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Rabbit Anti-Glucocorticoid Receptor/FITC Conjugated antibody
background:
Steroid receptors are ligand-dependent, intracellular proteins that stimulate transcription of specific genes by binding to specific DNA sequences following activation by the appropriate hormone. Glucocorticoids are a family of steroids necessary for the regulation of energy metabolism and the immune and inflammatory responses. These compounds exert their effect through their interaction with the glucocoticoid receptor (GR) and that complex's subsequent association with DNA. All normal mammalian tissues examined to date have been shown to contain glucocorticoid receptor.
Function:
Receptor for glucocorticoids (GC). Has a dual mode of action: as a transcription factor that binds to glucocorticoid response elements (GRE) 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. Involved in nuclear translocation.
Subunit:
Heteromultimeric cytoplasmic complex with HSP90, HSP70, and FKBP5 or another immunophilin, or the immunophilin homolog PPP5C. Directly interacts with UNC45A. Upon ligand binding FKBP5 dissociates from the complex and FKBP4 takes its place, thereby linking the complex to dynein and mediating transport to the nucleus, where the complex dissociates (By similarity). Binds to DNA as a homodimer, and as a heterodimer with NR3C2 or the retinoid X receptor. Binds STAT5A and STAT5B homodimers and heterodimers. Interacts with NRIP1, POU2F1, POU2F2 and TRIM28. Interacts with NCOA1, NCOA3, SMARCA4, SMARCC1, SMARCD1, and SMARCE1 (By similarity). Interacts with several coactivator complexes, including the SMARCA4 complex, CREBBP/EP300, TADA2L and p160 coactivators such as NCOA2 and NCOA6. Interaction with BAG1 inhibits transactivation. Interacts with HEXIM1, PELP1 and TGFB1I1.
Subcellular Location:
Cytoplasm. Nucleus. Cytoplasmic in the absence of ligand, nuclear after ligand-binding and Nucleus. Localized largely in the nucleus.
Tissue Specificity:
Widely expressed. In the heart, detected in left and right atria, left and right ventricles, aorta, apex, intraventricular septum, and atrioventricular node as well as whole adult and fetal heart.
Post-translational modifications:
Increased proteasome-mediated degradation in response to glucocorticoids.
Phosphorylated in the absence of hormone; becomes hyperphosphorylated in the presence of glucocorticoid. The Ser-203-phosphorylated form is mainly cytoplasmic, and the Ser-211-phosphorylated form is nuclear. Transcriptional activity correlates with the amount of phosphorylation at Ser-211.
Sumoylated; this reduces transcription transactivation.
Ubiquitinated; restricts glucocorticoid-mediated transcriptional signaling.
DISEASE:
Defects in NR3C1 are a cause of glucocorticoid resistance (GCRES) [MIM:27640]; also known as cortisol resistance. It is a hypertensive, hyperandrogenic disorder characterized by increased serum cortisol concentrations. Inheritance is autosomal dominant.
Similarity:
Belongs to the nuclear hormone receptor family. NR3 subfamily.
Contains 1 nuclear receptor DNA-binding domain.
Database links:
Entrez Gene: 2908 Human
Entrez Gene: 14815 Mouse
Entrez Gene: 24413 Rat
Omim: 27640 Human
SwissProt: P04150 Human
SwissProt: P06537 Mouse
SwissProt: P06536 Rat
Unigene: 122926 Human
Unigene: 129481 Mouse
Unigene: 90070 Rat
Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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