Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death
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- Type
- article
- Published
- 2001-04-27
- Cited by
- 4,233
- References
- 33
- Access
- Open access
- OpenAlex
- https://openalex.org/W1984547206
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:206506592
Keywords
Cell biology, Mitochondrion, Cytochrome c, Staurosporine, Apoptosis
References
- Bcl‐2 mutants with restricted subcellular location reveal spatially distinct pathways for apoptosis in different cell types.
- Apoptotic pathways: paper wraps stone blunts scissors.
- Mitochondrial control of cell death
- BAX-dependent transport of cytochrome c reconstituted in pure liposomes
- Bid-deficient mice are resistant to Fas-induced hepatocellular apoptosis
- Bcl-2 family proteins regulate the release of apoptogenic cytochrome c by the mitochondrial channel VDAC
- tBID, a membrane-targeted death ligand, oligomerizes BAK to release cytochrome c.
- The Bcl-2 protein family: arbiters of cell survival.
- Two CD95 (APO‐1/Fas) signaling pathways
- Reduced apoptosis and cytochrome c-mediated caspase activation in mice lacking caspase 9.
- A stable human-derived packaging cell line for production of high titer retrovirus/vesicular stomatitis virus G pseudotypes.
- Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors.
- Apoptotic crosstalk between the endoplasmic reticulum and mitochondria controlled by Bcl-2
- Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis.
- The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues.
- Bok is a pro-apoptotic Bcl-2 protein with restricted expression in reproductive tissues and heterodimerizes with selective anti-apoptotic Bcl-2 family members.
- Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-β
- p28 Bap31, a Bcl-2/Bcl-XL- and Procaspase-8–associated Protein in the Endoplasmic Reticulum
- Maintenance of Calcium Homeostasis in the Endoplasmic Reticulum by Bcl-2
- Apaf1 is required for mitochondrial pathways of apoptosis and brain development.
Cited by
- Investigation of the ubiquitin-specific protease UBP41 and of the lysosomal cysteine proteases cathepsin-L and cathepsin-B as potential mediators of proapoptotic signalling
- Apoptosis—New Opportunities for Novel Therapeutics for Heart Diseases
- Molecular Mechanisms of Programmed Necrotic Death Initiated by Intrinsic Death Signals
- Biophysical Insights into the Oligomerization of Bclxl Apoptotic Repressor
- Hsp70: anti-apoptotic and tumorigenic protein.
- The urokinase-system--role of cell proliferation and apoptosis.
- Insights into cancer therapeutic design based on p53 and TRAIL receptor signaling
- PTEN sensitizes prostate cancer cells to death receptor-mediated and drug-induced apoptosis through a FADD-dependent pathway
- Mitochondria-Dependent Caspase-9 Activation Is Necessary for Antigen Receptor-Mediated Effector Caspase Activation and Apoptosis in WEHI 231 Lymphoma Cells1
- Delayed Sclerosis, Neuroprotection, and Limbic Epileptogenesis After Status Epilepticus in the Rat
- Early events of target deprivation/axotomy‐induced neuronal apoptosis in vivo: oxidative stress, DNA damage, p53 phosphorylation and subcellular redistribution of death proteins
- Mitochondrion-targeted apoptosis regulators of viral origin.
- Alterations in the apoptotic machinery and their potential role in anticancer drug resistance
- c-Myc Sensitization to Oxygen Deprivation-induced Cell Death Is Dependent on Bax/Bak, but Is Independent of p53 and Hypoxia-inducible Factor-1*
- The Bcl-2 family: roles in cell survival and oncogenesis
- Development and maintenance of B and T lymphocytes requires antiapoptotic MCL-1
- Quantitation of mitochondrial dynamics by photolabeling of individual organelles shows that mitochondrial fusion is blocked during the Bax activation phase of apoptosis
- Genetic approaches to analyzing mitochondrial outer membrane permeability.
- Control of mitochondrial permeability by Bcl-2 family members.
- Acetylation of the C terminus of Ku70 by CBP and PCAF controls Bax-mediated apoptosis.
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