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TAK1 restricts spontaneous NLRP3 activation and cell death to control myeloid proliferation
The NOD-like receptor (NLR)–P3 inflammasome is a global sensor of infection and stress. Elevated NLRP3 activation levels are associated with human diseases, but the mechanisms controlling NLRP3 inflammasome activation are largely unknown. Here, we show that TGF-β activated kinase-1 (TAK1) is a centr...
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| 出版年: | J Exp Med |
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| 主要な著者: | , , , , , , |
| フォーマット: | Artigo |
| 言語: | Inglês |
| 出版事項: |
Rockefeller University Press
2018
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| 主題: | |
| オンライン･アクセス: | https://ncbi.nlm.nih.gov/pmc/articles/PMC5881469/ https://ncbi.nlm.nih.gov/pubmed/29500178 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1084/jem.20171922 |
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