Linked Life Data

1371120

Source:http://linkedlifedata.com/resource/pubmed/id/1371120

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1992-3-17
pubmed:abstractText
Glucocorticoid regulatory elements, denoted GREs and delayed secondary GREs (sGREs), bind the purified glucocorticoid receptors via distinctive sequence motifs and confer a primary and delayed secondary hormone inducibility, respectively, upon a linked reporter construct in stably transfected mammalian cells. The delayed secondary responses, but not the primary responses, are preceded by a time lag of several hours and blocked by protein synthesis inhibitors. In this report, we further characterized and distinguished these hormonal inductions. A 206-base pair DNA fragment from the hepatic rat alpha 2u-globulin (RUG) gene, containing at least two delayed sGREs, was specifically activated by glucocorticoids in a dose-dependent manner via a process which is sensitive to receptor antagonist RU486. Delayed sGRE-stimulated production of correctly initiated transcripts was preceded by a time lag of 2 h, a time when the GRE-mediated induction had reached maximal levels. A pulse of glucocorticoids sustained maximal activation of the delayed secondary response but not the primary response. In fact, hormone withdrawal triggered a premature induction of this delayed secondary response, suggesting that delayed sGREs are under both negative and positive control of the hormone receptor. Two separable elements of the 206-base pair fragment, including the 29-base pair sequence of a single receptor binding site, activated the reporter expression as effectively with transient, pulsatile exposure to hormone as with continuous exposure. Our results suggest that the information content of a hormonal pulse is retained, or "memorized," more persistently by a receptor binding site of delayed sGREs than those of the prototypical GREs.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
267
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3490-7
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:1371120-Alpha-Globulins, pubmed-meshheading:1371120-Animals, pubmed-meshheading:1371120-Cell Line, pubmed-meshheading:1371120-Chloramphenicol O-Acetyltransferase, pubmed-meshheading:1371120-Dexamethasone, pubmed-meshheading:1371120-Female, pubmed-meshheading:1371120-Gene Expression Regulation, pubmed-meshheading:1371120-Glucocorticoids, pubmed-meshheading:1371120-Kinetics, pubmed-meshheading:1371120-Liver, pubmed-meshheading:1371120-Mammary Tumor Virus, Mouse, pubmed-meshheading:1371120-Mice, pubmed-meshheading:1371120-Mifepristone, pubmed-meshheading:1371120-Rats, pubmed-meshheading:1371120-Recombinant Fusion Proteins, pubmed-meshheading:1371120-Regulatory Sequences, Nucleic Acid, pubmed-meshheading:1371120-Thymidine Kinase, pubmed-meshheading:1371120-Thyroid Hormones, pubmed-meshheading:1371120-Transcription, Genetic, pubmed-meshheading:1371120-Transcriptional Activation, pubmed-meshheading:1371120-Transfection
pubmed:year
1992
pubmed:articleTitle
Hormone withdrawal triggers a premature and sustained gene activation from delayed secondary glucocorticoid response elements.
pubmed:affiliation
E. A. Doisy Department of Biochemistry and Molecular Biology, Saint Louis University School of Medicine, Missouri 63104.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't