Damage-induced Bax N-terminal change, translocation to mitochondria and formation of Bax dimers/complexes occur regardless of cell fate.
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Interaction with a membrane surface triggers a reversible conformational change in Bax normally associated with induction of apoptosisIdentification of novel isoforms of the BH3 domain protein Bim which directly activate Bax to trigger apoptosisERK1/2-dependent phosphorylation of BimEL promotes its rapid dissociation from Mcl-1 and Bcl-xLMAP-1 is a mitochondrial effector of Bax.Bcl-2 regulator FKBP38 is activated by Ca2+/calmodulin.Role of Bax in resveratrol-induced apoptosis of colorectal carcinoma cells.Second-hand smoke-induced cardiac fibrosis is related to the Fas death receptor apoptotic pathway without mitochondria-dependent pathway involvement in rats.Bax and Bak can localize to the endoplasmic reticulum to initiate apoptosisBax forms an oligomer via separate, yet interdependent, surfaces.Essential role of the voltage-dependent anion channel (VDAC) in mitochondrial permeability transition pore opening and cytochrome c release induced by arsenic trioxide.Transforming growth factor beta-dependent sequential activation of Smad, Bim, and caspase-9 mediates physiological apoptosis in gastric epithelial cells.Combination of N-(4-hydroxyphenyl) retinamide and genistein increased apoptosis in neuroblastoma SK-N-BE2 and SH-SY5Y xenograftsN-(4-Hydroxyphenyl) Retinamide Potentiated Anti-tumor Efficacy of Genistein in Human Ewing's Sarcoma Xenografts.Vinblastine-induced apoptosis is mediated by discrete alterations in subcellular location, oligomeric structure, and activation status of specific Bcl-2 family membersSmall molecule inhibitor YM155-mediated activation of death receptor 5 is crucial for chemotherapy-induced apoptosis in pancreatic carcinoma.Commitment to apoptosis in CD4(+) T lymphocytes productively infected with human immunodeficiency virus type 1 is initiated by lysosomal membrane permeabilization, itself induced by the isolated expression of the viral protein NefA novel checkpoint in the Bcl-2-regulated apoptotic pathway revealed by murine cytomegalovirus infection of dendritic cells.Downregulation of Noxa by RAF/MEK inhibition counteracts cell death response in mutant B-RAF melanoma cells.Mechanisms of disease: mitochondria as new therapeutic targets in diabetic neuropathy.β-Elemene enhances susceptibility to cisplatin in resistant ovarian carcinoma cells via downregulation of ERCC-1 and XIAP and inactivation of JNKA role for HSP70 in protecting against indomethacin-induced gastric lesions.Chlamydia trachomatis infection inhibits both Bax and Bak activation induced by staurosporineThe N-terminal end of Bax contains a mitochondrial-targeting signal.To Prime, or Not to Prime: That Is the Question.Neuroprotection against neuroblastoma cell death induced by depletion of mitochondrial glutathione.GdCl3 induced Hep G2 cell death through mitochondrial and external death pathways without significant elevation of ROS generation.Translocation and oligomerization of Bax is regulated independently by activation of p38 MAPK and caspase-2 during MN9D dopaminergic neurodegeneration.An essential role for p73 in regulating mitotic cell death.Elucidation of some Bax conformational changes through crystallization of an antibody-peptide complex.Upregulation of BAK by butyrate in the colon is associated with increased Sp3 binding.Myxoma virus M11L blocks apoptosis through inhibition of conformational activation of Bax at the mitochondria.An anti-apoptotic viral protein that recruits Bax to mitochondria.BIM-mediated membrane insertion of the BAK pore domain is an essential requirement for apoptosis.Selective glucocorticoid receptor translational isoforms reveal glucocorticoid-induced apoptotic transcriptomes.Defective Bax activation in Hodgkin B-cell lines confers resistance to staurosporine-induced apoptosis.c-Myc induces cytochrome c release in Rat1 fibroblasts by increasing outer mitochondrial membrane permeability in a Bid-dependent manner.A caspase-8-independent signaling pathway activated by Fas ligation leads to exposure of the Bak N terminus.Contributions to Bax insertion and oligomerization of lipids of the mitochondrial outer membrane.AKT2 inhibition of cisplatin-induced JNK/p38 and Bax activation by phosphorylation of ASK1: implication of AKT2 in chemoresistance.Paclitaxel targets mitochondria upstream of caspase activation in intact human neuroblastoma cells.
P2860
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P2860
Damage-induced Bax N-terminal change, translocation to mitochondria and formation of Bax dimers/complexes occur regardless of cell fate.
description
2001 nî lūn-bûn
@nan
2001 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած
@hyw
2001 թվականի նոյեմբերին հրատարակված գիտական հոդված
@hy
2001年の論文
@ja
2001年論文
@yue
2001年論文
@zh-hant
2001年論文
@zh-hk
2001年論文
@zh-mo
2001年論文
@zh-tw
2001年论文
@wuu
name
Damage-induced Bax N-terminal ...... occur regardless of cell fate
@nl
Damage-induced Bax N-terminal ...... occur regardless of cell fate.
@ast
Damage-induced Bax N-terminal ...... occur regardless of cell fate.
@en
type
label
Damage-induced Bax N-terminal ...... occur regardless of cell fate
@nl
Damage-induced Bax N-terminal ...... occur regardless of cell fate.
@ast
Damage-induced Bax N-terminal ...... occur regardless of cell fate.
@en
prefLabel
Damage-induced Bax N-terminal ...... occur regardless of cell fate
@nl
Damage-induced Bax N-terminal ...... occur regardless of cell fate.
@ast
Damage-induced Bax N-terminal ...... occur regardless of cell fate.
@en
P2093
P2860
P356
P1433
P1476
Damage-induced Bax N-terminal ...... occur regardless of cell fate.
@en
P2093
A Thistlethwaite
G J Griffiths
J A Hickman
P2860
P304
P356
10.1093/EMBOJ/20.22.6306
P407
P577
2001-11-01T00:00:00Z