Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1997-6-17
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-3042
pubmed:author
pubmed:issnType
Print
pubmed:volume
68
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2308-16
pubmed:dateRevised
2006-11-15
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
pubmed:year
1997
pubmed:articleTitle
Regulation of corticotropin-releasing factor receptor function in human Y-79 retinoblastoma cells: rapid and reversible homologous desensitization but prolonged recovery.
pubmed:affiliation
Department of Molecular Neuroendocrinology, Max Planck Institute for Experimental Medicine, Goettingen, Germany.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't