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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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| Main Authors: | , , , , , , , , , , , , , , , |
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| Formato: | Artigo |
| Idioma: | Inglês |
| Publicado em: |
BlackWell Publishing Ltd
2014
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| 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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