Linked Life Data

8890934

Source:http://linkedlifedata.com/resource/pubmed/id/8890934

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
18
pubmed:dateCreated
1996-11-27
pubmed:abstractText
To better understand the molecular mechanisms that underlie the exaggerated bradykinin (BK)-stimulated release of Ins(1,4,5)P3 in fibroblasts from Alzheimer patients, the role of G-proteins, protein kinase C (PKC) and cyclic AMP in BK-induced Ins(1,4,5)P3 formation was determined. A role for G-proteins in the coupling of the BK receptor to intracellular signals was indicated by guanosine 5'-(3-O-thio)triphosphate (GTP gamma S) enhanced BK-stimulated Ins(1,4,5)P3 release. The coupling of G-proteins to Ins(1,4,5)P3 formation was sensitive to cholera toxin (CTX), but not pertussis toxin (PTX), and was not altered by PKC activation. The inhibition by CTX appeared to be secondary to its ability to increase cyclic AMP, because forskolin also inhibited the BK-mediated Ins (1,4,5)P3 release. Activation of PKC with TPA diminished the number of BK receptors by 33% and proportionally decreased BK-mediated Ins(1,4,5)P3 formation by 28%. The latter response was abolished by PKC inhibitors. Depletion of PKC by prolonged TPA treatment did not further alter the number of BK receptors but further decreased the Ins(1,4,5)P3 response by 65%. Thus, changes in PKC probably do not underlie the enhanced BK-induced Ins(1,4,5)P3 formation in AD fibroblasts, because both activation and depletion of the PKC diminished the Ins(1,4,5)P3 response.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0024-3205
pubmed:author
pubmed:issnType
Print
pubmed:volume
59
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1533-43
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Regulation of bradykinin-induced Ins(1,4,5)P3 formation by protein kinase C in human fibroblasts.
pubmed:affiliation
Department of Neurology and Neuroscience, Cornell Univ. Med. Coll., Burke Med. Res. Inst., White Plains, NY 10605, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.