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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1982-9-24
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pubmed:abstractText |
After 5 days of incubation with 10 nM tritiated dexamethasone, the amount of glucocorticoid displaceably-bound by the ACTH-secreting, glucocorticoid-responsive AtT-20 mouse pituitary tumor cell decreases by 70-80%. This decrease takes place in both the cytosolic and nuclear fractions. Although one might predict that there should be a decrease in agonist efficacy associated with this loss of nuclear binding, there was not; long-term incubations with dexamethasone revealed that the AtT-20 cells showed no tendency to resume secreting ACTH. Hence, although there was a dramatic decrease in the amount of nuclear-bound steroid, there was not a resulting decrease in the steroid's biopotency. These results suggest that the agonist-induced decrease in receptor content is either a means of removing redundant nuclear receptors, or a new, previously unrecognized, step in the mechanism of glucocorticoid hormone action.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0013-7227
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
111
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
699-702
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:6284490-Adrenocorticotropic Hormone,
pubmed-meshheading:6284490-Animals,
pubmed-meshheading:6284490-Cell Line,
pubmed-meshheading:6284490-Cell Nucleus,
pubmed-meshheading:6284490-Dexamethasone,
pubmed-meshheading:6284490-Mice,
pubmed-meshheading:6284490-Pituitary Neoplasms,
pubmed-meshheading:6284490-Receptors, Glucocorticoid,
pubmed-meshheading:6284490-Receptors, Steroid,
pubmed-meshheading:6284490-Time Factors
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pubmed:year |
1982
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pubmed:articleTitle |
Dissociation between the magnitude of nuclear binding and the biopotency of glucocorticoids.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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