Linked Life Data

7894339

Source:http://linkedlifedata.com/resource/pubmed/id/7894339

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1995-4-21
pubmed:abstractText
The corticosteroid receptors, including the glucocorticoid and mineralocorticoid receptors (GR and MR, respectively), are subject to ligand-mediated autoregulation like other members of the steroid receptor gene superfamily. Since it is the level of expression of these closely related intracellular receptors that determines cellular sensitivity to adrenal glucocorticoid and mineralocorticoid hormones, homologous as well as potential heterologous regulation of GR and MR levels constitute physiologically important homeostatic events. Although these autoregulatory responses are often exhibited in the form of receptor down-regulation (negative autoregulation), hormone-mediated up-regulation (positive autoregulation) has also been documented. Clearly, the extent as well as direction of hormone-mediated autoregulation of corticosteroid receptors vary considerably between different target tissues and cell types and may be altered during development or as a consequence of aging or disease state. Although historically the homologous as well as heterologous regulation of GR and MR were evaluated exclusively at the ligand binding levels, the cloning of the genes for these corticosteroid receptors has facilitated detailed analysis of hormonal regulation at the message and protein levels. Data generated in numerous laboratories have demonstrated that this regulation may be mediated at one or more molecular levels, including: the transcriptional level, as evidenced by the ability of ligand-receptor complexes to decrease the rate of receptor gene transcription; the posttranscriptional level, as evidenced by the ability of some ligands to alter the stability of their own receptor message; and at the posttranslational level, as evidenced by the ability of agonists to shorten the half-life of their own receptor protein. In this review we have focused on several basic questions (how, when, where, and why?) concerning this hormonal regulation of corticosteroid receptors. Clearly, many of these key questions concerning autoregulation of GR and MR levels remain unanswered and further studies in this area will enhance our understanding of the mechanisms involved in these cellular events.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1052-8040
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
229-57
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Autoregulation of corticosteroid receptors. How, when, where, and why?
pubmed:affiliation
Department of Physiology and Biophysics, University of Iowa, Iowa City 52242.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't