RIPK3 promotes cell death and NLRP3 inflammasome activation in the absence of MLKL

RIPK3 and its substrate MLKL are essential for necroptosis, a lytic cell death proposed to cause inflammation via the release of intracellular molecules. Whether and how RIPK3 might drive inflammation in a manner independent of MLKL and cell lysis remains unclear. Here we show that following LPS tre...

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Detaylı Bibliyografya
Yayımlandı:Nat Commun
Asıl Yazarlar: Lawlor, Kate E., Khan, Nufail, Mildenhall, Alison, Gerlic, Motti, Croker, Ben A., D’Cruz, Akshay A., Hall, Cathrine, Kaur Spall, Sukhdeep, Anderton, Holly, Masters, Seth L., Rashidi, Maryam, Wicks, Ian P., Alexander, Warren S., Mitsuuchi, Yasuhiro, Benetatos, Christopher A., Condon, Stephen M., Wong, W. Wei-Lynn, Silke, John, Vaux, David L., Vince, James E.
Materyal Türü: Artigo
Dil:Inglês
Baskı/Yayın Bilgisi: Nature Pub. Group 2015
Konular:
Article
Online Erişim:https://ncbi.nlm.nih.gov/pmc/articles/PMC4346630/
https://ncbi.nlm.nih.gov/pubmed/25693118
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1038/ncomms7282
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