it have a profound effect on the malignant phenotype. For example, it is now clear that some oncogenic mutations disrupt apoptosis, leading to tumor initiation, progression or metastasis. Conversely, compelling evidence indicates that other oncogenic changes promote apoptosis, thereby producing selective pressure to override apoptosis during multistage carcinogenesis. Finally, it is now well documented that most cytotoxic anticancer agents induce apoptosis, raising the intriguing possibility that defects in apoptotic programs contribute to treatment failure. Because the same mutations that suppress apoptosis during tumor development also reduce treatment sensitivity, apoptosis provides a conceptual framework to link cancer genetics with cancer therapy. An ...
Sigma-Aldrich offers abstracts and full-text articles by [Haiqin Wu, Huqing Wang, Wenting Zhang, Xuanhui Wei, Jiaxin Zhao, Pu Yan, Chao Liu].
The APO2.7 antigen (also named 7A6 antigen) is a 38 kDa protein localized on the membrane of mitochondria whose expression appears to be restricted to cells undergoing apoptosis. The APO2.7 antigen can be detected after apoptosis induction via CD95/Fas ligation, irradiation or drug treatment. Expression of APO2.7 appears as an early event in the apoptosis process. Normal viable cells are negative or weakly positive for APO2.7. Research studies have shown that less than 2% of peripheral T cells from normal donors expressed the APO2.7 antigen. Some level of APO2.7 expression associated with an on-going apoptotic process has been demonstrated in activated T cells.. ...
The APO2.7 antigen (also named 7A6 antigen) is a 38 kDa protein localized on the membrane of mitochondria whose expression appears to be restricted to cells undergoing apoptosis. The APO2.7 antigen can be detected after apoptosis induction via CD95/Fas ligation, irradiation or drug treatment. Expression of APO2.7 appears as an early event in the apoptosis process. Normal viable cells are negative or weakly positive for APO2.7. Research studies have shown that less than 2% of peripheral T cells from normal donors expressed the APO2.7 antigen. Some level of APO2.7 expression associated with an on-going apoptotic process has been demonstrated in activated T cells.. ...
Here, we analyzed the ability of C. vasculum-derived metabolites to inhibit proliferation, induce cytotoxicity, and trigger apoptotic signaling in NSCLC, SCLC, and ovarian carcinoma. It has previously been shown that compounds isolated from this sponge can kill tumor cells of different origin albeit through unknown mechanism of action (19). We show here that the two acetylenic compounds 1 and 2 as well as the parental mixture of these compounds from which they were separated, indeed cause tumor-specific cytotoxicity in NSCLC and SCLC. Importantly, we demonstrate that for both compounds this cytotoxicity is tumor specific, as all normal cells tested representing heart tissue, bronchial and retina epithelium, normal PBMCs, and foreskin or lung fibroblasts remained unaffected at concentrations that were toxic for NSCLC and SCLC. In ovarian carcinoma cells compound 1 but not compound 2 caused tumor-specific cell death. For compound 2, a cytotoxic effect was evident in NSCLC and SCLC whereas in ...
Death receptors were initially recognised as potent inducers of apoptotic cell death and soon ambitious attempts were made to exploit selective ignition of controlled cellular suicide as therapeutic strategy in malignant diseases. However, the complexity of death receptor signalling has increased substantially during recent years. Beyond activation of the apoptotic cascade, involvement in a variety of cellular processes including inflammation, proliferation and immune response was recognised. Mechanistically, these findings raised the question how multipurpose receptors can ensure selective activation of a particular pathway. A growing body of evidence points to an elegant spatiotemporal regulation of composition and assembly of the receptor-associated signalling complex. Upon ligand binding, receptor recruitment in specialized membrane compartments, formation of receptor-ligand clusters and internalisation processes constitute key regulatory elements. In this review, we will summarise the current
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 ...
We observed previously that cisplatin-resistant HeLa cells were cross-resistant to UV light due to accumulation of DDB2, a protein implicated in DNA repair. More recently, we found that cFLIP, which represents an anti-apoptotic protein whose level is induced by DDB2, was implicated in preventing apoptosis induced by deathreceptor signaling. In the present study, we investigated whether DDB2 has a protective role against UV irradiation and whether cFLIP is also involved in this process. Methods: We explored the role of DDB2 in mediating UV resistance in both human cells and Drosophila. ...
Background and Objective: Apoptosis or programmed cell death is an important process for cellular homeostasis and it can be initiated by both physiologic and pathologic stimuli. Defects in the apoptosis process may lead to serious disease such as autoimmune diseases, cancer, tumors drug resistance, and the acquired immunodeficiency syndrome (AIDS). ...
Apoptosis, the process by which cells orchestrate their own demise in response to intra- or extracellular events, plays a major role in normal, pathological, and iatrogenic processes in the nervous system (Cotter et al., 1990; Raff, 1992; Wyllie, 1992). In non-nervous system models, several endogenous factors have been shown to protect tumor and/or normal cells from apoptotic death (Brach et al., 1992; Tilly et al., 1992; Harrington et al., 1994; Ishizaki et al., 1994). These agents have been referred to collectively as "survival factors" (Collins et al., 1994). For both normal and neoplastic neural crest-derived cells, NGF acts as a survival factor that protects against apoptosis initiated by a variety of exogenous conditions (Ibanez et al., 1992; Rabizadeh et al., 1993). We have reported previously on antimitotic agent-induced apoptosis in neuroblastoma cells and the protection by NGF of these cells from apoptosis induced by such agents (Falcione et al., 1993; Cortazzo et al., 1995; Hartsell ...
in IEE Proceedings - Systems Biology (2005), 152(4), 221228. Analyses of different robustness aspects for models of the direct signal transduction pathway of receptor-induced apoptosis is presented. Apoptosis is a form of programmed cell death, removing unwanted ... [more ▼]. Analyses of different robustness aspects for models of the direct signal transduction pathway of receptor-induced apoptosis is presented. Apoptosis is a form of programmed cell death, removing unwanted cells within multicellular organisms to maintain a proper balance between cell reproduction and death. Its signalling pathway includes an activation feedback loop that generates bistable behaviour, where the two steady states can be seen as `life and `death. Inherent robustness, widely recognised in biological systems, is of major importance in apoptosis signalling, as it guarantees the same cell fate for similar conditions. First, the influence of the stochastic nature of reactions indicating a role for inhibition ...
In this study, we demonstrated that PC potentiated activation of survival pathways through PI-3 kinase signaling. Inhibition of PI-3 kinase with LY294002 abolished the protective effect of PC by stimulating apoptosis and DNA fragmentation without affecting LDH release from the myocytes. These data suggest that PI-3 kinase has an important role the in antiapoptotic effects of PC. Hypoxia followed by reoxygenation (H/R) was associated with both apoptotic and necrotic cell death, whereas hypoxia contributed to only a minimal amount of cell death. Therapeutic reperfusion is currently performed without any measure to protect myocardium from apoptosis during the treatment of myocardial infarction.23 Our results indicate that it may be possible to further limit the infarct size by inhibition of apoptosis, and PI-3 kinase might play a key role in this process. PC also stimulates phosphorylation of Akt, a kinase directly downstream of PI-3 kinase. Pretreatment with LY294002 blocks the PC-induced increase ...
Apoptosis regulator BAX TranslationBlocker™ siRNA. Tested in Human samples. The only siRNA validated in protein knockdown with detailed protocols. From: $219.
A few years ago, an original concept of cell biology was proposed: whereas the classic dogma postulates that transmembrane receptors are inactive unless bound by their specific ligand, it was suggested that some receptors may be active not only in the presence of their ligand, but also in their absence. In this latter case, the signaling downstream of these unbound receptors leads to apoptosis. These receptors were consequently named
A proof-of-concept study shows how a new compound selectively triggers cell suicide in acute myeloid leukemia cells without harming healthy cells.
Bax and Bak localized to the ER can initiate apoptosis. In addition to their mitochondrial localization and activity, Bax and Bak also reside at the ER. Upon ER
Gabriel Gil has directed the Apoptotic Signalling research group of the IMIM since 2000. Apoptosis, or programmed cell death, is a physiological process with an essential role both during development and in the adult organism.
Th1 cell differentiation is impaired in these mice. Primary murine embryonic fibroblasts prepared from mutant embryos have decreased viability and increased genomic DNA fragmentation with UV irradiation. This mutant mouse strain represents a model that may be useful in studies related to signal transduction.
The Lens serves almost all the patents and scholarly work in the world as a free, open and secure digital public good, with user privacy a paramount focus.
The Pa-PDT induced p-JNK caused down-regulation of the pro-apoptotic protein bcl-2 that facilitates the collapse of mitochondrial membrane and eventually initiates the intrinsic apoptotic pathway ...
Incheol Shin heeft geschreven in bericht ,8o0up8$9qn$1 at green.kreonet.re.kr,... ,Also, if you know the best apoptosis assay system ,for the adherent cells. I would like to avoid ,the system with microscopic observations since ,I need to include the floating (apoptotic) cells ,in my assay. Cant you just collect the medium with floating cells, and then trypsinize your adherent cells and do your thing? Regards, Bas ...
As much as the cellular viability is important for the living organisms, the elimination of unnecessary or damaged cells has the opposite necessity for the maintenance of homeostasis in tissues,...
DI-fusion, le Dépôt institutionnel numérique de lULB, est loutil de référencementde la production scientifique de lULB.Linterface de recherche DI-fusion permet de consulter les publications des chercheurs de lULB et les thèses qui y ont été défendues.
3 ap3h1 24 signarrays apoptosis 3 ap3h1 24 signarrays | order 3 ap3h1 24 signarrays apoptosis 3 ap3h1 24 signarrays | How to use: 3 ap3h1 24 signarrays apoptosis 3 ap3
It follows similar pacts by the likes of PPD, which is tapping another virtual trial specialist, Science 37, for its "siteless" approach to trials. https://www.fiercebiotech.com/cro/amid-pandemic-labcorp-s-cro-unit-covance-pens-decentralized-pact- ...
Expression analysis of BCL2L12, a new member of apoptosis-related genes, in colon cancer.: Apoptosis is an active process regulated by a variety of genes. Recen
Programmed cell death or apoptosis is an important physiological process in multicellular organisms. The equilibrium between cell growth and division and th...
Try Oncomin for Apoptosis from Bagdara Farms to gain from its multifaceted abilities to prevent and treat various kinds of cancer.
Gentaur molecular products has all kinds of products like :search , Biotium \ NUCVIEW488_MITOVIEW633 APOPTOSIS \ 30062 for more molecular products just contact us
Mice and primary neuronal cultures. Hq, Apaf1-/-, and Bax-/- mice were maintained and genotyped as described previously (Fortin et al., 2001; Klein et al., 2002). Cortical neurons and cerebellar granule neurons (CGNs) were cultured from cortices of E15.5 mice and cerebellums of postnatal day 7 mice, respectively, as described previously (Fortin et al., 2001). Recombinant adenoviral vectors carrying human AIF or LacZ expression cassettes were prepared and used at 50 multiplicity of infection as described previously (Cregan et al., 2002).. Camptothecin treatment and cell viability assays. Neurons were treated with 10 μm camptothecin with or without 10 μm Boc-aspartyl (Ome)-fluoromethylketone (BAF) (Enzyme System Products, Livermore, CA) after 2 d in vitro (DIV). Cell survival was measured by the following: live/dead staining (Molecular Probes, Eugene, OR), Hoechst staining, MTT assay (Cell Titer kit; Promega, Madison, WI), terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end ...
TY - JOUR. T1 - Mifepristone regulates expression of apoptosis related genes Fas and FasL in mouse endometrium. AU - Gao, F.. AU - Xu, F. H.. AU - Zhou, X. C.. AU - Han, X. B.. AU - Liu, Y. X.. PY - 2001/7/3. Y1 - 2001/7/3. N2 - AIM: To investigate the anti-implantation mechanism of mifepriston. METHODS: In situ hybridization and immunohistochemistry were applied to determine mRNA and protein. RESULTS: After mifepriston injection, the number of implantation sites were obviously reduced, mifepriston could inhibit the embryo implantation in mouse. The expression of apoptosis related genes, Fas and FasL, in mouse endometrium was also decreased after mifepriston treatment. CONCLUSION: The expression of apoptosis related genes Fas and FasL is regulated by mifepriston and the inhibitory effect of mifepriston on the embryo implantation may be mediated by action on the Fas/FasL system.. AB - AIM: To investigate the anti-implantation mechanism of mifepriston. METHODS: In situ hybridization and ...
title: Galpha12 Protects Vascular Endothelial Cells from Serum Withdrawal-Induced Apoptosis through Regulation of miR-155, doi: 10.3349/ymj.2016.57.1.247, category: Article
Vascular Endothelial Growth Inhibitor (VEGI) is an endothelial cell autocrine factor and a member of the tumor necrosis family of ligands. VEGI is able to specifically inhibit endothelial cell growth and is an efficient inhibitor of angiogenesis. The molecular mechanisms of VEGI activity on endothelial cells remain undefined. Here we focused on two important steps in the signal transduction of VEGI. We first determined a role of NF-κB in VEGI-induced apoptosis. We found that inhibition of the NF-κB pathway resulted in an increased apoptotic potential of VEGI. We conclude that the NF-κB pathway plays a role in suppressing the apoptotic potential of VEGI. We next investigated the receptor responsible for VEGI-induced endothelial cell apoptosis. DR3 is a receptor for VEGI and thus we first focused on confirming if DR3 is the receptor responsible for VEGI-mediated endothelial cell death. We determined VEGI had diminished apoptotic activity in endothelial cells that are depleted of DR3 by siRNA. ...
Pure ginsenoside standards (saponins Rh2, PD, and PT), along with an Rh2-enhanced North American ginseng (Panax quinquefolius) leaf extract (LFRh2), were tested for cytotoxic activity in cultured THP-1 leukemia cells. Thermal treatment of ginseng leaf resulted in production of both Rh2 and Rg3 content that was confirmed by liquid chromatography-mass spectrometry (LC-MS). Flow cytometry of cells stained with annexin V-fluorescein isothiocyanate and propidium iodide showed that the LFRh2 significantly (p ≤ 0.05) increased apoptosis (18% ± 0.4%) after 23 h at a concentration that inhibited cell viability by 50% (LC50 (72 h) = 52 μmg/mL. In comparison, a similar significant (p ≤ 0.05) increase in apoptotic cell numbers occurred at 41 h of exposure for pure ginsenoside standards, PD (LC50 (72 h) = 13 μg/mL), PT (LC50 (72 h) = 19 μg/mL), and Rh2 (LC 50 (72 h) = 15 μg/mL). Although no further increase in apoptosis was observed in THP-1 cells after exposure to increasing concentrations of LFRh2 ...
TY - JOUR. T1 - FADD/MORT1 is a common mediator of CD95 (Fas/APO-1) and tumor necrosis factor receptor-induced apoptosis. AU - Chinnaiyan, Arul M.. AU - Tepper, Clifford G. AU - Seldin, Michael F. AU - ORourke, Karen. AU - Kischkel, Frank C.. AU - Hellbardt, Stefan. AU - Krammer, Peter H.. AU - Peter, Marcus E.. AU - Dixit, Vishva M.. PY - 1996/3/1. Y1 - 1996/3/1. N2 - CD95 (Fas/APO-1) and tumor necrosis factor receptor-1 (TNFR-1) are related molecules that signal apoptosis. Recently, a number of novel binding proteins have been proposed to mediate the signaling of these death receptors. Here we report that an N-terminal truncation of one of these candidate signal transducers, FADD/MORT1, abrogates CD95-induced apoptosis, ceramide generation, and activation of the cell death protease Yama/CPP32. In addition, this dominant-negative derivative of FADD (FADD-DN) blocked TNF- induced apoptosis while not affecting NF-κB activation. FADD-DN bound both receptors, and in the case of CD95, it disrupted ...
We used cytoplasmic extracts from chicken DU249 cells at various stages along the apoptotic pathway to analyse the events of apoptotic exe-cution. So-called S/M extracts from morphologically normal committed-stage cells induce apoptotic morphology and DNA cleavage in substrate nuclei. These apoptotic changes appear to require the function of multiple caspases (cysteine aspar-tases, a specialized class of proteases) acting in parallel. Extracts from execution-stage apoptotic cells induce apoptotic events in added nuclei in a caspase-independent manner. Biochemical frac-tionation of these extracts reveals that a column fraction enriched in endogenous active caspases is un-able to induce DNA fragmentation or chromatin condensation in substrate nuclei, whereas a caspase-depleted fraction induces both changes. Execution-stage extracts contain an ICAD/DFF45-inhibitable nuclease resembling CAD, plus another activity that is required for the apoptotic chromatin condensation. Committed-stage S/M ...
In previous study we showed that caspase-2 plays the role of an apical caspase in cell death induction by taxanes in breast cancer cells. This study deals with the role of other caspases. We tested breast cancer cell lines SK-BR-3 (functional caspase-3) and MCF-7 (nonfunctional caspase-3). Using western blot analysis we demonstrated the activation of initiator caspase-8 and -9 as well as executioner caspase-6 and -7 in both tested cell lines after application of taxanes (paclitaxel, SB-T-1216) at death-inducing concentrations. Caspase-3 activation was also found in SK-BR-3 cells. Employing specific siRNAs after taxane application, suppression of caspase-3 expression significantly increased the number of surviving SK-BR-3 cells. Inhibition of caspase-7 expression also increased the number of surviving SK-BR-3 and MCF-7 cells. On the other hand, suppression of caspase-8 and caspase-9 expression had no significant effect on cell survival. However, caspase-9 seemed to be involved in the activation of
TY - JOUR. T1 - Nitric oxide-GAPDH-Siah. T2 - a novel cell death cascade.. AU - Hara, Makoto R.. AU - Snyder, Solomon H. PY - 2006/7. Y1 - 2006/7. N2 - 1. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is an extremely abundant glycolytic enzyme, and exemplifies the class of proteins with multiple, seemingly unrelated functions. Recent studies indicate that it is a major intracellular messenger mediating apoptotic cell death. This paper reviews the GAPDH cell death cascade and discusses its clinical relevance. 2. A wide range of apoptotic stimuli activate NO formation, which S-nitrosylates GAPDH. The S-nitrosylation abolishes catalytic activity and confers upon GAPDH the ability to bind to Siah, an E3-ubiquitin-ligase, which translocates GAPDH to the nucleus. In the nucleus, GAPDH stabilizes the rapidly turning over Siah, enabling it to degrade selected target proteins and affect apoptosis. 3. The cytotoxicity of mutant Huntingtin (mHtt) requires nuclear translocation which appears to be ...
3H]Thymidine Incorporation Studies. Thymidine incorporation studies were performed with cells grown in 35-mm culture dishes. The cells were labeled by the addition of methyl-[3H]thymidine (1 μCi/ml) to the medium, and the reactions were stopped after 1 h. The medium was drawn off, and the cells were rinsed twice with ice-cold phosphate-buffered saline (PBS). The cultures were then fixed with ice-cold 5% trichloracetic acid overnight at 4°C, after which the cells were extracted as previously described (Guo and Reiners, 2000). A second replicate set of nonfixed dishes was treated with 0.25% trypsin-EDTA to estimate cell numbers. [3H]Thymidine was detected by scintillation counting and expressed as disintegration per minute per 103 cells.. Assessment of Apoptosis. The effects of HET0016 to induced apoptosis in 9L cells were examined by fluorescence-activated cell sorting analysis after the cells were labeled with an annexin V-fluorescein isothiocyanate (FITC) antibody (Sigma Chemical, St. Louis, ...
Previous studies suggested that dithio-carbamates are potent apoptosis and anti-apoptosis inducing agents in various cancer cells. Here, the anti-proliferative and apoptosis inducing effects of a new derivative (2-NDC) from the dithio-carbamate family was examined in human leukemia K562 cells. We use thiazolyl blue tetrazolium bromide (MTT) to measure viability and cell growth inhibition. The 2-NDC showed effects on viability in a dose and time-dependent manner, inhibiting proliferation at concentrations of 10-30 M after 24-48 hours of treatment and increasing values after 72 hours at 40-120 M. The cytotoxic effect of the compound was calculated with an IC50 of 30 M after 24-hour. Apoptosis induction was confirmed by acridine orange-ethidium bromide (AO/EtBr) staining, DNA fragmentation assay, flow cytometric assessment and also caspase-3 activation assay. Furthermore, enzymes level such as superoxide dismutase (SOD) and catalase (CAT) involved in oxidative stress were evaluated. The results of this
Our results uncovered an unexpected role for MPO to influence the fate of neutrophils and consequently the duration of inflammation. By suppressing the constitutive cell death program, MPO prolonged the life span of neutrophils, thereby delaying the resolution of inflammation. These actions were specific for MPO, because other azurophilic granule constituents lactoferrin and elastase failed to affect neutrophil apoptosis.. Consistent with the commitment of neutrophils to apoptosis, MPO at clinically relevant concentrations delayed, rather than blocked apoptosis, resulting in prolonged survival of human neutrophils in vitro. We confirmed that increasing plasma concentrations of MPO in rats to levels comparable to those detected in patients with inflammatory vascular diseases20,21 was sufficient to retard the apoptotic machinery in neutrophils as assayed ex vivo. Furthermore, MPO also suppressed apoptosis in neutrophils that had emigrated into the airways and delayed resolution of inflammation in ...
TY - JOUR. T1 - The N-terminal helix of Bcl-xL targets mitochondria. AU - McNally, Melanie A.. AU - Soane, Lucian. AU - Roelofs, Brian A.. AU - Hartman, Adam L.. AU - Hardwick, J Marie. PY - 2013/3. Y1 - 2013/3. N2 - Anti- and pro-apoptotic Bcl-2 family members regulate the mitochondrial phase of apoptotic cell death. The mitochondrial targeting mechanisms of Bcl-2 family proteins are tightly regulated. Known outer mitochondrial membrane targeting sequences include the C-terminal tail and central helical hairpin. Bcl-xL also localizes to the inner mitochondrial membrane, but these targeting sequences are unknown. Here we investigate the possibility that the N-terminus of Bcl-xL also contains mitochondrial targeting information. Amino acid residues 1-28 of Bcl-xL fused to EGFP are sufficient to target mitochondria. Although positive charges and helical propensity are required for targeting, similar to import sequences the N-terminus is not sufficient for efficient mitochondrial import.. AB - ...
The effects of the acute phase proteins AGP and AAT on early (2-hour) and late (24-hour) apoptosis and inflammation after renal I/R were investigated. Both AGP and AAT administered at reperfusion decrease early as well as late apoptosis, as reflected by renal internucleosomal DNA cleavage, TUNEL histology, and caspase-like activities. In line, we previously demonstrated that abrogating acute early apoptosis with selective antiapoptotic agents prevents subsequent inflammation as well as secondary apoptosis caused by inflammation, whereas antiapoptotic treatment that is initiated after the onset of apoptosis does not reduce I/R-induced inflammation.1 In contrast, in the present study, treatment after 2 hours of reperfusion inhibited inflammation, which is supported by reports of anti-inflammatory effects mediated by AGP and AAT.12 13 Early primary19 20 as well as late secondary2 21 apoptosis after I/R has been reported to be caused by various means. The present results, showing that AGP and (to a ...
Background: Captopril is an angiotensin-converting enzyme inhibitor with sulphydryl groups in its chemical structure. It is commonly used as an antihypertensive drug. The occurrence of pemphigus vulgaris has repeatedly been reported in patients receiving captopril. The capacity of captopril and pemphigus serum to induce acantholysis, in vivo or in vitro, has been demonstrated experimentally. Objectives: To show that captopril and pemphigus serum, acting by a biochemical and immunological mechanism, respectively, trigger apoptosis. Methods: Human keratinocyte cells were treated with 15 mmol L)1 captopril or with pemphigus serum. DNA was extracted and the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labelling method was used to detect apoptosis. Results: DNA fragmentation occurred after 72 h of treatment. Increased expression of p53, c-myc and inducible nitric oxide (NO) synthase (iNOS) mRNA were observed by polymerase chain reaction (PCR) in the treated cells ...
Tu, S. P., Sun, Y. W., Cui, J. T., Zou, B., Lin, M. C. M., Gu, Q., Jiang, S. H., Kung, H. F., Korneluk, R. G. and Wong, B. C. Y. (2010), Tumor suppressor XIAP-Associated factor 1 (XAF1) cooperates with tumor necrosis factor-related apoptosis-inducing ligand to suppress colon cancer growth and trigger tumor regression. Cancer, 116: 1252-1263. doi: 10.1002/cncr.24814 ...
To identify the physiological functions of the retinoid-related orphan receptor γ (RORγ), a member of the nuclear receptor superfamily, mice deficient in RORγ function were generated by targeted disruption. RORγ−/− mice lack peripheral and mesenteric lymph nodes and Peyers patches, indicating that RORγ expression is indispensable for lymph node organogenesis. Although the spleen is enlarged, its architecture is normal. The number of peripheral blood CD3+ and CD4+ lymphocytes is reduced 6- and 10-fold, respectively, whereas the number of circulating B cells is normal. The thymus of RORγ−/− mice contains 74.4% ± 8.9% fewer thymocytes than that of wild-type mice. Flow cytometric analysis showed a decrease in the CD4+CD8+ subpopulation. Terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling (TUNEL) staining demonstrated a 4-fold increase in apoptotic cells in the cortex of the thymus of RORγ−/− mice. The latter was supported by the observed increase in annexin ...
Elders, R C and Baines, S J and Catchpole, B (2009) Susceptibility of the C2 canine mastocytoma cell line to the effects of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). VETERINARY IMMUNOLOGY AND IMMUNOPATHOLOGY, 130 (1-2). pp. 11-16. ...
Purpose : To evaluate the effects of ethanol extract of Diospyros kaki (EEDK) on dry eye in a murine model. Methods : Dry eye model was experimentally induced by topical administration of benzalkonium chloride (BAC) in a mouse. EEDK was orally administered throughout the experimental period. Tear break-up time (BUT) test, fluorescein staining, phenol red thread test, and histological analysis were performed on the ocular surface. Apoptotic cell death was tested by in situ terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay The protein expression levels of cytokeratin-10, interleukin-1 alpha (IL-1α), IL-1β, IL-6, tumor necrosis factor- alpha (TNF-α) and monocyte chemotactic protein- 1 (MCP-1) was detected by western blotting. The cellular proliferation of corneal epithelial cells was evaluated by immunohistochemistry (IHC). Results : Oral administration of EEDK resulted in prolonged tear break-up time (BUT), decreased fluorescein score, increased tear volume, and ...
TY - JOUR. T1 - Erratum. T2 - Human astrocytes are resistant to fas ligand and tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis (Journal of Neuroscience (March 22, 2006) (3299-3308)). AU - Song, Jin H.. AU - Bellail, Anita. AU - Tse, Margaret C.L.. AU - Yong, V. Wee. AU - Hao, Chunhai. PY - 2006/9/7. Y1 - 2006/9/7. UR - http://www.scopus.com/inward/record.url?scp=33748132489&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=33748132489&partnerID=8YFLogxK. M3 - Comment/debate. AN - SCOPUS:33748132489. VL - 26. JO - Journal of Neuroscience. JF - Journal of Neuroscience. SN - 0270-6474. IS - 18. ER - ...
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), a tumor necrosis factor superfamily member, targets death receptors and selectively kills malignant cells while leaving normal cells unaffected. However, unlike most cancers, many osteosarcomas are resistant to TRAIL. To investigate this resistance, we characterized the response of MG-63 osteosarcoma cells and hPOB-tert osteoblast-like cells to TRAIL and agonist antibodies to death receptor 4 (DR4) and death receptor 5 (DR5). We found that MG-63 osteosarcoma cells and hPOB-tert osteoblast-like cells show no or very little response to TRAIL or a DR4 agonist, but MG-63 cells undergo apoptosis in response to a DR5 agonist. Analysis of TRAIL receptor expression showed that normal osteoblastic and osteosarcoma cells express a variety of TRAIL receptors but this does not correlate to TRAIL responsiveness. Production of the soluble decoy receptor osteoprotegerin also could not explain TRAIL resistance. We show that TRAIL activates the canonical
DNA fragmentation factors 40 and 45 (DFF40/DFF45) and B-cell lymphoma 2 (Bcl-2) protein are underexpressed in uterine leiomyosarcomas and may predict survival Tomasz Banas,1 Kazimierz Pitynski,1 Krzysztof Okon,2 Aleksandra Czerw3,4 1Department of Gynecology and Oncology, 2Department of Pathomorphology, Jagiellonian University Medical College, Krakow, 3Department of Public Health, Faculty of Health Science, Medical University of Warsaw, 4Department of Health Promotion and Postgraduate Education, National Institute of Public Health – National Institute of Hygiene, Warsaw, Poland Objectives: DNA fragmentation factors 40 and 45 (DFF40 and DFF45) are responsible for final DNA-laddering during apoptosis, whereas Bcl-2 (B-cell lymphoma 2) is an apoptosis inhibitor. Our aim was to investigate the expression of DFF40, DFF45, and Bcl-2 in uterine leiomyosarcomas (uLMS), leiomyomas (uLM), and the normal myometrium. Furthermore, the correlation between DFF40, DFF45, and Bcl-2 expression and

Apoptosis (Inhibitors Agonists Modulators Antagonists)-MedChemExpress.comApoptosis (Inhibitors Agonists Modulators Antagonists)-MedChemExpress.com

Overview of Apoptosis:. Cell apoptosis, sometimes called programmed cell death, is a cellular self-destruction method to remove ... Apoptosis also occurs as a defense mechanism such as in immune reactions or when cells are damaged by disease or noxious agents ... Apoptosis is controlled by many genes and involves two fundamental pathways: the extrinsic pathway, which transmits death ... Abnormalities in cell apoptosis can be a significant component of diseases such as cancer, autoimmune lymphoproliferative ...
more infohttps://www.medchemexpress.com/Pathways/Apoptosis.html

Apoptosis - WikipediaApoptosis - Wikipedia

Apoptosis MiniCOPE Dictionary-list of apoptosis terms and acronyms. *Apoptosis (Programmed Cell Death) - The Virtual Library of ... Hyperactive apoptosis[edit]. On the other hand, loss of control of cell death (resulting in excess apoptosis) can lead to ... Apoptosis Interest Group (1999). "About apoptosis". Archived from the original on 28 December 2006. Retrieved 2006-12-15.. ... The study of apoptosis brought on by Bunyaviridae was initiated in 1996, when it was observed that apoptosis was induced by the ...
more infohttps://en.wikipedia.org/wiki/Pro-apoptotic

ApoptosisApoptosis

... is a form of necrosis and is sometimes referred to as single cell necrosis. Apoptotic cells and apoptotic bodies in ... Early development of apoptosis. Affected hepatocytes are hypereosinophilic and angular with fragmented and condensed nuclear ...
more infohttps://www.niehs.nih.gov/research/resources/visual-guides/liverpath/necrotic/apoptosis/

apoptosis | PNASapoptosis | PNAS

microRNA-378 promotes autophagy and inhibits apoptosis in skeletal muscle Yan Li, Jingjing Jiang, Wei Liu, Hui Wang, Lei Zhao, ... Akt-mediated platelet apoptosis and its therapeutic implications in immune thrombocytopenia Mengxing Chen, Rong Yan, Kangxi ...
more infohttps://www.pnas.org/keyword/apoptosis

Apoptosis - SpringerApoptosis - Springer

Apoptosis. Coverage. Volume 1 / 1996 - Volume 23 / 2018. Print ISSN. 1360-8185. Online ISSN. 1573-675X. Publisher. Springer US ... Apoptosis. An International Journal on Programmed Cell Death ISSN: 1360-8185 (Print) 1573-675X (Online) ... Apoptosis is an international peer-reviewed journal devoted to the rapid publication of innovative basic and clinically- ... It aims to stimulate research on the basis of mechanisms of apoptosis and on its role in various human disease processes ...
more infohttps://link.springer.com/journal/10495

Apoptosis | cytology | Britannica.comApoptosis | cytology | Britannica.com

Apoptosis, in biology, a mechanism that allows cells to self-destruct when stimulated by the appropriate trigger. Apoptosis can ... This realization has generated a massive research effort focused on apoptosis.. Regulation of apoptosis. Apoptosis occurs on a ... Apoptosis in medicine. Manipulating apoptosis is one avenue through which scientists can address a number of vexing medical ... cancer: Apoptosis and cancer development. Many cells undergo programmed cell death, or apoptosis, during fetal development. ...
more infohttps://www.britannica.com/science/apoptosis?oasmId=58073

Apoptosis inhibitor 5 (API5)Apoptosis inhibitor 5 (API5)

Homo sapiens apoptosis inhibitor 5 (API5), transcript variant 3, mRNA. PA. NM_001142930.1. Homo sapiens apoptosis inhibitor 5 ( ... Homo sapiens apoptosis inhibitor 5 (API5), transcript variant 5, mRNA. PA. NR_024625.1. Homo sapiens apoptosis inhibitor 5 ( ... apoptosis inhibitor 5-B. X. laevis. 89.5. 522. NP_955834.2 * Conserved domains (CDD) * * Gene summary * * Protein sequence * * ... apoptosis inhibitor 5. D. rerio. 88.2. 525. NP_509585.1 * Conserved domains (CDD) * * Gene summary * * Protein sequence * * ...
more infohttps://www.ncbi.nlm.nih.gov/UniGene/clust.cgi?ORG=Hs&CID=435771

Apoptosis and disease.  - PubMed - NCBIApoptosis and disease. - PubMed - NCBI

Apoptosis and disease.. Carson DA1, Ribeiro JM.. Author information. 1. Sam and Rose Stein Institute for Research on Aging, ... Such physiological cell death, in the absence of inflammation, is achieved by apoptosis, a structurally distinct programmed ... The pharmacological manipulation of apoptosis offers new possibilities for the prevention and treatment of these illnesses. ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/8098400?dopt=Abstract

Advances in apoptosis research | PNASAdvances in apoptosis research | PNAS

Apoptosis is the physiological way for nucleated cells to die. Apoptosis takes care of unwanted, injured, or virus-infected ... The elucidation of the apoptosis pathway in C. elegans has been helpful to better understand apoptosis signaling pathways in ... Key components of the apoptosis machinery seem to be conserved between humans and nematodes. However, neither an apoptosis- ... 1997) in Apoptosis: Biology, Mechanisms and Role in Disease, ed Kumar S(Springer, Heidelberg) , in press.. ...
more infohttps://www.pnas.org/content/94/24/12736.full

apoptosisapoptosis

... Painedog painedog at aol.com Sat Sep 17 12:57:02 EST 1994 *Previous message: Measuring Intracellular Calcium ...
more infohttp://www.bio.net/bionet/mm/bioforum/1994-September/010679.html

What is apoptosis? | HowStuffWorksWhat is apoptosis? | HowStuffWorks

See what apoptosis has to do with curing disease. ... Apoptosis is also known as programmed cell death, and is the ... This brings us to our discussion of the triggers of apoptosis. Rather than dying due to injury, cells that go through apoptosis ... while decreased apoptosis can signal lupus or cancer. Understanding how to regulate apoptosis could be the first step to ... Apoptosis, on the other hand, is relatively civil, even though it may not sound so at first -- its when a cell commits suicide ...
more infohttps://science.howstuffworks.com/life/cellular-microscopic/apoptosis.htm

Apoptosis questionsApoptosis questions

... David Voehringer ylek at utmdacc.uth.tmc.edu Tue Jun 27 17:05:57 EST 1995 *Previous message: Apoptosis ... Using the Oncor ApopTag kit, I have gotten beautiful ,pictures of cells undergoing apoptosis, however, there are a few , ... phenomenas that I notice that I cant explain- namely: , 1. Apoptosis is supposed to be marked by cell shrinkage whereas ,my ... Cells undergoing apoptosis do tend to shrink during the loss of cytoplasm as apoptotic bodies are formed and released. Cells ...
more infohttp://www.bio.net/bionet/mm/cellbiol/1995-June/002440.html

NASA - ROle of Apoptosis in Lymphocyte DepressionNASA - ROle of Apoptosis in Lymphocyte Depression

ROle of Apoptosis in Lymphocyte Depression (ROALD) will to determine the role of programmed cell death (apoptosis) in loss of T ... ROle of Apoptosis in Lymphocyte Depression (ROALD) will determine the role of programmed apoptosis (cell death) in loss of T- ... ROle of Apoptosis in Lymphocyte Depression (ROALD) - 03.23.17. Overview , Description , Applications , Operations , Results , ... In this project, we plan to ascertain whether or not Space conditions might induce apoptosis in human lymphocytes through a 5- ...
more infohttps://www.nasa.gov/mission_pages/station/research/experiments/424.html

Apoptosis - incl. option to publish open accessApoptosis - incl. option to publish open access

Apoptosis is an international peer-reviewed journal devoted to the rapid publication of innovative basic and clinically- ... Apoptosis is an international peer-reviewed journal, published monthly. The Journal is devoted to the rapid publication of ... Apoptosis is an international peer-reviewed journal devoted to the rapid publication of innovative basic and clinically- ... It aims to stimulate both research on the basis of mechanisms of apoptosis and on its role in various human disease processes ...
more infohttps://www.springer.com/biomed/cancer/journal/10495

System Modeling of Receptor-Induced Apoptosis | SpringerLinkSystem Modeling of Receptor-Induced Apoptosis | SpringerLink

Receptor-induced apoptosis is a complex signal transduction pathway involving numerous protein-protein interactions and post- ... Spencer SL, Sorger PK (2011) Measuring and modeling apoptosis in single cells. Cell 144:926-939CrossRefPubMedPubMedCentral ... Schleich K, Lavrik IN (2013) Mathematical modeling of apoptosis. Cell Commun Signal 11:44CrossRefPubMedPubMedCentralGoogle ... Lavrik IN (2010) Systems biology of apoptosis signaling networks. Curr Opin Biotechnol 21:551-555CrossRefPubMedGoogle Scholar ...
more infohttps://link.springer.com/chapter/10.1007/978-3-319-56805-8_12

PPAR and Apoptosis in CancerPPAR and Apoptosis in Cancer

Depending on cell types or ligands, induction of apoptosis in cancer cells by PPAR. 𝛾. ligands can be either PPAR. 𝛾. - ... ligand-induced apoptosis, we can develop better strategies which may include combining other antitumor agents for PPAR. 𝛾. - ... and Apoptosis in Cancer. Heath A. Elrod and Shi-Yong Sun Department of Hematology and Medical Oncology, Winship Cancer ... ligands including endogenous prostaglandins and the synthetic thiazolidinediones (TZDs) can induce apoptosis of cancer cells ...
more infohttps://www.hindawi.com/journals/ppar/2008/704165/abs/

Apoptosis - Burial LyricsApoptosis - Burial Lyrics

Burial lyrics performed by Apoptosis: Dark night, Frozen light This is the end of your decadent life ... Feel the power and fear apoptosis strength Now your world is over Your world is over ...
more infohttps://www.lyricsmania.com/burial_lyrics_apoptosis.html

apoptosis | Modern medicineapoptosis | Modern medicine

Apoptosis may be the best characterized form of programmed cell death-but it isnt in isolation, said Joan W. Miller, MD. ... Apoptosis not only culprit in cell death. November 16, 2013By Michele Barrere ...
more infohttp://www.modernmedicine.com/tag/apoptosis

Studies of apoptosis in breast cancer | The BMJStudies of apoptosis in breast cancer | The BMJ

Increased apoptosis with increased proliferation is associated with malignant tumours. Breast tumours with increased apoptosis ... All of these act in part by inducing apoptosis.4-6 Thus it is possible to delineate the biology of individual tumours at the ... The balance between proliferation and apoptosis is crucial in determining the overall growth or regression of the tumour 2 3 in ... Here we summarise and integrate the data on apoptosis and its role in the development, prognosis, and treatment of breast ...
more infohttp://www.bmj.com/content/322/7301/1528

Patent US20030211108 - Monoclonal antibody inducing apoptosis - Google PatentsPatent US20030211108 - Monoclonal antibody inducing apoptosis - Google Patents

... while also having an action of inducing apoptosis of nucleated blood cells; these properties can be utilized to prepare useful ... and the antigens that induce apoptosis of nucleated blood cells having human Integrin Associated Protein. Accordingly, they are ... 7-9 and 10-11, the culture supernatants of 7D2-E3 and 11C8 increase a proportion of apoptosis cells of Jurkat cells and the ... 18 shows the apoptosis-inducing effect of MABL-1(10 μg/ml) on L1210 cells transfected with the human IAP gene (incubation for ...
more infohttp://www.google.com/patents/US20030211108?dq=oakley+D523,461

Systems Biology of Apoptosis | Inna N. Lavrik | SpringerSystems Biology of Apoptosis | Inna N. Lavrik | Springer

Apoptosis is a process common to all multicellular organisms. Apoptosis leads to the elimination of cells via a complex but ... Defects in the regulation of apoptosis result in ... Systems Biology of Apoptosis. Editors. * Inna N. Lavrik ... Systems Biology of Apoptosis summarizes all current achievements in this emerging field. ... Systems Biology of Apoptosis summarizes all current achievements in this emerging field. Apoptosis is a process common to all ...
more infohttps://www.springer.com/us/book/9781461440086

Apoptosis in AIDS - & related info | MendeleyApoptosis in AIDS - & related info | Mendeley

Apoptosis. Infection with the human immunodeficiency virus type 1 (HIV-1) leads to progressive immunodeficiency and onset of ... This review focuses on the various molecular determinants from HIV-1 that play a role in induction of apoptosis in T- ... and signaling and effector pathways leading to apoptosis. The types of pro- and anti-apoptotic stimuli that have been ...
more infohttps://www.mendeley.com/research-papers/apoptosis-aids/

Stress and the Control of ApoptosisStress and the Control of Apoptosis

... Douglas R. Green La Jolla Institute for Allergy and Immunology, 10355 Science Center Dr., ...
more infohttps://www.hindawi.com/journals/tswj/2001/826549/abs/

RIPK1 maintains epithelial homeostasis by inhibiting apoptosis and necroptosis | NatureRIPK1 maintains epithelial homeostasis by inhibiting apoptosis and necroptosis | Nature

RIPK1 is shown to have a crucial role-independent of its known kinase function-in suppressing epithelial cell apoptosis and ... RIPK1 suppresses epithelial cell apoptosis and necroptosis by preventing FADD/caspase-8-mediated apoptosis and RIPK3-dependent ... RIPK1 maintains epithelial homeostasis by inhibiting apoptosis and necroptosis. *Marius Dannappel1. n5*, Katerina Vlantis1. n5* ... IAP antagonists induce autoubiquitination of c-IAPs, NF-κB activation, and TNFα-dependent apoptosis. . Cell 131, 669-681 (2007) ...
more infohttps://www.nature.com/articles/nature13608?error=cookies_not_supported&code=bb346d66-1544-41a4-85da-a0b53bc18596

Apoptosis Reagents and KitsApoptosis Reagents and Kits

Contains the instructions and reagents required for measuring apoptosis in cells. APO-DIRECT™ Apoptosis Detection Kit is a 2- ... eBioscience™ Annexin V Apoptosis Detection Kit APC Compatible with intracellular staining. Pre-titrated and tested on mouse ... eBioscience™ Annexin V Apoptosis Detection Kit FITC Compatible with intracellular staining. Pre-titrated and tested on mouse ... R&D Systems™ TACS TdT In Situ Apoptosis Detection Kit, Fluorescein A TUNEL assay designed for fixed cells, embedded tissue, and ...
more infohttps://www.fishersci.com/us/en/products/I9C8KX62/apoptosis-reagents-kits.html
  • ROle of Apoptosis in Lymphocyte Depression (ROALD) will determine the role of programmed apoptosis (cell death) in loss of T-lymphocyte (white blood cells originating in the thymus) activity in microgravity. (nasa.gov)
  • Current research is focused on a greater understanding of the response and resistance to treatment, including the role of apoptosis. (bmj.com)
  • 1 . A monoclonal antibody that induces apoptosis of nucleated blood cells having Integrin Associated Protein (IAP). (google.com)
  • 2 . A fragment, a peptide or a low molecular compound of a monoclonal antibody that induces apoptosis of nucleated blood cells having Integrin Associated Protein (IAP). (google.com)
  • Gouazè V, Mirault ME, Carpentier S, Salvayre R, Levade T, Andrieu-Abadie N: Glutathione peroxidase-1 overexpression prevents ceramide production and partially inhibits apoptosis in doxorubicin-treated human breast carcinoma cells. (springer.com)
  • The 2002 Nobel Prize in Medicine was awarded to Sydney Brenner , Horvitz and John E. Sulston for their work identifying genes that control apoptosis. (wikipedia.org)
  • First, studies with the small nematode Caenorhabditis elegans have identified a number of apoptosis regulating genes-the first evidence that cell death is an active process under genetic control. (pnas.org)
  • The conservation in both sequence and function between nematode and mammalian cell death genes indicates that apoptosis is of ancient evolutionary origin, and it suggests that worms and humans use similar conserved mechanisms to get rid of cells. (pnas.org)
  • Activation of p53 promotes the transcriptional activation of many target genes involved in several cellular responses: apoptosis, cell cycle arrest, DNA repair and senescence. (els.net)
  • Intestinal epithelial cell (IEC)-specific RIPK1 knockout caused IEC apoptosis, villus atrophy, loss of goblet and Paneth cells and premature death in mice. (nature.com)
  • Abnormalities in cell apoptosis can be a significant component of diseases such as cancer, autoimmune lymphoproliferative syndrome, AIDS, ischemia, and neurode-generative diseases. (medchemexpress.com)
  • This protein family, which provides the framework for controlling apoptosis, takes its name from a type of cancer called B-cell lymphoma . (britannica.com)
  • Anti-cancer drugs and radiation, for example, work by triggering apoptosis in diseased cells. (howstuffworks.com)
  • Many diseases and disorders are linked with the life and death of cells -- increased apoptosis is a characteristic of AIDS , Alzheimer's and Parkinson's disease, while decreased apoptosis can signal lupus or cancer . (howstuffworks.com)
  • It aims to stimulate research on the basis of mechanisms of apoptosis and on its role in various human disease processes including: cancer, autoimmune disease, viral infection, AIDS, cardiovascular disease, neurodegenerative disorders, osteoporosis and ageing. (springer.com)
  • Hassan M, Watari H, AbuAlmaaty A, Ohba Y, Sakuragi N (2014) Apoptosis and molecular targeting therapy in cancer. (springer.com)
  • Here we summarise and integrate the data on apoptosis and its role in the development, prognosis, and treatment of breast cancer. (bmj.com)
  • Additionally, a dysregulation of apoptosis is underlying in numerous pathological situations such as Parkinson, Alzheimer s disease and cancer. (novapublishers.com)
  • Apoptosis is important in many biological contexts and deregulation of apoptosis may cause diseases, either in the case of insufficient apoptosis, which may contribute to excessive cell proliferation and cancer, or excessive apoptosis, which may cause degenerative and other disorders. (els.net)
  • The second breakthrough is related to the discovery of a family of receptors that can specifically trigger apoptosis. (pnas.org)
  • These findings revealed that RIPK1 inhibits RIPK3-mediated necroptosis in keratinocytes in vivo and identified necroptosis as a more potent trigger of inflammation compared with apoptosis. (nature.com)
  • Its rediscovery in the second half of this century, and the coining of the term apoptosis in 1972 by Kerr, Wyllie, and Currie, ignited an unparalleled interest in this field of science. (pnas.org)
  • Epithelial FADD ablation inhibited IEC apoptosis and prevented the premature death of mice with IEC-specific RIPK1 knockout. (nature.com)
  • Epidermis-specific RIPK1 knockout triggered keratinocyte apoptosis and necroptosis and caused severe skin inflammation that was prevented by RIPK3 but not FADD deficiency. (nature.com)
  • Kerr, Wyllie and Currie credited James Cormack, a professor of Greek language at University of Aberdeen , with suggesting the term apoptosis. (wikipedia.org)
  • Ferroptosis and necroptosis are recently recognized forms of regulated cell death that differs considerably from apoptosis. (medchemexpress.com)
  • Antisense eNOS depressed DOX-induced oxidative stress and apoptosis. (springer.com)
  • A simple, non-lytic assay that allows real-time monitoring of apoptosis progression, without the need for multiple plates or complicated processing. (fishersci.com)
  • It has been suggested that reduced growth response in lymphocytes during spaceflight might be linked to apoptosis, based on morphological anomalies and cDNA microarray analysis of space-flown human lymphoblastoid (Jurkat) cells. (nasa.gov)
  • In this context, 5-Lipoxygenase (5-LOX) plays a central role in interleukin-2 expression and activation of human lymphocytes, and is involved in the initiation of programmed death (apoptosis) triggered by several stimuli in different human cells. (nasa.gov)
  • The story of apoptosis as an aborted mitosis derives from lymphocytes and is not necessarily valid, though the signalling mechansisms are interesting. (bio.net)
  • Apoptosis is also the regulatory mechanism involved in the removal of unnecessary cells during development and in tissue homeostasis in a wide range of organisms from insects to mammals. (novapublishers.com)
  • Apoptosis can also be triggered in otherwise normal cells by external stimuli, including nutrient removal, toxins , hormones , heat, and radiation . (britannica.com)
  • The editors intend to encourage the development of clinical therapies against apoptosis-related diseases. (springer.com)
  • Research on apoptosis has increased substantially since the early 1990s. (wikipedia.org)
  • John E. Sulston won the Nobel Prize in Medicine in 2002, for his pioneering research on apoptosis. (wikipedia.org)
  • This realization has generated a massive research effort focused on apoptosis. (britannica.com)
  • In the early 1840s, a biological use for the mechanism of planned apoptosis became apparent when scientists realized that the development from fertilized egg to adult is not a linear process. (britannica.com)