Innate immune signaling and programmed cell death are intimately linked, andmany signaling pathways can regulate and induce both, transcription of inflammatorymediators or autonomous cell death. The best-characterized examples for these dualoutcomes are members of the TNF superfamily, the inflammasome receptors, andthe toll-like receptors. Signaling via the intracellular peptidoglycan receptors NOD1and NOD2, however, does not appear to follow this trend, despite involving signalingproteins, or proteins with domains that are linked to programmed cell death, such asRIP kinases, inhibitors of apoptosis (IAP) proteins or the CARD domains on NOD1/2. Tobetter understand the connections between NOD signaling and cell death induction, wehere review the latest findings on the molecular regulation of signaling downstream ofthe NOD receptors and explore the links between this immune signaling pathway andthe regulation of cell death.
Innate immune signaling and programmed cell death are intimately linked, and<br>many signaling pathways can regulate and induce both, transcription of inflammatory<br>mediators or autonomous cell death. The best-characterized examples for these dual<br>outcomes are members of the TNF superfamily, the inflammasome receptors, and<br>the toll-like receptors. Signaling via the intracellular peptidoglycan receptors NOD1<br>and NOD2, however, does not appear to follow this trend, despite involving signaling<br>proteins, or proteins with domains that are linked to programmed cell death, such as<br>RIP kinases, inhibitors of apoptosis (IAP) proteins or the CARD domains on NOD1/2. To<br>better understand the connections between NOD signaling and cell death induction, we<br>here review the latest findings on the molecular regulation of signaling downstream of<br>the NOD receptors and explore the links between this immune signaling pathway and<br>the regulation of cell death.
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