Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1996-2-21
pubmed:abstractText
ATP-sensitive K+ (KATP) channels play a key role in stimulus-secretion coupling in pancreatic beta-cells. Recent studies have shown that the beta-cell KATP channel comprises two subunits: a novel member of the inwardly rectifying K+ channel family, designated BIR and expressed at highest levels in pancreatic islets, and the sulfonylurea receptor (SUR). Moreover, the genes encoding these two proteins are adjacent to one another on human chromosome 11. Genetic factors contribute to the development of NIDDM, and it seems likely that mutations in genes encoding proteins involved in insulin secretion or action may contribute to NIDDM susceptibility. The present study examined the contribution of the linked BIR and SUR genes to the development of NIDDM. These genes were localized to the same yeast artificial chromosome as two microsatellite DNA polymorphisms, D11S902 and D11S921. These microsatellite DNA polymorphisms were typed in 140 Japanese NIDDM-affected sib pairs. There was no evidence for linkage between these markers and NIDDM, suggesting that genetic variation in the BIR and SUR genes does not play a major role in susceptibility to NIDDM in Japanese.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
267-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Identification of microsatellite markers near the human genes encoding the beta-cell ATP-sensitive K+ channel and linkage studies with NIDDM in Japanese.
pubmed:affiliation
Diabetes Center, Tokyo Women's Medical College, Japan.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't