Caspase 8

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  Subject Areas on Research

  • A Fas-associated death domain protein/caspase-8-signaling axis promotes S-phase entry and maintains S6 kinase activity in T cells responding to IL-2. 
  • A RIPK3-caspase 8 complex mediates atypical pro-IL-1β processing. 
  • A double hit to kill tumor and endothelial cells by TRAIL and antiangiogenic 3TSR. 
  • A role for c-FLIP(L) in the regulation of apoptosis, autophagy, and necroptosis in T lymphocytes. 
  • A role for tumor necrosis factor receptor-2 and receptor-interacting protein in programmed necrosis and antiviral responses. 
  • A20 protects endothelial cells from TNF-, Fas-, and NK-mediated cell death by inhibiting caspase 8 activation. 
  • Analysis of FasL and TRAIL induced apoptosis pathways in glioma cells. 
  • Apoptosis induction by caspase-8 is amplified through the mitochondrial release of cytochrome c. 
  • Apoptotic caspases regulate induction of iPSCs from human fibroblasts. 
  • Association between CASP8 and CASP10 polymorphisms and toxicity outcomes with platinum-based chemotherapy in Chinese patients with non-small cell lung cancer. 
  • Association of two CASP8 polymorphisms with breast cancer risk: a meta-analysis. 
  • CASP8 polymorphisms contribute to cancer susceptibility: evidence from a meta-analysis of 23 publications with 55 individual studies. 
  • Caspase 8 is absent or low in many ex vivo gliomas. 
  • Caspase-8 and RIP kinases regulate bacteria-induced innate immune responses and cell death. 
  • Caspase-8 and caspase-3 small interfering RNA decreases ischemia/reperfusion injury to the liver in mice. 
  • Caspase-8 levels affect necessity for mitochondrial amplification in death ligand-induced glioma cell apoptosis. 
  • Caspase-8 levels correlate with the expression of signal transducer and activator of transcription 1 in high-grade but not lower grade neuroblastoma. 
  • Caspase-8-mediated PAR-4 cleavage is required for TNFα-induced apoptosis. 
  • Caspase-8-mediated apoptosis in human RPE cells. 
  • Cellular FLIP Inhibits Myeloid Cell Activation by Suppressing Selective Innate Signaling. 
  • Competitive control of independent programs of tumor necrosis factor receptor-induced cell death by TRADD and RIP1. 
  • Consortium analysis of 7 candidate SNPs for ovarian cancer. 
  • Engineering a BCR-ABL-activated caspase for the selective elimination of leukemic cells. 
  • Fueling the flames: Mammalian programmed necrosis in inflammatory diseases. 
  • Genetic variants and haplotypes of the caspase-8 and caspase-10 genes contribute to susceptibility to cutaneous melanoma. 
  • HIV-1 viral protein r induces ERK and caspase-8-dependent apoptosis in renal tubular epithelial cells. 
  • Heat shock protein 90 suppresses tumor necrosis factor alpha induced apoptosis by preventing the cleavage of Bid in NIH3T3 fibroblasts. 
  • Identification of high caspase-3 mRNA expression as a unique signature profile for extremely old individuals. 
  • Interferon regulatory factor-1-induced apoptosis mediated by a ligand-independent fas-associated death domain pathway in breast cancer cells. 
  • Mechanisms of synthetic serine protease inhibitor (FUT-175)-mediated cell death. 
  • Mind bomb 1 regulation of cFLIP interactions. 
  • Mouse translation elongation factor eEF1A-2 interacts with Prdx-I to protect cells against apoptotic death induced by oxidative stress. 
  • Physiological consequences of programmed necrosis, an alternative form of cell demise. 
  • RIP3 induces apoptosis independent of pronecrotic kinase activity. 
  • RIPK1-RIPK3-MLKL-Associated Necroptosis Drives Leishmania infantum Killing in Neutrophils. 
  • Smac mimetic Birinapant induces apoptosis and enhances TRAIL potency in inflammatory breast cancer cells in an IAP-dependent and TNF-α-independent mechanism. 
  • The Mitochondrial Phosphatase PGAM5 Is Dispensable for Necroptosis but Promotes Inflammasome Activation in Macrophages. 
  • The c-FLIPL cleavage product p43FLIP promotes activation of extracellular signal-regulated kinase (ERK), nuclear factor κB (NF-κB), and caspase-8 and T cell survival. 
  • The combination of TPL2 knockdown and TNFα causes synthetic lethality via caspase-8 activation in human carcinoma cell lines. 
  • The role of membrane lipids in the induction of macrophage apoptosis by microparticles. 
  • The six-nucleotide deletion/insertion variant in the CASP8 promoter region is inversely associated with risk of squamous cell carcinoma of the head and neck. 
  • Uncoupling phototoxicity-elicited neural dysmorphology and death by insidious function and selective impairment of Ran-binding protein 2 (Ranbp2). 
  • Upstream regulatory role for XIAP in receptor-mediated apoptosis. 
  • Validating the meta-analytical results on MDM2, CASP8, XRCC3 polymorphisms and breast cancer risk: examination of Hardy-Weinberg Equilibrium. 
  • c-FLIP maintains tissue homeostasis by preventing apoptosis and programmed necrosis. 
  • c-FLIP protects mature T lymphocytes from TCR-mediated killing. 
  • cFLIP regulates skin homeostasis and protects against TNF-induced keratinocyte apoptosis. 
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  Keywords of People

  • Berchuck, Andrew, James M. Ingram Distinguished Professor of Gynecologic Oncology, Obstetrics and Gynecology, Gynecologic Oncology
  • Moorman, Patricia Gripka, Professor Emeritus in Family Medicine and Community Health, Duke Cancer Institute