Linked Life Data

3808033

Source:http://linkedlifedata.com/resource/pubmed/id/3808033

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6102
pubmed:dateCreated
1987-2-26
pubmed:abstractText
Glucocorticoids, a class of steroid hormones, associate specifically with intracellular receptors, facilitating a conformational change that converts the receptor in vitro to a DNA-binding protein and in vivo to a nuclear species that activates a class of transcriptional enhancers termed glucocorticoid response elements (GREs). The DNA sequences recognized specifically by the hormone-receptor complex correspond directly to those required for GRE enhancement. The structural transition that accompanies steroid binding, 'receptor transformation', has been monitored by changes in receptor chromatographic properties, accessibility to monoclonal antibodies, association with other receptor subunits or with heterologous proteins, and aqueous two-phase partition coefficient. However, the significance of the structural change for the biological activity of the receptor is not understood. We have used cloned rat glucocorticoid-receptor coding sequences to produce and characterize a novel class of receptor mutants that elicit GRE enhancer function in transfected cells even in the absence of hormone. The constitutive activity of those receptor derivatives, together with mapping studies that distinguish between the DNA- and hormone-binding domains of the receptor, imply that the conformational change corresponding to receptor transformation may simply unmask pre-existing functional domains for DNA binding, enhancer activation, or both.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0028-0836
pubmed:author
pubmed:issnType
Print
pubmed:volume
325
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
365-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
Glucocorticoid receptor mutants that are constitutive activators of transcriptional enhancement.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't