| http://purl.uniprot.org/citations/11901108 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/11901108 | http://www.w3.org/2000/01/rdf-schema#comment | "The Sir2 protein is an NAD(+)-dependent protein deacetylase that is required for silencing at the silent mating-type loci, telomeres, and the ribosomal DNA (rDNA). Mutations in the NAD(+) salvage gene NPT1 weaken all three forms of silencing and also cause a reduction in the intracellular NAD(+) level. We now show that mutation of a highly conserved histidine residue in Npt1p results in a silencing defect, indicating that Npt1p enzymatic activity is required for silencing. Deletion of another NAD(+) salvage pathway gene called PNC1 caused a less severe silencing defect and did not significantly reduce the intracellular NAD(+) concentration. However, silencing in the absence of PNC1 was completely dependent on the import of nicotinic acid from the growth medium. Deletion of a gene in the de novo NAD(+) synthesis pathway BNA1 resulted in a significant rDNA silencing defect only on medium deficient in nicotinic acid, an NAD(+) precursor. By immunofluorescence microscopy, Myc-tagged Bna1p was localized throughout the whole cell in an asynchronously growing population. In contrast, Myc-tagged Npt1p was highly concentrated in the nucleus in approximately 40% of the cells, indicating that NAD(+) salvage occurs in the nucleus in a significant fraction of cells. We propose a model in which two components of the NAD(+) salvage pathway, Pnc1p and Npt1p, function together in recycling the nuclear nicotinamide generated by Sir2p deacetylase activity back into NAD(+)."xsd:string |
| http://purl.uniprot.org/citations/11901108 | http://purl.org/dc/terms/identifier | "doi:10.1093/genetics/160.3.877"xsd:string |
| http://purl.uniprot.org/citations/11901108 | http://purl.uniprot.org/core/author | "Boeke J.D."xsd:string |
| http://purl.uniprot.org/citations/11901108 | http://purl.uniprot.org/core/author | "Celic I."xsd:string |
| http://purl.uniprot.org/citations/11901108 | http://purl.uniprot.org/core/author | "Smith J.S."xsd:string |
| http://purl.uniprot.org/citations/11901108 | http://purl.uniprot.org/core/author | "Sandmeier J.J."xsd:string |
| http://purl.uniprot.org/citations/11901108 | http://purl.uniprot.org/core/date | "2002"xsd:gYear |
| http://purl.uniprot.org/citations/11901108 | http://purl.uniprot.org/core/name | "Genetics"xsd:string |
| http://purl.uniprot.org/citations/11901108 | http://purl.uniprot.org/core/pages | "877-889"xsd:string |
| http://purl.uniprot.org/citations/11901108 | http://purl.uniprot.org/core/title | "Telomeric and rDNA silencing in Saccharomyces cerevisiae are dependent on a nuclear NAD(+) salvage pathway."xsd:string |
| http://purl.uniprot.org/citations/11901108 | http://purl.uniprot.org/core/volume | "160"xsd:string |
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