NOD Signaling and Cell Death

Frontiers in Cell and Developmental Biology

Valentin J. Heim¹  Ueli Nachbur¹  Che A. Stafford² 

[1] Department of Medical Biology, University of Melbourne, Melbourne, VIC, Australia;Gene Center and Department of Biochemistry, Ludwig-Maximilians-Universität München, Munich, Germany;The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia;

关键词: RIPK2;    NOD2;    ubiquitin;    inflammation;    cell signaling;   

DOI  :  10.3389/fcell.2019.00208

来源: DOAJ

【 摘 要 】

Innate immune signaling and programmed cell death are intimately linked, and many signaling pathways can regulate and induce both, transcription of inflammatory mediators or autonomous cell death. The best-characterized examples for these dual outcomes are members of the TNF superfamily, the inflammasome receptors, and the toll-like receptors. Signaling via the intracellular peptidoglycan receptors NOD1 and NOD2, however, does not appear to follow this trend, despite involving signaling proteins, or proteins with domains that are linked to programmed cell death, such as RIP kinases, inhibitors of apoptosis (IAP) proteins or the CARD domains on NOD1/2. To better understand the connections between NOD signaling and cell death induction, we here review the latest findings on the molecular regulation of signaling downstream of the NOD receptors and explore the links between this immune signaling pathway and the regulation of cell death.

【 授权许可】

Unknown