Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1993-7-2
pubmed:abstractText
In this study we report that a synthetic peptide of the effector domain of rab3A (rab3AL(33-48)) stimulates both amylase secretion and inositol 1,4,5-trisphosphate (IP3)-accumulation in digitonin-permeabilized pancreatic acini in an analogous way to cholecystokinin-octapeptide (CCK8). Maximum CCK8-induced IP3-accumulation was observed at five seconds after addition of CCK8 to the acini. Maximum rab3AL(33-48)-induced IP3-production occurred 15 to 30 seconds after addition of rab3AL(33-48); then the acinar IP3 content declined towards the basal level. Heparin, an inhibitor of IP3 binding to its receptor, inhibited both rab3AL(33-48)- and CCK8-stimulated amylase secretion without affecting the response to vasoactive intestinal polypeptide. rab3AL(33-48) had no effect in intact acini, indicating that the site of action of rab3AL(33-48) is intracellular. We conclude that rab-like small molecular weight GTP-binding proteins regulate phospholipase C activity and thereby amylase secretion from inside of the cell.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0006-291X
pubmed:author
pubmed:issnType
Print
pubmed:day
14
pubmed:volume
192
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1030-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
A synthetic peptide of the effector domain of rab3A stimulates inositol 1,4,5-trisphosphate production in digitonin-permeabilized pancreatic acini.
pubmed:affiliation
Department of Internal Medicine, University of Frankfurt/Main, Germany.
pubmed:publicationType
Journal Article, In Vitro