scholarly article | Q13442814 |
P356 | DOI | 10.1016/S0006-291X(03)00615-6 |
P953 | full work available at URL | https://api.elsevier.com/content/article/PII:S0006291X03006156?httpAccept=text/plain |
https://api.elsevier.com/content/article/PII:S0006291X03006156?httpAccept=text/xml | ||
P698 | PubMed publication ID | 12729577 |
P5875 | ResearchGate publication ID | 10774861 |
P50 | author | Stanley J. Korsmeyer | Q138795 |
Luca Scorrano | Q16854174 | ||
P2860 | cites work | Genes & Development | Q1524533 |
Bax interacts with the permeability transition pore to induce permeability transition and cytochrome c release in isolated mitochondria | Q22008484 | ||
Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC | Q22009974 | ||
Bax oligomerization is required for channel-forming activity in liposomes and to trigger cytochrome c release from mitochondria | Q22011013 | ||
Bmf: a proapoptotic BH3-only protein regulated by interaction with the myosin V actin motor complex, activated by anoikis | Q24291662 | ||
Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors | Q24310559 | ||
Cleavage of BID by caspase 8 mediates the mitochondrial damage in the Fas pathway of apoptosis | Q24310597 | ||
Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death | Q24311298 | ||
X-linked IAP is a direct inhibitor of cell-death proteases | Q24318710 | ||
Bim: a novel member of the Bcl-2 family that promotes apoptosis | Q24532974 | ||
IAPs block apoptotic events induced by caspase-8 and cytochrome c by direct inhibition of distinct caspases | Q24533214 | ||
Enforced dimerization of BAX results in its translocation, mitochondrial dysfunction and apoptosis | Q24533270 | ||
Proapoptotic BH3-only Bcl-2 family members induce cytochrome c release, but not mitochondrial membrane potential loss, and do not directly modulate voltage-dependent anion channel activity | Q24680994 | ||
A novel, high conductance channel of mitochondria linked to apoptosis in mammalian cells and Bax expression in yeast | Q24685400 | ||
Structure of Bax: coregulation of dimer formation and intracellular localization | Q27628839 | ||
The dynamin-related GTPase, Mgm1p, is an intermembrane space protein required for maintenance of fusion competent mitochondria | Q27938333 | ||
Noxa, a BH3-only member of the Bcl-2 family and candidate mediator of p53-induced apoptosis | Q28144256 | ||
BCL-2, BCL-X(L) sequester BH3 domain-only molecules preventing BAX- and BAK-mediated mitochondrial apoptosis | Q28189945 | ||
Activation of mitochondrial voltage-dependent anion channel by apro-apoptotic BH3-only protein Bim | Q28214708 | ||
BH3 domain of BAD is required for heterodimerization with BCL-XL and pro-apoptotic activity | Q28249553 | ||
Bax and adenine nucleotide translocator cooperate in the mitochondrial control of apoptosis | Q28283313 | ||
Bad is a BH3 domain-containing protein that forms an inactivating dimer with Bcl-XL. | Q40024055 | ||
Transient and long-lasting openings of the mitochondrial permeability transition pore can be monitored directly in intact cells by changes in mitochondrial calcein fluorescence | Q40137371 | ||
Bid acts on the permeability transition pore complex to induce apoptosis | Q40827697 | ||
Mitochondrial ultracondensation, but not swelling, is involved in TNF alpha-induced apoptosis in human T-lymphoblastic leukaemic cells. | Q41076130 | ||
Mitochondrial proliferation and paradoxical membrane depolarization during terminal differentiation and apoptosis in a human colon carcinoma cell line | Q41098628 | ||
The coordinate release of cytochrome c during apoptosis is rapid, complete and kinetically invariant | Q41723645 | ||
Injected cytochrome c induces apoptosis | Q42832504 | ||
Rate-limiting step preceding cytochrome c release in cells primed for Fas-mediated apoptosis revealed by analysis of cellular mosaicism of respiratory changes | Q43508166 | ||
Bax is present as a high molecular weight oligomer/complex in the mitochondrial membrane of apoptotic cells | Q43514949 | ||
Cytochrome c release occurs via Ca2+-dependent and Ca2+-independent mechanisms that are regulated by Bax. | Q43551075 | ||
The apoptotic protein tBid promotes leakage by altering membrane curvature | Q44039942 | ||
Oligomycin, inhibitor of the F0 part of H+-ATP-synthase, suppresses the TNF-induced apoptosis. | Q44224227 | ||
The inner mitochondrial membrane contains ion-conducting channels similar to those found in bacteria. | Q44810762 | ||
Ultrastructural localization of cytochrome c in apoptosis demonstrates mitochondrial heterogeneity. | Q49078003 | ||
Quantitative cytochemistry of the diaminobenzidine cytochrome oxidase reaction product in mitochondria of cardiac muscle and pancreas | Q52433623 | ||
Interactions of cyclophilin with the mitochondrial inner membrane and regulation of the permeability transition pore, and cyclosporin A-sensitive channel. | Q52518634 | ||
A thermodynamic model describing the nature of the crista junction: a structural motif in the mitochondrion. | Q53674378 | ||
Mitochondria are excitable organelles capable of generating and conveying electrical and calcium signals. | Q53967833 | ||
Tumor Necrosis Factor-α Increases the Steady-state Reduction of Cytochromebof the Mitochondrial Respiratory Chain in Metabolically Inhibited L929 Cells | Q58885458 | ||
Functional consequences of the sustained or transient activation by Bax of the mitochondrial permeability transition pore | Q73107174 | ||
Cytochrome c release from mitochondria: all or nothing | Q73521425 | ||
The overexpression of Bax produces cell death upon induction of the mitochondrial permeability transition | Q74358996 | ||
Bcl-xL prevents cell death following growth factor withdrawal by facilitating mitochondrial ATP/ADP exchange | Q74607067 | ||
Serine phosphorylation of death agonist BAD in response to survival factor results in binding to 14-3-3 not BCL-X(L) | Q28297419 | ||
Proapoptotic BAX and BAK: a requisite gateway to mitochondrial dysfunction and death | Q28363890 | ||
Apaf1 is required for mitochondrial pathways of apoptosis and brain development | Q28505574 | ||
Survival factor-mediated BAD phosphorylation raises the mitochondrial threshold for apoptosis | Q28509136 | ||
Bid-deficient mice are resistant to Fas-induced hepatocellular apoptosis | Q28511080 | ||
The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues | Q28512628 | ||
Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis | Q28512752 | ||
Cytochrome c release from mitochondria proceeds by a two-step process | Q28571562 | ||
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 death | Q28586301 | ||
Bax directly induces release of cytochrome c from isolated mitochondria | Q28588847 | ||
Bid induces the oligomerization and insertion of Bax into the outer mitochondrial membrane | Q28647586 | ||
Posttranslational N-myristoylation of BID as a molecular switch for targeting mitochondria and apoptosis | Q28647600 | ||
Mitochondria and apoptosis | Q29547905 | ||
BCL-2 family members and the mitochondria in apoptosis | Q29614427 | ||
Bid, Bax, and lipids cooperate to form supramolecular openings in the outer mitochondrial membrane | Q29616354 | ||
The role of dynamin-related protein 1, a mediator of mitochondrial fission, in apoptosis | Q29616568 | ||
Reduced apoptosis and cytochrome c-mediated caspase activation in mice lacking caspase 9 | Q29618617 | ||
Identification of calcineurin as a key signalling enzyme in T-lymphocyte activation | Q29620223 | ||
BAX and BAK regulation of endoplasmic reticulum Ca2+: a control point for apoptosis | Q29620466 | ||
Distinct BH3 domains either sensitize or activate mitochondrial apoptosis, serving as prototype cancer therapeutics | Q29620467 | ||
A distinct pathway remodels mitochondrial cristae and mobilizes cytochrome c during apoptosis | Q29620536 | ||
The machinery of mitochondrial inheritance and behavior | Q33538526 | ||
Mitochondrial transport of cations: channels, exchangers, and permeability transition. | Q33744633 | ||
Endogenous inhibitors of caspases | Q33816829 | ||
Organelle division: Self-assembling GTPase caught in the middle | Q33912827 | ||
BAX-dependent transport of cytochrome c reconstituted in pure liposomes | Q33912996 | ||
The internal structure of mitochondria | Q33953227 | ||
Bid, a widely expressed proapoptotic protein of the Bcl-2 family, displays lipid transfer activity. | Q34012615 | ||
Imaging the permeability pore transition in single mitochondria | Q34167671 | ||
Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice | Q34408475 | ||
Topology of the mitochondrial inner membrane: dynamics and bioenergetic implications. | Q34499144 | ||
A reversible component of mitochondrial respiratory dysfunction in apoptosis can be rescued by exogenous cytochrome c. | Q34582647 | ||
BH3-only proteins that bind pro-survival Bcl-2 family members fail to induce apoptosis in the absence of Bax and Bak | Q35079498 | ||
Bax-induced cytochrome C release from mitochondria is independent of the permeability transition pore but highly dependent on Mg2+ ions | Q36255553 | ||
The pro-apoptotic proteins, Bid and Bax, cause a limited permeabilization of the mitochondrial outer membrane that is enhanced by cytosol | Q36301514 | ||
Intrinsic curvature hypothesis for biomembrane lipid composition: a role for nonbilayer lipids | Q37689757 | ||
The BH3 domain of Bcl-x(S) is required for inhibition of the antiapoptotic function of Bcl-x(L). | Q39447996 | ||
P433 | issue | 3 | |
P407 | language of work or name | English | Q1860 |
P921 | main subject | biochemistry | Q7094 |
biophysics | Q7100 | ||
cell biology | Q7141 | ||
P304 | page(s) | 437-444 | |
P577 | publication date | 2003-05-01 | |
2003-05-09 | |||
P1433 | published in | Biochemical and Biophysical Research Communications | Q864228 |
P1476 | title | Mechanisms of cytochrome c release by proapoptotic BCL-2 family members | |
P478 | volume | 304 |
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