GLUCOCORTICOID AND MINERALOCORTICOID RECEPTORS: Biology and Clinical Relevance
Mineralocorticoid and glucocorticoid receptors act as homodimers via canonical pentadecamer hormone response elements to regulate transcription. Glucocorticoid, but as yet not mineralocorticoid, receptors have been shown also to modulate AP-1- and NFκB-induced transcription by direct protein-protein...
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| Veröffentlicht in: | Annual review of medicine 1997-01, Vol.48 (1), p.231-240 |
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| container_title | Annual review of medicine |
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| creator | Funder, MD, John W |
| description | Mineralocorticoid and glucocorticoid receptors act as homodimers via
canonical pentadecamer hormone response elements to regulate transcription.
Glucocorticoid, but as yet not mineralocorticoid, receptors have been shown
also to modulate AP-1- and NFκB-induced transcription by direct
protein-protein interactions. The role of 11β-hydroxysteroid dehydrogenase
in conferring aldosterone specificity on epithelial mineralocorticoid receptors
has been proven by the demonstration of sequence mutations in all cases of
apparent mineralocorticoid excess examined to date. The autosomal form of
aldosterone resistance (pseudohypoaldosteronism) has been shown to reflect
loss-of-function mutations in epithelial sodium channel subunit sequence.
(Patho)physiological roles for aldosterone and glucocorticoid membrane
receptors, and for the recently described nuclear receptors for
11-ketosteroids in 11β-hydroxysteroid
dehydrogenase-protected epithelia, remain to be established. |
| doi_str_mv | 10.1146/annurev.med.48.1.231 |
| format | Article |
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canonical pentadecamer hormone response elements to regulate transcription.
Glucocorticoid, but as yet not mineralocorticoid, receptors have been shown
also to modulate AP-1- and NFκB-induced transcription by direct
protein-protein interactions. The role of 11β-hydroxysteroid dehydrogenase
in conferring aldosterone specificity on epithelial mineralocorticoid receptors
has been proven by the demonstration of sequence mutations in all cases of
apparent mineralocorticoid excess examined to date. The autosomal form of
aldosterone resistance (pseudohypoaldosteronism) has been shown to reflect
loss-of-function mutations in epithelial sodium channel subunit sequence.
(Patho)physiological roles for aldosterone and glucocorticoid membrane
receptors, and for the recently described nuclear receptors for
11-ketosteroids in 11β-hydroxysteroid
dehydrogenase-protected epithelia, remain to be established.</description><identifier>ISSN: 0066-4219</identifier><identifier>EISSN: 1545-326X</identifier><identifier>DOI: 10.1146/annurev.med.48.1.231</identifier><identifier>PMID: 9046958</identifier><identifier>CODEN: ARMCAH</identifier><language>eng</language><publisher>Palo Alto, CA 94303-0139: Annual Reviews</publisher><subject>11-HSD2 ; Adrenals. Adrenal axis. Renin-angiotensin system (diseases) ; Aldosterone - physiology ; Animals ; AP-1 ; apparent mineralocorticoid excess ; Biological and medical sciences ; DNA Mutational Analysis ; Endocrinopathies ; Gene Expression - physiology ; hormone response elements ; Humans ; Medical sciences ; Mice ; NF-kappa B - genetics ; NFκB ; Non tumoral diseases. Target tissue resistance. Benign neoplasms ; nonclassical receptors ; pseudohypoaldosteronism ; Receptors, Glucocorticoid - genetics ; Receptors, Glucocorticoid - physiology ; Receptors, Mineralocorticoid - genetics ; Receptors, Mineralocorticoid - physiology ; Transcription Factor AP-1 - genetics</subject><ispartof>Annual review of medicine, 1997-01, Vol.48 (1), p.231-240</ispartof><rights>Copyright © 1997 by Annual Reviews Inc. All rights reserved</rights><rights>1997 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-a447t-7349515f6998c16a834c99e7733950f06a54a9dc39a900b7f7ed7131b7d5f1403</citedby><cites>FETCH-LOGICAL-a447t-7349515f6998c16a834c99e7733950f06a54a9dc39a900b7f7ed7131b7d5f1403</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.annualreviews.org/content/journals/10.1146/annurev.med.48.1.231?crawler=true&mimetype=application/pdf$$EPDF$$P50$$Gannualreviews$$H</linktopdf><linktohtml>$$Uhttps://www.annualreviews.org/content/journals/10.1146/annurev.med.48.1.231$$EHTML$$P50$$Gannualreviews$$H</linktohtml><link.rule.ids>70,314,780,784,4182,27924,27925,78254,78255</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2589329$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9046958$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Funder, MD, John W</creatorcontrib><title>GLUCOCORTICOID AND MINERALOCORTICOID RECEPTORS: Biology and Clinical Relevance</title><title>Annual review of medicine</title><addtitle>Annu Rev Med</addtitle><description>Mineralocorticoid and glucocorticoid receptors act as homodimers via
canonical pentadecamer hormone response elements to regulate transcription.
Glucocorticoid, but as yet not mineralocorticoid, receptors have been shown
also to modulate AP-1- and NFκB-induced transcription by direct
protein-protein interactions. The role of 11β-hydroxysteroid dehydrogenase
in conferring aldosterone specificity on epithelial mineralocorticoid receptors
has been proven by the demonstration of sequence mutations in all cases of
apparent mineralocorticoid excess examined to date. The autosomal form of
aldosterone resistance (pseudohypoaldosteronism) has been shown to reflect
loss-of-function mutations in epithelial sodium channel subunit sequence.
(Patho)physiological roles for aldosterone and glucocorticoid membrane
receptors, and for the recently described nuclear receptors for
11-ketosteroids in 11β-hydroxysteroid
dehydrogenase-protected epithelia, remain to be established.</description><subject>11-HSD2</subject><subject>Adrenals. Adrenal axis. Renin-angiotensin system (diseases)</subject><subject>Aldosterone - physiology</subject><subject>Animals</subject><subject>AP-1</subject><subject>apparent mineralocorticoid excess</subject><subject>Biological and medical sciences</subject><subject>DNA Mutational Analysis</subject><subject>Endocrinopathies</subject><subject>Gene Expression - physiology</subject><subject>hormone response elements</subject><subject>Humans</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>NF-kappa B - genetics</subject><subject>NFκB</subject><subject>Non tumoral diseases. Target tissue resistance. Benign neoplasms</subject><subject>nonclassical receptors</subject><subject>pseudohypoaldosteronism</subject><subject>Receptors, Glucocorticoid - genetics</subject><subject>Receptors, Glucocorticoid - physiology</subject><subject>Receptors, Mineralocorticoid - genetics</subject><subject>Receptors, Mineralocorticoid - physiology</subject><subject>Transcription Factor AP-1 - genetics</subject><issn>0066-4219</issn><issn>1545-326X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkF1PgzAUhhujmfPjH2jChfEObGlLW-8mw0kyh8Et8a7poBgMg0nHzP69XYbGS69Oct7nnNM-AFwh6CFEgjtV112rt95K5x7hHvJ8jI7AEFFCXewHb8dgCGEQuMRH4hScGfMBIRQY8wEYCEgCQfkQzCbTRZiESTqPwyQeO6PZ2HmOZ1E6mv7pplEYvcyT9PXeeSibqnnfOarOnbAq6zJTlZPqSm9VnekLcFKoyujLvp6DxWM0D5_caTKJw9HUVYSwjcswERTRIhCCZyhQHJNMCM0YxoLCAgaKEiXyDAslIFyygumcIYyWLKcFIhCfg9vD3nXbfHbabOSqNJmuKlXrpjOScU4xxMSC5ABmbWNMqwu5bsuVancSQbnXKHuN0mqUhEskrUY7dt3v75b74Geo92bzmz5XxgooWvv50vxiPuUC-8Ji4oDtj6jKnin1l_nfE74Bg4eNDQ</recordid><startdate>19970101</startdate><enddate>19970101</enddate><creator>Funder, MD, John W</creator><general>Annual Reviews</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19970101</creationdate><title>GLUCOCORTICOID AND MINERALOCORTICOID RECEPTORS: Biology and Clinical Relevance</title><author>Funder, MD, John W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-a447t-7349515f6998c16a834c99e7733950f06a54a9dc39a900b7f7ed7131b7d5f1403</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>11-HSD2</topic><topic>Adrenals. Adrenal axis. Renin-angiotensin system (diseases)</topic><topic>Aldosterone - physiology</topic><topic>Animals</topic><topic>AP-1</topic><topic>apparent mineralocorticoid excess</topic><topic>Biological and medical sciences</topic><topic>DNA Mutational Analysis</topic><topic>Endocrinopathies</topic><topic>Gene Expression - physiology</topic><topic>hormone response elements</topic><topic>Humans</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>NF-kappa B - genetics</topic><topic>NFκB</topic><topic>Non tumoral diseases. Target tissue resistance. Benign neoplasms</topic><topic>nonclassical receptors</topic><topic>pseudohypoaldosteronism</topic><topic>Receptors, Glucocorticoid - genetics</topic><topic>Receptors, Glucocorticoid - physiology</topic><topic>Receptors, Mineralocorticoid - genetics</topic><topic>Receptors, Mineralocorticoid - physiology</topic><topic>Transcription Factor AP-1 - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Funder, MD, John W</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Annual review of medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Funder, MD, John W</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>GLUCOCORTICOID AND MINERALOCORTICOID RECEPTORS: Biology and Clinical Relevance</atitle><jtitle>Annual review of medicine</jtitle><addtitle>Annu Rev Med</addtitle><date>1997-01-01</date><risdate>1997</risdate><volume>48</volume><issue>1</issue><spage>231</spage><epage>240</epage><pages>231-240</pages><issn>0066-4219</issn><eissn>1545-326X</eissn><coden>ARMCAH</coden><abstract>Mineralocorticoid and glucocorticoid receptors act as homodimers via
canonical pentadecamer hormone response elements to regulate transcription.
Glucocorticoid, but as yet not mineralocorticoid, receptors have been shown
also to modulate AP-1- and NFκB-induced transcription by direct
protein-protein interactions. The role of 11β-hydroxysteroid dehydrogenase
in conferring aldosterone specificity on epithelial mineralocorticoid receptors
has been proven by the demonstration of sequence mutations in all cases of
apparent mineralocorticoid excess examined to date. The autosomal form of
aldosterone resistance (pseudohypoaldosteronism) has been shown to reflect
loss-of-function mutations in epithelial sodium channel subunit sequence.
(Patho)physiological roles for aldosterone and glucocorticoid membrane
receptors, and for the recently described nuclear receptors for
11-ketosteroids in 11β-hydroxysteroid
dehydrogenase-protected epithelia, remain to be established.</abstract><cop>Palo Alto, CA 94303-0139</cop><cop>4139 El Camino Way, P.O. Box 10139</cop><cop>USA</cop><pub>Annual Reviews</pub><pmid>9046958</pmid><doi>10.1146/annurev.med.48.1.231</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
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| ispartof | Annual review of medicine, 1997-01, Vol.48 (1), p.231-240 |
| issn | 0066-4219 1545-326X |
| language | eng |
| recordid | cdi_proquest_miscellaneous_78853034 |
| source | Annual Reviews Complete A-Z List; MEDLINE |
| subjects | 11-HSD2 Adrenals. Adrenal axis. Renin-angiotensin system (diseases) Aldosterone - physiology Animals AP-1 apparent mineralocorticoid excess Biological and medical sciences DNA Mutational Analysis Endocrinopathies Gene Expression - physiology hormone response elements Humans Medical sciences Mice NF-kappa B - genetics NFκB Non tumoral diseases. Target tissue resistance. Benign neoplasms nonclassical receptors pseudohypoaldosteronism Receptors, Glucocorticoid - genetics Receptors, Glucocorticoid - physiology Receptors, Mineralocorticoid - genetics Receptors, Mineralocorticoid - physiology Transcription Factor AP-1 - genetics |
| title | GLUCOCORTICOID AND MINERALOCORTICOID RECEPTORS: Biology and Clinical Relevance |
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