Selective knockdown of the long variant of cellular FLICE inhibitory protein augments death receptor-mediated caspase-8 activation and apoptosis.
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The Fas death signaling pathway connecting reactive oxygen species generation and FLICE inhibitory protein down-regulationS-nitrosylation of FLICE inhibitory protein determines its interaction with RIP1 and activation of NF-kappa BTAK1 is required for survival of mouse fibroblasts treated with TRAIL, and does so by NF-kappaB dependent induction of cFLIPL.β-Elemene piperazine derivatives induce apoptosis in human leukemia cells through downregulation of c-FLIP and generation of ROS.Inhibition of SREBP1 sensitizes cells to death ligands.HIV infection enhances TRAIL-induced cell death in macrophage by down-regulating decoy receptor expression and generation of reactive oxygen species.Differential inhibition of TRAIL-mediated DR5-DISC formation by decoy receptors 1 and 2.Identification of a conserved anti-apoptotic protein that modulates the mitochondrial apoptosis pathway.Model-based dissection of CD95 signaling dynamics reveals both a pro- and antiapoptotic role of c-FLIPL.The role of cellular FLICE inhibitory protein (c-FLIP) in the pathogenesis and treatment of cancer.TRAIL sensitisation by arsenic trioxide is caspase-8 dependent and involves modulation of death receptor components and Akt.Bcl-2 family proteins contribute to apoptotic resistance in lung cancer multicellular spheroids.B lymphocytes are resistant to death receptor 5-induced apoptosis.Understanding the Role of the Death Receptor 5/FADD/caspase-8 Death Signaling in Cancer MetastasisA New Player in the Development of TRAIL Based Therapies for Hepatocarcinoma Treatment: ATM Kinase.Death receptor 5 signaling promotes hepatocyte lipoapoptosis4-(4-Chloro-2-methylphenoxy)-N-hydroxybutanamide (CMH) targets mRNA of the c-FLIP variants and induces apoptosis in MCF-7 human breast cancer cells.Effects of histone deacetylase inhibitor trichostatin A combined with cisplatin on apoptosis of A549 cell lineTargeting the Anti-Apoptotic Protein c-FLIP for Cancer Therapy.Regulation of chemoresistance via alternative messenger RNA splicingCellular FLICE-like Inhibitory Protein (c-FLIP) and PS1-associated Protein (PSAP) Mediate Presenilin 1-induced γ-Secretase-dependent and -independent Apoptosis, Respectively.Cellular FLICE-like inhibitory protein (C-FLIP): a novel target for cancer therapy.On the TRAIL of a new therapy for leukemia.Withanolide E sensitizes renal carcinoma cells to TRAIL-induced apoptosis by increasing cFLIP degradation.TNF-related apoptosis-inducing ligand as a therapeutic agent in autoimmunity and cancer.Association of TRAF2 with the short form of cellular FLICE-like inhibitory protein prevents TNFR1-mediated apoptosis.TRAIL, caspases and maturation of normal and leukemic myeloid precursors.Deregulation of apoptotic factors Bcl-xL and Bax confers apoptotic resistance to myeloid-derived suppressor cells and contributes to their persistence in cancer.Cells surviving fractional killing by TRAIL exhibit transient but sustainable resistance and inflammatory phenotypes.c-FLIP knockdown induces ligand-independent DR5-, FADD-, caspase-8-, and caspase-9-dependent apoptosis in breast cancer cells.Differential responses of FLIPLong and FLIPShort-overexpressing human myeloid leukemia cells to TNF-alpha and TRAIL-initiated apoptotic signalsTo kill a tumor cell: the potential of proapoptotic receptor agonistsAkt-mediated eminent expression of c-FLIP and Mcl-1 confers acquired resistance to TRAIL-induced cytotoxicity to lung cancer cells.The natural product honokiol preferentially inhibits cellular FLICE-inhibitory protein and augments death receptor-induced apoptosis.Valproate activates the Notch3/c-FLIP signaling cascade: a strategy to attenuate white matter hyperintensities in bipolar disorder in late life?The therapeutic potential of TRAIL receptor signalling in cancer cells.Systems biology of death receptor networks: live and let die.Apoptotic Caspases in Promoting Cancer: Implications from Their Roles in Development and Tissue Homeostasis.Prognostic and therapeutic relevance of c-FLIP in acute myeloid leukaemia.Cbl-b-dependent degradation of FLIP(L) is involved in ATO-induced autophagy in leukemic K562 and gastric cancer cells.
P2860
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P2860
Selective knockdown of the long variant of cellular FLICE inhibitory protein augments death receptor-mediated caspase-8 activation and apoptosis.
description
2005 nî lūn-bûn
@nan
2005年の論文
@ja
2005年学术文章
@wuu
2005年学术文章
@zh-cn
2005年学术文章
@zh-hans
2005年学术文章
@zh-my
2005年学术文章
@zh-sg
2005年學術文章
@yue
2005年學術文章
@zh
2005年學術文章
@zh-hant
name
Selective knockdown of the lon ...... se-8 activation and apoptosis.
@en
type
label
Selective knockdown of the lon ...... se-8 activation and apoptosis.
@en
prefLabel
Selective knockdown of the lon ...... se-8 activation and apoptosis.
@en
P2093
P2860
P356
P1476
Selective knockdown of the lon ...... se-8 activation and apoptosis.
@en
P2093
Avi Ashkenazi
Darcie A Sharp
David A Lawrence
P2860
P304
19401-19409
P356
10.1074/JBC.M413962200
P407
P577
2005-03-10T00:00:00Z