| First Author | Erener S | Year | 2012 |
| Journal | Mol Cell | Volume | 46 |
| Issue | 2 | Pages | 200-11 |
| PubMed ID | 22464733 | Mgi Jnum | J:188026 |
| Mgi Id | MGI:5438909 | Doi | 10.1016/j.molcel.2012.02.016 |
| Citation | Erener S, et al. (2012) Inflammasome-activated caspase 7 cleaves PARP1 to enhance the expression of a subset of NF-kappaB target genes. Mol Cell 46(2):200-11 |
| abstractText | Caspase 1 is part of the inflammasome, which is assembled upon pathogen recognition, while caspases 3 and/or 7 are mediators of apoptotic and nonapoptotic functions. PARP1 cleavage is a hallmark of apoptosis yet not essential, suggesting it has another physiological role. Here we show that after LPS stimulation, caspase 7 is activated by caspase 1, translocates to the nucleus, and cleaves PARP1 at the promoters of a subset of NF-kappaB target genes negatively regulated by PARP1. Mutating the PARP1 cleavage site D214 renders PARP1 uncleavable and inhibits PARP1 release from chromatin and chromatin decondensation, thereby restraining the expression of cleavage-dependent NF-kappaB target genes. These findings propose an apoptosis-independent regulatory role for caspase 7-mediated PARP1 cleavage in proinflammatory gene expression and provide insight into inflammasome signaling. |
