BAK/BAX macropores facilitate mitochondrial herniation and mtDNA efflux during apoptosis
By K. McArthur, L. Whitehead, John M. Heddleston, L. Li, B. Padman, V. Oorschot, N. Geoghegan, S. Chappaz, Sophia Davidson, Hui San Chin and 15 more. Science, 2018
936 citations recorded by the source corpus.
Subfields: Epidemiology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/1db8cc782638f3a7e3da4175363289eff9f86363
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In Molecular Biology
Citations in the corpus
- Mitochondrial DNA in inflammation and immunity (2020, neutral): “In the context of cell death, it is now clear that BAX and BAK form the pores on the mitochondrial outer membrane through which the inner membrane herniates, leading to mtDNA release, although how the inner membrane permeabilises is as yet not fully resolved [61,62].”
- Mitochondrial ROS promote mitochondrial dysfunction and inflammation in ischemic acute kidney injury by disrupting TFAM-mediated mtDNA maintenance (2021, background): “A recent study showed that mitochondrial macropores formed by activated Bax protein under stress allow the release of mtDNA into the cytosol [59].”
- The senescence-associated secretory phenotype and its physiological and pathological implications (2024, neutral): “A recent study showed that, in senescent cells with minority mitochondrial outer membrane permeabilization (miMOMP), the BAX and BAK macropores allowed the mitochondrial inner membrane to herniate into the cytosol to release mitochondrial DNA 102 , leading to activation of cGAS–STING and SASP 103 (F”
- TDP-43 Triggers Mitochondrial DNA Release via mPTP to Activate cGAS/STING in ALS (2020, methodology): “It has been reported that TDP-43 is capable of inducing apoptosis under certain conditions, which could trigger Bak/Bax permeabilization of the outer mitochondrial membrane and leakage of DNA into the cytoplasm (McArthur et al., 2018).”