Proapoptotic BAX and BAK: A Requisite Gateway to Mitochondrial Dysfunction and Death

By M. Wei, W. Zong, E. Cheng, T. Lindsten, V. Panoutsakopoulou, Andrea J. Ross, K. Roth, G. MacGregor, Craig B. Thompson, S. Korsmeyer. Science, 2001

4,220 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/803b1672ed76dc13f50b020abd30e76a010be24b

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Citations in the corpus

Mitochondria and Mitophagy: The Yin and Yang of Cell Death Control (2012, background): “The proapoptotic members can be separated into 2 distinct subfamilies: the BH3-only proteins, which include BH3 interacting domain death agonist (BID), BCL2/adenovirus E1B 19-kDa proteininteracting protein 3 (BNIP3), Nip3-like protein X (NIX)/ BCL2/adenovirus E1B 19-kDa protein-interacting protein 3”
BCL-2 family antagonists for cancer therapy (2008, background): “Cells in which both BAK and BAX have been deleted are essentially resistant to apoptosi”
CHOP induces death by promoting protein synthesis and oxidation in the stressed endoplasmic reticulum. (2004, background): “Various downstream effectors of cell death induced by ER stress have been identified (Nakagawa et al. 2000; Rao et al. 2001; Wei et al. 2001); however, the proximal steps that mobilize them during ER stress are poorly understood.”
Caspase-9, caspase-3 and caspase-7 have distinct roles during intrinsic apoptosis (2013, background): “Activation of the BCL-2 family members Bax and Bak results in MOMP and the release of pro-apoptotic proteins, including cytochrome c, from the inter-membrane space into the cytosol [3-5].”
Mitochondria and cell death: outer membrane permeabilization and beyond (2010, background): “Activation of either BCL-2-associated X protein ( BAX ) or BCL-2 antagonist or killer ( BAK ) is essential for MOMP as cells lacking both proteins fail to undergo MOMP and apoptosis in response to diverse intrinsic stimul”
Drug-induced death signaling strategy rapidly predicts cancer response to chemotherapy (2015, positive): “…in the mitochondrial outer membrane that induce release of cytochrome c and the loss of mitochondrial transmembrane potential, as well as release of SMAC/DIABLO and other proteins that trigger apoptosome formation, caspase activation , and finally apoptosis (Kluck et al., 1997; Wei et al., 2001).”
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “panel of cell types profoundly resistant to diverse lethal stimuli [74], a phenotype that in some settings can be”
Control of mitochondrial apoptosis by the Bcl-2 family (2009, background): “Apoptosis that is caused by BH3-only proteins absolutely requires Bax and Bak (Kuwana et al., 2005; Lindsten et al., 2000; Wei et al., 2000; Wei et al., 2001).”
The expanding role of mitochondria in apoptosis. (2001, background): “Instead, they block the oligomerization of Bax and Bak and abort the apoptotic program at this stage (Nechushtan et al. 2001; Sundarajan and White 2001; Wei et al. 2001).”
Neuronal Cell Death. (2018, positive): “The pro-apoptotic members Bax and Bak contain BH1–3 and are thought to be almost entirely essential for the execution of apoptosis via the intrinsic pathway (107, 722, 807), although a novel but as yet unknown Bax/Bak-independent intrinsic apoptotic pathway has recently been reported (787).”