Linked Life Data

8102365

Source:http://linkedlifedata.com/resource/pubmed/id/8102365

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
23
pubmed:dateCreated
1993-9-15
pubmed:abstractText
Purified Gs is a substrate for ADP-ribosylation catalyzed by cholera toxin (CTx). In S49 cyc- membranes complemented with in vitro translated Gs alpha, the beta-adrenergic agonist isoproterenol enhanced the ADP-ribosylation rate. This effect was maximal if all guanyl nucleotides were suppressed but was blocked by the beta-adrenergic antagonist alprenolol. Enhancement was partially diminished if addition of GDP followed that of isoproterenol. When added in the absence of agonist, the GTP analogues guanosine 5'-O-(gamma-thiotriphosphate) and guanosine 5'-(beta, gamma-imido)triphosphate potentiated CTx-catalyzed ADP-ribosylation of Gs alpha consistent with their activating ADP-ribosylation factors. However, this effect was lessened when the same nucleotides were tested in the presence of agonist. Taken altogether, these results indicate that like Gt and Gi, Gs is an optimal substrate for CTx when coupled to an agonist-activated receptor and depleted of nucleotide. Therefore, coupling to the receptor and subsequent departure of the GDP turn out to be the common features underlying the sensitivity of all GTP-binding proteins to CTx-catalyzed ADP-ribosylation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
268
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
17026-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
ADP-ribosylation of Gs by cholera toxin is potentiated by agonist activation of beta-adrenergic receptors in the absence of GTP.
pubmed:affiliation
Centre National de la Recherche Scientifique, Institut de Pharmacologie Moléculaire et Cellulaire, Valbonne, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't