Linked Life Data

2516306

Source:http://linkedlifedata.com/resource/pubmed/id/2516306

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1990-3-21
pubmed:abstractText
ATP-sensitive K-channels in the cloned beta-cell line HIT T15 were studied by patch-clamp methods; by measurement of 86Rb efflux; and by [3H]glibenclamide binding to isolated membrane preparations. In inside-out patches a 50 pS K-channel was found which was blocked by ATP or tolbutamide applied to the intracellular membrane surface. A minimum estimate of about 500 channels per beta-cell was obtained by combining whole-cell and single-channel data. The rate of efflux of 86Rb from 86RbCl-loaded HIT cells was markedly increased by intracellular ATP-depletion; 86Rb-efflux was progressively inhibited by increasing concentrations of glibenclamide or tolbutamide. In non-ATP-depleted cells, diazoxide elicited a concentration-dependent stimulation of 86Rb-efflux which was completely blocked by 1 microM glibenclamide. Isolated membranes showed dose-dependent saturable binding of [3H]glibenclamide to both high (Kd = 1.12 nM) and low (Kd = 136 nM) affinity binding sites. We estimate about 5000 high-affinity binding sites per cell. [3H]-glibenclamide binding was inhibited by tolbutamide (IC50 = 125 microM) but was not affected by diazoxide. ADP (0.5 or 1.0 mM) markedly reduced binding; other nucleotides tested were ineffective.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0031-6768
pubmed:author
pubmed:issnType
Print
pubmed:volume
415
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
47-55
pubmed:dateRevised
2009-9-29
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
ATP-sensitive K-channels in HIT T15 beta-cells studied by patch-clamp methods, 86Rb efflux and glibenclamide binding.
pubmed:affiliation
Nuffield Department of Clinical Biochemistry, John Radcliffe Hospital, Headington, Oxford, Great Britain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't