Mitochondria and cell death: outer membrane permeabilization and beyond

By S. Tait, Douglas R. Green. Nature reviews. Molecular cell biology, 2010

2,557 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/b4d7058e5b924a0073cbea8bf68369b700f16551

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Citations in the corpus

PGC1α Expression Defines a Subset of Human Melanoma Tumors with Increased Mitochondrial Capacity and Resistance to Oxidative Stress (2013, positive): “One of the mechanisms by which mitochondrial failure causes apoptosis is through the loss of membrane potential and generation of ROS (Tait and Green, 2010).”
Mitochondrial apoptosis: killing cancer using the enemy within (2015, background): “In general terms, caspase activity can be initiated either via cellsurface death-receptors—the so-called death receptor or extrinsic pathway (reviewed in Dickens et al (2012)) or through the mitochondrial, also called intrinsic, pathway of apoptosis (Tait and Green, 2010).”
Initiation and perpetuation of NLRP3 inflammasome activation and assembly (2015, background): “As Bak and Bax are not required for NLRP3 activation, it is possible that MOMP is irrelevant (121, 127).”
13 reasons why the brain is susceptible to oxidative stress (2018, background): “Beyond oxidative phosphorylation, mitochondria are essential signalling hubs regulating a veritable plethora of essential processes, from Ca homeostasis, Fe-S cluster synthesis to cell fate [55,108,109].”
Consensus guidelines for the detection of immunogenic cell death (2014, background): “239241 The externalization of phosphatidylserine (a phospholipid normally restricted to the inner leaflet of the plasma membrane) indeed accompanies multiple (though not all) instances of apoptotic cell death,(16,242-245) while the permanent dissipation of the Dcm as a result of mitochondrial outer ”
Molecular definitions of cell death subroutines: recommendations of the Nomenclature Committee on Cell Death 2012 (2011, background): “membrane owing to the pore-forming activity of pro-apoptotic members of the BCL-2 protein family such as BAK and BAX or can result from a phenomenon (the so-called mitochondrial permeability transition, MPT) that originates at the inner mitochondrial membrane due to the opening of a multiprotein com”
Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA (2014, background): “Bax/Bak-Dependent Induction of Type I IFNs The intrinsic pathway of apoptosis is activated upon MOMP by the Bax/Bak channel (Jiang and Wang, 2004).”