The expanding role of mitochondria in apoptosis.

By X. Wang. Genes & Development, 2001

2,557 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/2641d74ec0bcd464a2597474bcd2a2930f9a3171

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Citations in the corpus

The role of the unfolded protein response in tumour development: friend or foe? (2004, unknown): “In response to extrinsic and intrinsic signals, they are activated through cleavage by upstream caspases, setting in place a cascade, which leads to apoptotic cell deat”
OPA1 controls apoptotic cristae remodeling independently from mitochondrial fusion. (2006, unknown): “They release cytochrome c and other proapoptotic proteins activating a postmitochondrial pathway that culminates in cell demise (Wang, 2001).”
Ways of dying: multiple pathways to apoptosis. (2003, background): “Because Bcl-2 can prevent this change, it has been widely assumed that commitment to all forms of stress-induced apoptosis, that is, all those regulated by the Bcl-2 family, requires this step to initiate all relevant caspase activation, and hence that Bcl-2 and its anti-apoptotic relatives function”
Bax and Bak can localize to the endoplasmic reticulum to initiate apoptosis (2003, background): “It has been well established that these proteins function at mitochondria to prevent or promote the release of apoptogenic factors such as cytochrome c, AIF, Smac/Diablo, endonuclease G, and Omi (Wang, 2001).”
The Bcl2 family: regulators of the cellular life-or-death switch (2002, background): “Progression from lymphoid hyperplasia to high-grade malignant lymphoma in mice transgenic for the t(14;18).”
Comprehending crystalline β-carotene accumulation by comparing engineered cell models and the natural carotenoid-rich system of citrus (2011, unknown): “In animal cells, mitochondria have a pivotal role in an apoptosis response to various extracellular stimuli (Kroemer et al., 1998; Wang, 2001; Wang and Youle, 2009).”
Luteolin, a flavonoid with potential for cancer prevention and therapy. (2008, background): “The intrinsic pathway involves functional incapacitation of mitochondria by pro-apoptotic Bcl2 family members, including Bax, Bak, and Bik, that cause mitochondria potential loss and release cytochrome c to activate caspase 9, which in turn activates executor caspases (−3, −7) and destroys cellular ”
Role of Mitochondria in Ferroptosis (2018, background): “In mitochondria-mediated apoptosis, the mitochondrion serves as a reservoir, storing apoptosis-regulatory proteins such as cytochrome c and Smac, which upon release to the cytoplasm, promote caspase activation (Jiang and Wang, 2004; Wang, 2001).”
Bcl11b is required for differentiation and survival of αβ T lymphocytes (2003, result): “This was consistent with there being no alteration in the expression of Kip1 (ref”
Control of mitochondrial apoptosis by the Bcl-2 family (2009, background): “Bax and Bak oligomers participate in forming pores in and cause permeabilization of the outer mitochondrial membrane, leading to the release of the contents of the mitochondrial intermembrane space, including cytochrome c and Smac, into the cytosol ( Wang, 2001 ).”
Radiation-induced cell death mechanisms (2010, background): “MOMP releases several potentially lethal proteins from the intermembrane space into the cytoplasm [ 53 ].”
Validating survivin as a cancer therapeutic target (2003, background): “An 'intrinsic' pathway is triggered by intracellular and environmental cues and is centred on dysregulation of mitochondrial functio”