期刊
PLOS ONE
卷 7, 期 7, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0041005
关键词
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资金
- Fond National de la Recherche Scientifique (FNRS, Brussels, Belgium) [3.4543.08]
- Televie program (FNRS, Brussels, Belgium) [7.4568.09, 7.4533.11F]
- Interuniversity Attraction Poles, Bruxelles, Belgium [IAP6/18, 6/18]
- Fond de la Recherche Industrielle et Agricole (FRIA - FNRS, Brussels, Belgium)
SHIP-1 is an inositol phosphatase predominantly expressed in hematopoietic cells. Over the ten past years, SHIP-1 has been described as an important regulator of immune functions. Here, we characterize a new inhibitory function for SHIP-1 in NOD2 signaling. NOD2 is a crucial cytoplasmic bacterial sensor that activates proinflammatory and antimicrobial responses upon bacterial invasion. We observed that SHIP-1 decreases NOD2-induced NF-kappa B activation in macrophages. This negative regulation relies on its interaction with XIAP. Indeed, we observed that XIAP is an essential mediator of the NOD2 signaling pathway that enables proper NF-kappa B activation in macrophages. Upon NOD2 activation, SHIP-1 C-terminal proline rich domain (PRD) interacts with XIAP, thereby disturbing the interaction between XIAP and RIP2 in order to decrease NF-kappa B signaling.
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