GLUCOCORTICOID RECEPTOR

GWB-B53426

2908

8000000000

Spleen cells from immunised BALB/c mice were fused with cells of the mouse Sp-2/0 Ag14 myeloma cell line.

Purified IgG prepared by affinity chromatography on Protein G from tissue culture supernatant

ELISA - 1:1000Western Blotting - 1:1000

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.

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.

Increased proteasome-mediated degradation in response to glucocorticoids.

Sumoylated; this reduces transcription transactivation.

Carriers of the 22-Glu-Lys-23 allele are relatively more resistant to the effects of GCs with respect to the sensitivity of the adrenal feedback mechanism than non-carriers resulting in a better metabolic health profile. Carriers have a better survival than non-carriers as well as lower serum CRP levels. The 22-Glu-Lys-23 polymorphism is associated with a sex-specific beneficial body composition at young-adult age as well as greater muscle strength in males.

High constitutive expression of isoform beta by neutrophils may provide a mechanism by which these cells escape glucocorticoid-induced cell death. Up-regulation by proinflammatory cytokines such as IL8 further enhances their survival in the presence of glucocorticoids during inflammation.

Belongs to the nuclear hormone receptor family. NR3 subfamily.