Tumor necrosis factor-alpha induces Bax-Bak interaction and apoptosis, which is inhibited by adenovirus E1B 19K
about
Caspase-dependent processing activates the proapoptotic activity of deleted in breast cancer-1 during tumor necrosis factor-alpha-mediated death signalingInteraction of F1L with the BH3 domain of Bak is responsible for inhibiting vaccinia-induced apoptosisProapoptotic Bak is sequestered by Mcl-1 and Bcl-xL, but not Bcl-2, until displaced by BH3-only proteins.The vaccinia virus protein F1L interacts with Bim and inhibits activation of the pro-apoptotic protein BaxBax and Bak independently promote cytochrome C release from mitochondriaBcl-XL is qualitatively different from and ten times more effective than Bcl-2 when expressed in a breast cancer cell lineBIK, the founding member of the BH3-only family proteins: mechanisms of cell death and role in cancer and pathogenic processes.DNA damage response and MCL-1 destruction initiate apoptosis in adenovirus-infected cellsDepletion of physiological levels of the human TID1 protein renders cancer cell lines resistant to apoptosis mediated by multiple exogenous stimuli.Cytomegalovirus cell death suppressor vMIA blocks Bax- but not Bak-mediated apoptosis by binding and sequestering Bax at mitochondria.Oligomerization of the mitochondrial protein voltage-dependent anion channel is coupled to the induction of apoptosisE1A sensitizes cells to tumor necrosis factor alpha by downregulating c-FLIP S.Viral versus cellular BCL-2 proteins.Transformations of the macromolecular landscape at mitochondria during DNA-damage-induced apoptotic cell death.Viral product trafficking to mitochondria, mechanisms and roles in pathogenesis.Key role for Bak activation and Bak-Bax interaction in the apoptotic response to vinblastineInterferon-gamma augments CD95(APO-1/Fas) and pro-caspase-8 expression and sensitizes human vascular endothelial cells to CD95-mediated apoptosis.Bax dimerizes via a symmetric BH3:groove interface during apoptosisHepatic IGFBP1 is a prosurvival factor that binds to BAK, protects the liver from apoptosis, and antagonizes the proapoptotic actions of p53 at mitochondriaVDAC1: from structure to cancer therapy.Mechanisms of apoptosis regulation by viral oncogenes in infection and tumorigenesis.The antiapoptotic role of pregnane X receptor in human colon cancer cells.Cisplatin-induced apoptosis in p53-deficient renal cells via the intrinsic mitochondrial pathway.Execution of superoxide-induced cell death by the proapoptotic Bcl-2-related proteins Bid and Bak.The fowlpox virus BCL-2 homologue, FPV039, interacts with activated Bax and a discrete subset of BH3-only proteins to inhibit apoptosis.A proapoptotic signaling pathway involving RasGRP, Erk, and Bim in B cells.Enterovirus 71 2B Induces Cell Apoptosis by Directly Inducing the Conformational Activation of the Proapoptotic Protein BaxAdenovirus E1A and E1B-19K proteins protect human hepatoma cells from transforming growth factor beta1-induced apoptosis.Tumour necrosis factor in infectious disease.Inhibition of TNF receptor 1 internalization by adenovirus 14.7K as a novel immune escape mechanism.Adenoviral vector-based strategies against infectious disease and cancer.Role of Bax/Bcl-2 family members in green tea polyphenol induced necroptosis of p53-deficient Hep3B cells.Benzo(a)pyrene-7,8-diol-9,10-epoxide induced p53-independent necrosis via the mitochondria-associated pathway involving Bax and Bak activation.BAX to basics: How the BCL2 gene family controls the death of retinal ganglion cells.The oncolytic adenovirus AdΔΔ enhances selective cancer cell killing in combination with DNA-damaging drugs in pancreatic cancer models.Translocation and oligomerization of Bax is regulated independently by activation of p38 MAPK and caspase-2 during MN9D dopaminergic neurodegeneration.The vaccinia virus F1L protein interacts with the proapoptotic protein Bak and inhibits Bak activationBNip3 is a mediator of TNF-induced necrotic cell death.Requirement of BAX for efficient adenovirus-induced apoptosis.Bak and Bax function to limit adenovirus replication through apoptosis induction.
P2860
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P2860
Tumor necrosis factor-alpha induces Bax-Bak interaction and apoptosis, which is inhibited by adenovirus E1B 19K
description
2001 nî lūn-bûn
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2001 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած
@hyw
2001 թվականի նոյեմբերին հրատարակված գիտական հոդված
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2001年の論文
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2001年学术文章
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2001年学术文章
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2001年学术文章
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2001年学术文章
@zh-my
2001年学术文章
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2001年學術文章
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name
Tumor necrosis factor-alpha in ...... nhibited by adenovirus E1B 19K
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Tumor necrosis factor-alpha in ...... nhibited by adenovirus E1B 19K
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Tumor necrosis factor-alpha in ...... nhibited by adenovirus E1B 19K
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Tumor necrosis factor-alpha in ...... nhibited by adenovirus E1B 19K
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Tumor necrosis factor-alpha in ...... nhibited by adenovirus E1B 19K
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Tumor necrosis factor-alpha in ...... nhibited by adenovirus E1B 19K
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Tumor necrosis factor-alpha in ...... nhibited by adenovirus E1B 19K
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Tumor necrosis factor-alpha in ...... nhibited by adenovirus E1B 19K
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Tumor necrosis factor-alpha in ...... nhibited by adenovirus E1B 19K
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Tumor necrosis factor-alpha in ...... nhibited by adenovirus E1B 19K
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Tumor necrosis factor-alpha in ...... nhibited by adenovirus E1B 19K
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Tumor necrosis factor-alpha in ...... nhibited by adenovirus E1B 19K
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P2093
P2860
P3181
P356
P1476
Tumor necrosis factor-alpha in ...... nhibited by adenovirus E1B 19K
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P2093
A Cuconati
R Sundararajan
P2860
P304
P3181
P356
10.1074/JBC.M106386200
P407
P50
P577
2001-11-30T00:00:00Z