Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5 Pt 1
pubmed:dateCreated
1994-12-7
pubmed:abstractText
Bombesin stimulates cholecystokinin (CCK) secretion, presumably by a direct effect on the intestinal CCK cell. The present objectives were to characterize bombesin-stimulated CCK release and to investigate the role of calcium in CCK secretion in an intestinal CCK-producing cell line (STC-1). Bombesin caused a dose-dependent release of CCK, which was reduced either in the absence of extracellular calcium or by calcium channel blockade, suggesting that influx of calcium is necessary for CCK secretion. Bombesin caused an increase in intracellular calcium concentration ([Ca2+]i) and increased efflux of 45Ca2+ from 45Ca(2+)-loaded cells. Radioligand binding studies and Northern analysis were consistent with the expression of a bombesin receptor. Thus bombesin stimulation of CCK release occurs via binding to a receptor and is dependent on increased [Ca2+]i. We propose that the STC-1 cell line may provide a useful model for studying the regulation of intestinal CCK secretion.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
267
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
G859-65
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Regulation of cholecystokinin secretion by bombesin in STC-1 cells.
pubmed:affiliation
Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't