Divergent signalling via APO-1/Fas and the TNF receptor, two homologous molecules involved in physiological cell death.
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Overexpression of acid ceramidase protects from tumor necrosis factor-induced cell deathMitochondrial hyperpolarization and ATP depletion in patients with systemic lupus erythematosusMechanisms of necroptosis in T cellsEffects of siRNA on RET/PTC3 junction oncogene in papillary thyroid carcinoma: from molecular and cellular studies to preclinical investigationsElevation of mitochondrial transmembrane potential and reactive oxygen intermediate levels are early events and occur independently from activation of caspases in Fas signalingIncreased levels of soluble Fas ligand in serum in Plasmodium falciparum malaria.TNF-induced necroptosis and PARP-1-mediated necrosis represent distinct routes to programmed necrotic cell deathProtooncogene bcl-2 gene transfer abrogates Fas/APO-1 antibody-mediated apoptosis of human malignant glioma cells and confers resistance to chemotherapeutic drugs and therapeutic irradiationDynamics of physical interaction between HIV-1 Nef and ASK1: identifying the interacting motif(s).Superoxide anion is a natural inhibitor of FAS-mediated cell death.Human hsp27, Drosophila hsp27 and human alphaB-crystallin expression-mediated increase in glutathione is essential for the protective activity of these proteins against TNFalpha-induced cell deathDichotomy between RIP1- and RIP3-mediated necroptosis in tumor necrosis factor-α-induced shock.Genetic and metabolic status of NGF-deprived sympathetic neurons saved by an inhibitor of ICE family proteases.Sequential reduction of mitochondrial transmembrane potential and generation of reactive oxygen species in early programmed cell death.Biochemical pathways of apoptosis: nicotinamide adenine dinucleotide-deficient cells are resistant to tumor necrosis factor or ultraviolet light activation of the 24-kD apoptotic protease and DNA fragmentationActivation of CPP32-like proteases is not sufficient to trigger apoptosis: inhibition of apoptosis by agents that suppress activation of AP24, but not CPP32-like activity.The peptide derived from the Ig-like domain of human herpesvirus 8 K1 protein induces death in hematological cancer cells.Constitutive activation of NF-kappaB during progression of breast cancer to hormone-independent growth.Antigen-mediated T cell expansion regulated by parallel pathways of death.Influence of Insulin Resistance and TNF-α on the Inflammatory Process, Oxidative Stress, and Disease Activity in Patients with Rheumatoid Arthritis.Management of multicellular senescence and oxidative stress.Multiple pathways originate at the Fas/APO-1 (CD95) receptor: sequential involvement of phosphatidylcholine-specific phospholipase C and acidic sphingomyelinase in the propagation of the apoptotic signal.Mechanisms of cell death in acute liver failure.Cell Death Signaling.Failure of poly(ADP-ribose) polymerase cleavage by caspases leads to induction of necrosis and enhanced apoptosis.Posttranslational modification of Bcl-2 facilitates its proteasome-dependent degradation: molecular characterization of the involved signaling pathway.Fas (CD95)-Fas ligand interactions are responsible for monocyte apoptosis occurring as a result of phagocytosis and killing of Staphylococcus aureus.Activation and caspase-mediated inhibition of PARP: a molecular switch between fibroblast necrosis and apoptosis in death receptor signaling.Caspase activation by adenovirus e4orf4 protein is cell line specific and Is mediated by the death receptor pathway.Tumor necrosis factor alpha-induced interleukin-8 production via NF-kappaB and phosphatidylinositol 3-kinase/Akt pathways inhibits cell apoptosis in human hepatocytes.Activation of CPP32-like protease in tumor necrosis factor-induced apoptosis is dependent on mitochondrial function.Tumor necrosis factor receptor p55 is essential for intrahepatic granuloma formation and hepatocellular apoptosis in a murine model of bacterium-induced fulminant hepatitis.Blockade of T-cell activation by dithiocarbamates involves novel mechanisms of inhibition of nuclear factor of activated T cells.PARP is important for genomic stability but dispensable in apoptosis.Stimulation of Fas agonistic antibody-mediated apoptosis by heparin-like agents suppresses Hsp27 but not Bcl-2 protective activity.Apoptosis by a cytosolic extract from Fas-activated cellsEffect of gene transfer of tumor necrosis factor receptors into human lung carcinoma cell line.Bcl-2 down-regulates the activity of transcription factor NF-kappaB induced upon apoptosis.Looking beneath the surface: the cell death pathway of Fas/APO-1 (CD95).Self-renewal of multipotent long-term repopulating hematopoietic stem cells is negatively regulated by Fas and tumor necrosis factor receptor activation.
P2860
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P2860
Divergent signalling via APO-1/Fas and the TNF receptor, two homologous molecules involved in physiological cell death.
description
1994 nî lūn-bûn
@nan
1994年の論文
@ja
1994年学术文章
@wuu
1994年学术文章
@zh-cn
1994年学术文章
@zh-hans
1994年学术文章
@zh-my
1994年学术文章
@zh-sg
1994年學術文章
@yue
1994年學術文章
@zh
1994年學術文章
@zh-hant
name
Divergent signalling via APO-1 ...... d in physiological cell death.
@en
type
label
Divergent signalling via APO-1 ...... d in physiological cell death.
@en
prefLabel
Divergent signalling via APO-1 ...... d in physiological cell death.
@en
P2093
P2860
P1433
P1476
Divergent signalling via APO-1 ...... d in physiological cell death.
@en
P2093
Krammer PH
Schulze-Osthoff K
P2860
P304
P407
P577
1994-10-01T00:00:00Z