The mitochondrial phosphatase PGAM5 functions at the convergence point of multiple necrotic death pathways.
By Zhigao Wang, Hui Jiang, She Chen, Fenghe Du, Xiaodong Wang. Cell, 2012
954 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/8b990e53a9b9efe1d0fdfc1007bf4ce88d7f4e08
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In Molecular Biology
- Guido Kroemer
- Douglas R. Green
- L. Galluzzi
- Beth Levine
- Simone Fulda
- D. Tang
- Junying Yuan
- D. Klionsky
Citations in the corpus
- Crosstalk between apoptosis, necrosis and autophagy. (2013, background): “Inte-restingly, PGAM5, a mitochondrial phosphoglyceratemutase, was also recently reported to associate with the necrosome, providing a potential point of convergence for increased mitochondrial fi ssion and necroptosis ([40,41]; reviewed in [37]).”
- Toll-like Receptor 3-mediated Necrosis via TRIF, RIP3, and MLKL* (2013, background): “Following preparation of cell extracts, immunoprecipitation, and electrophoretic separation on denaturing polyacrylamide gels followed by transfer (4, 9), immunoblot analysis was performed on the following antibodies: mouse anti-(cid:2) -actin (clone AC-74; Sigma); rabbit anti-Casp8 (Cell Signaling)”
- Necroptosis: Mechanisms and Relevance to Disease (2016, neutral): “Initial beliefs that necroptosis would proceed upon mitochondrial fragmentation mediated by PGAM family member 5, serine/ threonine protein phosphatase, mitochondrial (PGAM5) and dynamin 1-like (DNM1L) (25) have been conclusively rejected (26–29).”
- Apoptosis, autophagy, necroptosis, and cancer metastasis (2015, background): “At the second checkpoint, activated caspase-8 cleaves and abolishes the activities of RIP1, RIP3, and CYLD [118-120].”