Glucocorticoid receptor

1M2Z, 1NHZ, 1P93, 3BQD, 3CLD, 3E7C, 3H52, 3K22, 3K23, 4CSJ, 4HN5, 4HN6, 4LSJ, 4MDD, 4P6W, 4P6X, 5CBY, 5CBX, 4UDC, 4UDD, 5CBZ, 5CC1, 5EMQ, 5EMC, 5EMP290814815ENSG00000113580ENSMUSG00000024431P04150Q3MSN4P06537NM_001020825NM_001024094NM_001204258NM_001204259NM_001204260NM_001204261NM_001204262NM_001204263NM_001204264NM_001204265NM_001364180NM_001364181NM_001364182NM_001364183NM_001364184NM_001364185NM_008173NM_001361209NM_001361210NM_001361211NM_001361212NP_001018661NP_001019265NP_001191187NP_001191188NP_001191189NP_001191190NP_001191191NP_001191192NP_001191193NP_001191194NP_001351109NP_001351110NP_001351111NP_001351112NP_001351113NP_001351114NP_000167.1NP_001018084.1NP_001018085.1NP_001018086.1NP_001018087.1NP_001018661.1NP_001019265.1NP_001191187.1NP_001191188.1NP_001191189.1NP_001191190.1NP_001191191.1NP_001191192.1NP_001191193.1n/aThe glucocorticoid receptor (GR, or GCR) also known as NR3C1 (nuclear receptor subfamily 3, group C, member 1) is the receptor to which cortisol and other glucocorticoids bind.1gdc: REFINED SOLUTION STRUCTURE OF THE GLUCOCORTICOID RECEPTOR DNA-BINDING DOMAIN1glu: CRYSTALLOGRAPHIC ANALYSIS OF THE INTERACTION OF THE GLUCOCORTICOID RECEPTOR WITH DNA1m2z: Crystal structure of a dimer complex of the human glucocorticoid receptor ligand-binding domain bound to dexamethasone and a TIF2 coactivator motif1nhz: Crystal Structure of the Antagonist Form of Glucocorticoid Receptor1p93: CRYSTAL STRUCTURE OF THE AGONIST FORM OF GLUCOCORTICOID RECEPTOR1r4o: Crystallographic analysis of the interaction of the glucocorticoid receptor with DNA1r4r: Crystallographic analysis of the interaction of the glucocorticoid receptor with DNA1rgd: STRUCTURE REFINEMENT OF THE GLUCOCORTICOID RECEPTOR-DNA BINDING DOMAIN FROM NMR DATA BY RELAXATION MATRIX CALCULATIONS2gda: REFINED SOLUTION STRUCTURE OF THE GLUCOCORTICOID RECEPTOR DNA-BINDING DOMAIN The glucocorticoid receptor (GR, or GCR) also known as NR3C1 (nuclear receptor subfamily 3, group C, member 1) is the receptor to which cortisol and other glucocorticoids bind. The GR is expressed in almost every cell in the body and regulates genes controlling the development, metabolism, and immune response. Because the receptor gene is expressed in several forms, it has many different (pleiotropic) effects in different parts of the body. When glucocorticoids bind to GR, its primary mechanism of action is the regulation of gene transcription. The unbound receptor resides in the cytosol of the cell. After the receptor is bound to glucocorticoid, the receptor-glucocorticoid complex can take either of two paths. The activated GR complex up-regulates the expression of anti-inflammatory proteins in the nucleus or represses the expression of pro-inflammatory proteins in the cytosol (by preventing the translocation of other transcription factors from the cytosol into the nucleus). In humans, the GR protein is encoded by NR3C1 gene which is located on chromosome 5 (5q31). Like the other steroid receptors, the glucocorticoid receptor is modular in structure and contains the following domains (labeled A - F): In the absence of hormone, the glucocorticoid receptor (GR) resides in the cytosol complexed with a variety of proteins including heat shock protein 90 (hsp90), the heat shock protein 70 (hsp70) and the protein FKBP52 (FK506-binding protein 52). The endogenous glucocorticoid hormone cortisol diffuses through the cell membrane into the cytoplasm and binds to the glucocorticoid receptor (GR) resulting in release of the heat shock proteins. The resulting activated form GR has two principal mechanisms of action, transactivation and transrepression, described below. A direct mechanism of action involves homodimerization of the receptor, translocation via active transport into the nucleus, and binding to specific DNA responsive elements activating gene transcription. This mechanism of action is referred to as transactivation. The biological response depends on the cell type. In the absence of activated GR, other transcription factors such as NF-κB or AP-1 themselves are able to transactivate target genes. However activated GR can complex with these other transcription factors and prevent them from binding their target genes and hence repress the expression of genes that are normally upregulated by NF-κB or AP-1. This indirect mechanism of action is referred to as transrepression. The GR is abnormal in familial glucocorticoid resistance.