| Literature DB >> 17335870 |
Armando van der Horst1, Jolanda M Schavemaker, Wendy Pellis-van Berkel, Boudewijn M T Burgering.
Abstract
In yeast, increasing the copy number of the nicotinamide adenine dinucleotide (NAD)-dependent deacetylase Sir2 extends lifespan, which can be inhibited by nicotinamide (Nam), the end-product of Sir2-mediated NAD-breakdown. Furthermore, the yeast pyrazinamidase/nicotinamidase PNC-1 can extend yeast lifespan by converting Nam. In Caenorhabditis elegans (C. elegans), increased dosage of the gene encoding SIR-2.1 also increases lifespan. Here, we report that knockdown of the C. elegans homologue of yeast PNC-1 as well as growing worms on Nam-containing medium significantly decreases adult lifespan. Accordingly, increased gene dosage of pnc-1 increases adult survival under conditions of oxidative stress. These data show for the first time the involvement of PNC-1/Nam in the survival of a multicellular organism and may also contribute to our understanding of lifespan regulation in mammals.Entities:
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Year: 2007 PMID： 17335870 DOI： 10.1016/j.mad.2007.01.004
Source DB: PubMed Journal: Mech Ageing Dev ISSN： 0047-6374 Impact factor: 5.432