Linked Life Data

15683739

Source:http://linkedlifedata.com/resource/pubmed/id/15683739

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2005-2-1
pubmed:abstractText
Despite acutely inhibiting adenylate cyclase, prolonged activation of Galpha(i/o)-coupled receptors leads to a subsequent heterologous sensitization of adenylate cyclase responsiveness. Recently, protein kinase signaling and phosphorylation have been implicated in the sensitization of adenylate cyclase type 6 (AC6). To examine the sensitization specifically of AC6, we constructed human embryonic kidney cells (HEK293) cells stably expressing AC6 and the Galpha(i/o)-coupled D2L dopamine receptor. In contrast to observations in delta-opioid-expressing Chinese hamster ovary (CHO) cells that express endogenous AC6 and AC7, neither protein kinase C (PKC) nor tyrosine kinase inhibitors attenuated D2L receptor-mediated sensitization of AC6. Inhibition of Raf1 modestly inhibited the magnitude of D2L receptor-induced sensitization of AC6; however, activation of PKC robustly enhanced D2L receptor-mediated AC6 sensitization in a Raf1-dependent manner. These data indicate that, although PKC and Raf1 are not required for sensitization, activation of the PKC-Raf1 pathway robustly potentiated D2L receptor-mediated sensitization of AC6.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0898-6568
pubmed:author
pubmed:issnType
Print
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
647-53
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Activation of a novel PKC isoform synergistically enhances D2L dopamine receptor-mediated sensitization of adenylate cyclase type 6.
pubmed:affiliation
Department of Medicinal Chemistry and Molecular Pharmacology, Purdue University, West Lafayette, IN 47907-2091, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't