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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
1997-6-17
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pubmed:abstractText |
Homologous receptor desensitization is an important regulatory response to continuous activation by agonist that involves the uncoupling of a receptor from its G protein. When human retinoblastoma Y-79 cells expressing corticotropin-releasing factor (CRF) receptors were preincubated with CRF for 10 min-4 h, a time-dependent reduction in both the peak and sensitivity of CRF-stimulated intracellular cyclic AMP (cAMP) accumulation developed with a t1/2 of 38 min and an EC50 of 6-7 nM CRF. CRF receptor desensitization was slowly reversible after a 4-h CRF preincubation with a t1/2 of 13 h and a full restoration of cAMP responsiveness to CRF at 24 h following the removal of 10 nM CRF. Because the ability of vasoactive intestinal peptide, forskolin, or (-)-isoproterenol to stimulate cAMP accumulation was not diminished in Y-79 cells desensitized with 10 nM CRF, the observed desensitization was considered to be a specific homologous action of CRF. CRF receptor desensitization was markedly attenuated by CRF receptor antagonists, which alone did not produce any appreciable reduction in CRF-stimulated cAMP accumulation. Although recent reports have demonstrated a rapid decline in steady-state levels of CRF receptor type 1 (CRF-R1) mRNA in anterior pituitary cells during several hours of exposure to CRF, there was no observed reduction in CRF-R1 mRNA levels when Y-79 cells were preincubated with 10 nM CRF for 10 min-24 h despite a rapid time- and concentration-dependent loss of CRF receptors from the retinoblastoma cell surface.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenylate Cyclase,
http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic beta-Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/Corticotropin-Releasing Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/Forskolin,
http://linkedlifedata.com/resource/pubmed/chemical/Isoproterenol,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Corticotropin-Releasing...,
http://linkedlifedata.com/resource/pubmed/chemical/Vasoactive Intestinal Peptide
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0022-3042
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
68
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2308-16
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:9166723-Adenylate Cyclase,
pubmed-meshheading:9166723-Adrenergic beta-Agonists,
pubmed-meshheading:9166723-Blotting, Northern,
pubmed-meshheading:9166723-Corticotropin-Releasing Hormone,
pubmed-meshheading:9166723-Cyclic AMP,
pubmed-meshheading:9166723-Dose-Response Relationship, Drug,
pubmed-meshheading:9166723-Forskolin,
pubmed-meshheading:9166723-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:9166723-Humans,
pubmed-meshheading:9166723-Isoproterenol,
pubmed-meshheading:9166723-Membrane Proteins,
pubmed-meshheading:9166723-RNA, Messenger,
pubmed-meshheading:9166723-Receptors, Corticotropin-Releasing Hormone,
pubmed-meshheading:9166723-Retinoblastoma,
pubmed-meshheading:9166723-Sensitivity and Specificity,
pubmed-meshheading:9166723-Time Factors,
pubmed-meshheading:9166723-Tumor Cells, Cultured,
pubmed-meshheading:9166723-Vasoactive Intestinal Peptide
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pubmed:year |
1997
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pubmed:articleTitle |
Regulation of corticotropin-releasing factor receptor function in human Y-79 retinoblastoma cells: rapid and reversible homologous desensitization but prolonged recovery.
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pubmed:affiliation |
Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, Goettingen, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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