Necroptosis
Necroptosis also known as programmed necrosis is a mechanism that regulates cell death. Necrotic cell death has been considered a form of passive cell death. However, the discovery that TNFalpha mediated necrosis can be inhibited by a specific inhibitor of RIP1 kinase, necrostatin-1, led to the concept of necroptosis Cite error: A <ref> tag is missing the closing </ref> (see the help page).
Under conditions that are insufficient to trigger apoptosis, TNFα activates TNFR1 and in turn induces recruitment of RIP1 kinase and other proteins to form complex I. Subsequently, these proteins dissociate from TNFR1 and RIP1 can be found in the cytosol in complex IIb, which includes RIP1, RIP3, caspase 8 and FADD. The formation of complex IIb leads to necroptosis.[1]
Necroptosis plays a role in various pathological forms of cell death, including ischemic brain injury, neurodegenerative diseases and viral infections.[2]
References
- ^ Cite error: The named reference
pmid20045303was invoked but never defined (see the help page). - ^ Dunai, Z (2011). "Necroptosis: biochemical, physiological and pathological aspects". Pathol. Oncol. Res.: POR. 17 (4): 791–800. PMID 21773880.
{{cite journal}}: Unknown parameter|coauthors=ignored (|author=suggested) (help); Unknown parameter|month=ignored (help)
 | This molecular or cell biology article is a stub. You can help Wikipedia by expanding it. |