3cld: Difference between revisions
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{{STRUCTURE_3cld| PDB=3cld | SCENE= }} | {{STRUCTURE_3cld| PDB=3cld | SCENE= }} | ||
===Ligand binding domain of the glucocorticoid receptor complexed with fluticazone furoate=== | |||
{{ABSTRACT_PUBMED_18522385}} | |||
=== | ==Disease== | ||
[[http://www.uniprot.org/uniprot/GCR_HUMAN GCR_HUMAN]] Defects in NR3C1 are a cause of glucocorticoid resistance (GCRES) [MIM:[http://omim.org/entry/138040 138040]]; also known as cortisol resistance. It is a hypertensive, hyperandrogenic disorder characterized by increased serum cortisol concentrations. Inheritance is autosomal dominant.<ref>PMID:12050230</ref><ref>PMID:1704018</ref><ref>PMID:7683692</ref><ref>PMID:11589680</ref><ref>PMID:11701741</ref> | |||
==Function== | |||
[[http://www.uniprot.org/uniprot/GCR_HUMAN GCR_HUMAN]] Receptor for glucocorticoids (GC). Has a dual mode of action: as a transcription factor that binds to glucocorticoid response elements (GRE), both for nuclear and mitochondrial DNA, and as a modulator of other transcription factors. Affects inflammatory responses, cellular proliferation and differentiation in target tissues. Could act as a coactivator for STAT5-dependent transcription upon growth hormone (GH) stimulation and could reveal an essential role of hepatic GR in the control of body growth. Involved in chromatin remodeling. Plays a significant role in transactivation.<ref>PMID:21664385</ref> | |||
==About this Structure== | ==About this Structure== | ||
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==Reference== | ==Reference== | ||
<ref group="xtra">PMID:018522385</ref><references group="xtra"/> | <ref group="xtra">PMID:018522385</ref><references group="xtra"/><references/> | ||
[[Category: Homo sapiens]] | [[Category: Homo sapiens]] | ||
[[Category: Biggadike, K B.]] | [[Category: Biggadike, K B.]] | ||
