Linked Life Data

8776735

Source:http://linkedlifedata.com/resource/pubmed/id/8776735

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1996-12-30
pubmed:abstractText
Stably transfected human kidney 293 cells expressing the wild type rat LH/CG receptor (rLHR) or receptors with C-terminal tails truncated at residues 653, 631, or 628 (designated rLHR-t653, rLHR-t631, and rLHR-t628) were used to probe the importance of this region on the regulation of hormonal responsiveness. The chosen cells line express comparable densities of cell surface rLHR, bind human CG (hCG) with high affinity, and respond to hCG with increases in cAMP and inositol phosphate accumulation. Cells expressing rLHR-wt or rLHR-t653 responded to hCG, or phorbol 12-myristate-13-acetate (PMA) stimulation with a similar increase in rLHR phosphorylation. Neither of these two stimuli increased rLHR phosphorylation in cells expressing rLHR-t631 or rLHR-t628, however. The cell line expressing rLHR-t653, the phosphorylation-positive receptor mutant, desensitized normally in response to PMA or hCG stimulation. This truncated form of rLHR also was down-regulated normally in response to hCG stimulation. In contrast, the cell lines expressing rLHR-t631 or rLHR-t628, the two phosphorylation-negative receptor mutants, showed a delay in the early phase of hCG-induced desensitization, a complete loss of PMA-induced desensitization, and an increase in the rate of hCG-induced receptor down-regulation. These results clearly show that residues 632-653 in the C-terminal tail of the rLHR are involved in PMA-induced desensitization, hCG-induced de-sensitization, and hCG-induced down-regulation. These results also establish a positive correlation between rLHR phosphorylation and desensitization and a negative correlation between rLHR phosphorylation and down-regulation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0888-8809
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
748-59
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Progressive cytoplasmic tail truncations of the lutropin-choriogonadotropin receptor prevent agonist- or phorbol ester-induced phosphorylation, impair agonist- or phorbol ester-induced desensitization, and enhance agonist-induced receptor down-regulation.
pubmed:affiliation
Department of Pharmacology, University of Iowa, College of Medicine Iowa City 52242-1109, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't