A role for mitochondrial Bak in apoptotic response to anticancer drugs

scientific article

A role for mitochondrial Bak in apoptotic response to anticancer drugs is …
instance of (P31):
scholarly articleQ13442814

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P356DOI10.1074/JBC.M103526200
P698PubMed publication ID11447222

P2093author name stringKim TH
Wang GQ
Fang B
Gambotto A
Rabinowich H
Goldstein LA
Gastman BR
Wieckowski E
Yin XM
Rabinovitz A
P2860cites workMolecular characterization of mitochondrial apoptosis-inducing factorQ22001452
Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondriaQ22008484
Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptorsQ24310559
Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosisQ24310597
Cytochrome c and dATP-dependent formation of Apaf-1/caspase-9 complex initiates an apoptotic protease cascadeQ24311006
Bcl-xL regulates the membrane potential and volume homeostasis of mitochondriaQ24311858
Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell deathQ24312211
BID: a novel BH3 domain-only death agonistQ24320091
Apaf-1, a human protein homologous to C. elegans CED-4, participates in cytochrome c-dependent activation of caspase-3Q24324482
Investigation of bax-induced release of cytochrome c from yeast mitochondria permeability of mitochondrial membranes, role of VDAC and ATP requirementQ28140258
Bax and adenine nucleotide translocator cooperate in the mitochondrial control of apoptosisQ28283313
Cloning of a bcl-2 homologue by interaction with adenovirus E1B 19KQ28299861
Induction of apoptosis by the Bcl-2 homologue BakQ28299871
Modulation of apoptosis by the widely distributed Bcl-2 homologue BakQ28299882
Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and deathQ28363890
Bid-deficient mice are resistant to Fas-induced hepatocellular apoptosisQ28511080
The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissuesQ28512628
Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosisQ28512752
Caspase cleaved BID targets mitochondria and is required for cytochrome c release, while BCL-XL prevents this release but not tumor necrosis factor-R1/Fas deathQ28586301
Bax directly induces release of cytochrome c from isolated mitochondriaQ28588847
Bax-deficient mice with lymphoid hyperplasia and male germ cell deathQ28589360
BAX is required for neuronal death after trophic factor deprivation and during developmentQ28592997
Bid induces the oligomerization and insertion of Bax into the outer mitochondrial membraneQ28647586
BCL-2 family members and the mitochondria in apoptosisQ29614427
The release of cytochrome c from mitochondria: a primary site for Bcl-2 regulation of apoptosisQ29616513
Mitochondrial control of cell deathQ29617739
Role of BAX in the apoptotic response to anticancer agentsQ31523620
Mitochondria and cell death. Mechanistic aspects and methodological issuesQ33734610
Bcl-2 proteins: regulators of apoptosis or of mitochondrial homeostasis?Q33787932
Bid, a critical mediator for apoptosis induced by the activation of Fas/TNF-R1 death receptors in hepatocytesQ33996179
Pro-apoptotic cascade activates BID, which oligomerizes BAK or BAX into pores that result in the release of cytochrome c.Q34139321
Apoptotic pathways: the roads to ruinQ34753431
bax-deficiency promotes drug resistance and oncogenic transformation by attenuating p53-dependent apoptosisQ36040551
Regulated targeting of BAX to mitochondria.Q36255507
Bax-induced cytochrome C release from mitochondria is independent of the permeability transition pore but highly dependent on Mg2+ ionsQ36255553
Granzyme B-mediated cytochrome c release is regulated by the Bcl-2 family members bid and Bax.Q36368546
Initiation of apoptosis by granzyme B requires direct cleavage of bid, but not direct granzyme B-mediated caspase activation.Q36368577
Withdrawal of IL-7 induces Bax translocation from cytosol to mitochondria through a rise in intracellular pH.Q36746298
Bid-induced conformational change of Bax is responsible for mitochondrial cytochrome c release during apoptosisQ38326924
Role of Bak in UV-induced apoptosis in skin cancer and abrogation by HPV E6 proteinsQ40445624
Lysosomal protease pathways to apoptosis. Cleavage of bid, not pro-caspases, is the most likely routeQ40843079
Bax-induced caspase activation and apoptosis via cytochrome c release from mitochondria is inhibitable by Bcl-xL.Q40980272
BAX frameshift mutations in cell lines derived from human haemopoietic malignancies are associated with resistance to apoptosis and microsatellite instabilityQ41043279
Evaluation of GAL4/TATA in vivo. Induction of transgene expression by adenovirally mediated gene codeliveryQ41056260
Aberrant expression and function of p53 in T-cells immortalized by HTLV-I Tax1.Q41116189
Mutant p53: epigenetic mutator of the T-cell receptor via induction of methylation.Q53422686
On the voltage dependence of the mitochondrial permeability transition pore. A critical appraisal.Q53969386
Analysis of the membrane potential of rat- and mouse-liver mitochondria by flow cytometry and possible applications.Q54085818
P433issue36
P407language of work or nameEnglishQ1860
P921main subjectapoptotic processQ14599311
P304page(s)34307-34317
P577publication date2001-07-10
P1433published inJournal of Biological ChemistryQ867727
P1476titleA role for mitochondrial Bak in apoptotic response to anticancer drugs
P478volume276

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cites work (P2860)
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