Journal
CELL CYCLE
Volume 16, Issue 19, Pages 1748-1760Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15384101.2017.1371889
Keywords
Necroptosis; RIPK3; MLKL; ESCRT; cell death; plasma membrane repair
Categories
Funding
- US NIH [R01 CA169291, R01 AI44828]
- ALSAC
- NATIONAL CANCER INSTITUTE [R01CA169291] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R37AI044828] Funding Source: NIH RePORTER
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Necroptosis is a form of programmed necrotic cell death mediated by the kinase RIPK3 and its substrate MLKL. MLKL, which displays plasma membrane (PM) pore-forming activity upon phosphorylation, functions as the executionerduring necroptosis. Thus, it was previously assumed that MLKL phosphorylation is the endpoint of the necroptotic signaling pathway. Here, we summarize several events that characterize the dying necroptotic cells after MLKL phosphorylation, including Ca2+ influx, phosphatidylserine (PS) externalization, PM repair by ESCRT-III activation, and the final compromise of PM integrity. These processes add several unexpected regulatory events downstream of MLKL signaling. We have also observed that CoCl2, which may mimic hypoxia, can induce necroptosis, which suggests that in vivo triggers of necroptosis might include a transient lack of O-2.
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