Endonuclease G is an apoptotic DNase when released from mitochondria
By Lily Y. Li, Xu Luo, Xiaodong Wang. Nature, 2001
1,875 citations recorded by the source corpus.
Subfields: Molecular Biology, Nutrition and Dietetics
View Paper: https://www.semanticscholar.org/paper/beee476b7f3c9239200ae52307d1a3372aaa80ec
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In Molecular Biology
- Guido Kroemer
- Douglas R. Green
- Jerry M. Adams
- L. Galluzzi
- Simone Fulda
- Beth Levine
- D. Tang
- Suzanne Cory
In Nutrition and Dietetics
Citations in the corpus
- Pathophysiology of Acute Kidney Injury (2012, neutral): “For example, Endonuclease G (Endo G) is a small 27 kDa protein residing in the inner membrane space of mitochondria and can traverse to the nucleus under apoptotic conditions (313).”
- On the origin, evolution, and nature of programmed cell death: a timeline of four billion years (2002, background): “Similarly, when localized inside the mitochondria, endonuclease G seems to play an important role in mitochondrial DNA replication,(237) and once released from the mitochondria, it seems to participate in caspaseindependent cell death.(85) Also, the cytoplasmic dynaminrelated Drp1 protein, that may ”
- The role of mitochondrial factors in apoptosis: a Russian roulette with more than one bullet (2002, methodology): “Therefore, it is conceivable that endonuclease G is responsible for the nuclear DNA degradation observed in embryonic fibroblasts from these mice after induction of apoptosis by TNF treatment or ultraviolet radiation.(15) DNA degradation during apoptosis generally occurs in two stages: first when hi”
- Distinct BH3 domains either sensitize or activate mitochondrial apoptosis, serving as prototype cancer therapeutics. (2002, neutral): “The latter displace (Li et al., 2001; Terradillos et al., 2002).”
- Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “Indeed, the actual contribution of ENDOG to RCD in mammals [675] has been questioned by the generation of Endog mice, whose cells display normal sensitivity to multiple lethal triggers [676, 677].”
- Bcl-2-family proteins and the role of mitochondria in apoptosis. (2003, background): “The contribution of the intrinsic pathway in such cases could be mediated by any of several IMS proteins, including cytochrome c, Smac/DIABLO [20,21], Omi/Htra2 [22–24], endonuclease G [25] and apoptosis-inducing factor (AIF) [26,27].”