| Literature DB >> 10556969 |
L Liu1, J S Stamler.
Abstract
Nitric oxide (NO) or related molecules of both endogenous and exogenous origin inhibit programmed cell death in a variety of cells and tissues. This general protective function is largely independent of the apoptotic stimulus. S-nitrosylation of the catalytic-site cysteine of caspases is a well-established and possibly widespread mechanism of enzyme inhibition that protects from cell death. However, NO may inhibit apoptosis by additional mechanisms. The physiological and pathological significance of NO's anti-apoptotic activity remains to be determined in most cases.Entities:
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Year: 1999 PMID: 10556969 DOI: 10.1038/sj.cdd.4400578
Source DB: PubMed Journal: Cell Death Differ ISSN: 1350-9047 Impact factor: 15.828