Rapid turnover of c-FLIPshort is determined by its unique C-terminal tail.
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The Fas death signaling pathway connecting reactive oxygen species generation and FLICE inhibitory protein down-regulationNitric oxide negatively regulates Fas CD95-induced apoptosis through inhibition of ubiquitin-proteasome-mediated degradation of FLICE inhibitory proteinInhibition of DNA binding by differential sumoylation of heat shock factors.DED or alive: assembly and regulation of the death effector domain complexesc-FLIP, a master anti-apoptotic regulatorHyperthermia enhances mapatumumab-induced apoptotic death through ubiquitin-mediated degradation of cellular FLIP(long) in human colon cancer cellsThe antidiabetic drug ciglitazone induces high grade bladder cancer cells apoptosis through the up-regulation of TRAILTAK1 is required for survival of mouse fibroblasts treated with TRAIL, and does so by NF-kappaB dependent induction of cFLIPL.Herpes simplex virus type 1 (HSV-1)-induced apoptosis in human dendritic cells as a result of downregulation of cellular FLICE-inhibitory protein and reduced expression of HSV-1 antiapoptotic latency-associated transcript sequences.Early growth response-1 is a regulator of DR5-induced apoptosis in colon cancer cells.The eIF4E/eIF4G interaction inhibitor 4EGI-1 augments TRAIL-mediated apoptosis through c-FLIP Down-regulation and DR5 induction independent of inhibition of cap-dependent protein translationβ-Elemene piperazine derivatives induce apoptosis in human leukemia cells through downregulation of c-FLIP and generation of ROS.Rocaglamide breaks TRAIL resistance in HTLV-1-associated adult T-cell leukemia/lymphoma by translational suppression of c-FLIP expression.FLASH knockdown sensitizes cells to Fas-mediated apoptosis via down-regulation of the anti-apoptotic proteins, MCL-1 and Cflip shortChemistry and biology of rocaglamides (= flavaglines) and related derivatives from aglaia species (meliaceae)Parthenolide Sensitizes Human Colorectal Cancer Cells to Tumor Necrosis Factor-related Apoptosis-inducing Ligand through Mitochondrial and Caspase Dependent Pathway.Modeling dynamics of cell-to-cell variability in TRAIL-induced apoptosis explains fractional killing and predicts reversible resistanceRoles of c-FLIP in Apoptosis, Necroptosis, and Autophagy.KSR1 is overexpressed in endometrial carcinoma and regulates proliferation and TRAIL-induced apoptosis by modulating FLIP levels.p53 mediates cigarette smoke-induced apoptosis of pulmonary endothelial cells: inhibitory effects of macrophage migration inhibitor factorThe nuclear splicing factor RNA binding motif 5 promotes caspase activation in human neuronal cells, and increases after traumatic brain injury in mice.The NEDD8-activating enzyme inhibitor, MLN4924, cooperates with TRAIL to augment apoptosis through facilitating c-FLIP degradation in head and neck cancer cellsWogonin and related natural flavones overcome tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) protein resistance of tumors by down-regulation of c-FLIP protein and up-regulation of TRAIL receptor 2 expression.Fractional killing arises from cell-to-cell variability in overcoming a caspase activity thresholdTargeting the Anti-Apoptotic Protein c-FLIP for Cancer Therapy.The novel Akt inhibitor API-1 induces c-FLIP degradation and synergizes with TRAIL to augment apoptosis independent of Akt inhibition.Cellular FLICE-like inhibitory protein (C-FLIP): a novel target for cancer therapy.Doxorubicin generates a proapoptotic phenotype by phosphorylation of elongation factor 2.Caspase-containing complexes in the regulation of cell death and inflammation.Transformation, translation and TRAIL: an unexpected intersection.Distinct Activation Mechanisms of NF-κB Regulator Inhibitor of NF-κB Kinase (IKK) by Isoforms of the Cell Death Regulator Cellular FLICE-like Inhibitory Protein (cFLIP).Apoptosis and antiapoptotic mechanisms in the progression of myelodysplastic syndrome.Differential responses of FLIPLong and FLIPShort-overexpressing human myeloid leukemia cells to TNF-alpha and TRAIL-initiated apoptotic signalsc-FLIP(S) reduces activation of caspase and NF-kappaB pathways and decreases T cell survivalThe natural product honokiol preferentially inhibits cellular FLICE-inhibitory protein and augments death receptor-induced apoptosis.Essential role of MALT1 protease activity in activated B cell-like diffuse large B-cell lymphoma.Systems biology of death receptor networks: live and let die.Molecular mechanisms and anti-cancer aspects of the medicinal phytochemicals rocaglamides (=flavaglines).The BET bromodomain inhibitor, JQ1, facilitates c-FLIP degradation and enhances TRAIL-induced apoptosis independent of BRD4 and c-Myc inhibition.Celecoxib promotes c-FLIP degradation through Akt-independent inhibition of GSK3.
P2860
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P2860
Rapid turnover of c-FLIPshort is determined by its unique C-terminal tail.
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
Rapid turnover of c-FLIPshort is determined by its unique C-terminal tail.
@en
type
label
Rapid turnover of c-FLIPshort is determined by its unique C-terminal tail.
@en
prefLabel
Rapid turnover of c-FLIPshort is determined by its unique C-terminal tail.
@en
P2093
P2860
P356
P1476
Rapid turnover of c-FLIPshort is determined by its unique C-terminal tail.
@en
P2093
Aura Kaunisto
John E Eriksson
Konstantin Denessiouk
Lea Sistonen
Mark S Johnson
Minna Poukkula
Tuire Katajamäki
Ville Hietakangas
P2860
P304
27345-27355
P356
10.1074/JBC.M504019200
P407
P577
2005-05-10T00:00:00Z