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Mitochondrial apoptosis is dispensable for NLRP3 inflammasome activation but non-apoptotic caspase-8 is required for inflammasome priming

A current paradigm proposes that mitochondrial damage is a critical determinant of NLRP3 inflammasome activation. Here, we genetically assess whether mitochondrial signalling represents a unified mechanism to explain how NLRP3 is activated by divergent stimuli. Neither co-deletion of the essential e...

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Detalhes bibliográficos
Main Authors: Allam, Ramanjaneyulu, Lawlor, Kate E, Yu, Eric Chi-Wang, Mildenhall, Alison L, Moujalled, Donia M, Lewis, Rowena S, Ke, Francine, Mason, Kylie D, White, Michael J, Stacey, Katryn J, Strasser, Andreas, O’Reilly, Lorraine A, Alexander, Warren, Kile, Benjamin T, Vaux, David L, Vince, James E
Formato: Artigo
Idioma:Inglês
Publicado em: BlackWell Publishing Ltd 2014
Assuntos:
Acesso em linha:https://ncbi.nlm.nih.gov/pmc/articles/PMC4198042/
https://ncbi.nlm.nih.gov/pubmed/24990442
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.15252/embr.201438463
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