期刊
JOURNAL OF IMMUNOLOGY
卷 178, 期 3, 页码 1256-1260出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.178.3.1256
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资金
- NIAID NIH HHS [T32-AI007273-22, AI063031] Funding Source: Medline
- NIDCR NIH HHS [DE016326] Funding Source: Medline
- NIDDK NIH HHS [DK38108] Funding Source: Medline
CATERPILLER (NOD, NBD-LRR) proteins are rapidly emerging as important mediators of innate and adaptive immunity. Among these, Monarch-1 operates as a novel attenuating factor of inflammation by suppressing inflammatory responses in activated monocytes. However, the molecular mechanisms by which Monarch-1 performs this important function are not well understood. In this report, we show that Monarch-1 inhibits CD40-mediated activation of NF-kappa B via the non-canonical pathway in human monocytes. This inhibition stems from the ability of Monarch-1 to associate with and induce proteasome-mediated degradation of NF-kappa B inducing kinase. Congruently, silencing Monarch-1 with shRNA enhances the expression of p52-dependent chemokines.
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