Linked Life Data

19149601

Source:http://linkedlifedata.com/resource/pubmed/id/19149601

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2009-1-19
pubmed:abstractText
The intersection between regulatory pathways responsive to metabolic fluctuation on one hand, and to cellular stress on the other, is a fascinating area within which NAD/NADH responsive proteins play a major role [1, 2]. A key player amongst these is SIRT1, a member of the mammalian sirtuin family (SIRT1-7). SIRT1 is an NAD-dependent deacetylase with critical functions in the maintenance of homeostasis and cell survival. In this review I shall focus upon (i) the cellular regulation of SIRT1 expression and (ii) the cellular regulation of SIRT1 activity. In addition the distinction between basal and stress-induced functions will be addressed: do they simply reflect a sliding scale of response, or are they mechanistically distinct? Elevated levels of SIRT1 are evident in cancer and SIRT1 can function as a cancer-specific survival factor in human cell lines. However, in a mouse model SIRT1 is reported to function as a tumour suppressor. Possible explanations for this apparent discrepancy will be considered. Given the high profile of SIRT1 as a potential therapeutic target it is clearly important to clarify its basal functioning in relation to differentiation, cell type, intercellular communication, and to age-related disease states including neurodegeneration and cancer.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1873-4286
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
39-44
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Cellular regulation of SIRT1.
pubmed:affiliation
Yorkshire Cancer Research P53 Research Unit, Department of Biology, University of York, York, UK, YO10 5DD. ajm24@york.ac.uk
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't