Status
Please wait ...

Details for receptor: glucocorticoid receptor

  • Top
  • General information
  • Subunits
    •
  • External resources
  • General information
  • Hormones
  • Anatomical structures
  • Click to access the toolbox
EndoNet ID: ENR00691

To link to the content of EndoNet use the EndoNet ID that is given on the detail pages in the format ENX0000, where X is a place holder for the type of the component (e. g. R for receptor or C for anatomical structure).
As URL for the linking append this ID to the detail page for this type of component.
For an hormone that would be: 

http://endonet.bioinf.med.uni-goettingen.de/hormone/ENH00000

It is also possible to use the search of EndoNet to link to the right detail page. The URL should look like 

http://endonet.bioinf.med.uni-goettingen.de/search/ENC00000
If the search pattern is unambigious the user is directed to the corresponding detail page.

Synonyms

  • GR
  • GR-alpha
  • glucocorticoid receptor alpha
  • glucocorticoid receptor

General information

  • IL-2 increased the number of GRs, while it reduced binding affinity in PBMCs. [1]
  • Dexamethasone-activated glucocorticoid receptor increases the expression of CAR mRNA in hepatocytes by enhancing its transcription. [2]
  • The CYP 2C8 and 2C9 promoters contain a glucocorticoid-responsive element that is recognized and transactivated by glucocorticoid receptor. Identification of this functional element provides a rational mechanistic basis for the induction of CYP 2C protein and an increase in EDHF-mediated responses in porcine coronary arteries by cortisol. [3]
  • Expressed in the lung. [4]
  • GR-alpha mRNA abundance (×106 cDNA copies/µg total RNA) was as follows: brain (3.83 ± 0.80) > skeletal muscle > macrophages > lung > kidney > liver > heart > eosinophils > peripheral blood mononuclear cells (PBMCs) > nasal mucosa > neutrophils > colon (0.33 ± 0.04). [5]
  • The default splicing pathway is the one leading to GR-alpha. The alternative splicing event leading to GR-beta is minimally activated. [5]

Links to other resources

UniProt P04150
Ensembl ENST00000454007

Subunit information

alpha isoform

Sequence 
MDSKESLTP GREENPSSV LAQERGDVM 
DFYKTLRGG ATVKVSASS PSLAVASQS 
DSKQRRLLV DFPKGSVSN AQQPDLSKA 
VSLSMGLYM GETETKVMG NDLGFPQQG 
QISLSSGET DLKLLEESI ANLNRSTSV 
PENPKSSAS TAVSAAPTE KEFPKTHSD 
VSSEQQHLK GQTGTNGGN VKLYTTDQS 
TFDILQDLE FSSGSPGKE TNESPWRSD 
LLIDENCLL SPLAGEDDS FLLEGNSNE 
DCKPLILPD TKPKIKDNG DLVLSSPSN 
VTLPQVKTE KEDFIELCT PGVIKQEKL 
GTVYCQASF PGANIIGNK MSAISVHGV 
STSGGQMYH YDMNTASLS QQQDQKPIF 
NVIPPIPVG SENWNRCQG SGDDNLTSL 
GTLNFPGRT VFSNGYSSP SMRPDVSSP 
PSSSSTATT GPPPKLCLV CSDEASGCH 
YGVLTCGSC KVFFKRAVE GQHNYLCAG 
RNDCIIDKI RRKNCPACR YRKCLQAGM 
NLEARKTKK KIKGIQQAT TGVSQETSE 
NPGNKTIVP ATLPQLTPT LVSLLEVIE 
PEVLYAGYD SSVPDSTWR IMTTLNMLG 
GRQVIAAVK WAKAIPGFR NLHLDDQMT 
LLQYSWMFL MAFALGWRS YRQSSANLL 
CFAPDLIIN EQRMTLPCM YDQCKHMLY 
VSSELHRLQ VSYEEYLCM KTLLLLSSV 
PKDGLKSQE LFDEIRMTY IKELGKAIV 
KREGNSSQN WQRFYQLTK LLDSMHEVV 
ENLLNYCFQ TFLDKTMSI EFPEMLAEI 
ITNQIPKYS NGNIKKLLF HQK
UniProt P04150-1

Binding hormones

  • cortisol
    (trough: blood
    )
  • cortisone
    (trough: blood
    )
  • corticosterone
    (trough: blood
    )

Anatomical structures with this receptor

  • pituitary_gland_of_diencephalon

  • brain

  • lung

  • kidney

  • heart

  • colon

  • macrophage

    Induced phenotypes

    • hypertension
      • Oxidative stress and nitric oxide deficiency are emerging as key components in the pathogenesis of glucocorticoid-induced hypertension. [6]
      • This highlights the role of inflammation and oxidative stress in the pathogenesis of glucocorticoid-induced hypertension and this is consistent with a role for macrophages in this pathology. [7]
    • abdominal obesity-metabolic syndrome
      • Glucocorticoids play a role in adipocyte maturation, function and distribution. Differentiating adipocytes produce increasing levels of the enzyme 11-beta-hydroxysteroid dehydrogenase 1 to convert inactive cortisone into cortisol, in turn amplifying local glucocorticoid levels. [8]
      • Many findings implicate macrophages, GR and 11βHSD1 in the pro-inflammatory phenotype of metabolic dysfunction. [7]
    • negative regulation of immune response
      • A recent study exploring the effect of corticosterone on isolated peritoneal macrophages has demonstrated that high corticosterone concentrations suppress macrophage immune functions. [9]
      • Responses to high corticosteroid levels are a consequence of GR activation. [9]
    • osteoporosis
      • Glucocorticoids suppress osteoblast activity in vivo. [10]
      • Glucocorticoid signalling via GR inhibits proliferation of osteoclastogenic cells, apoptosis of mature osteoclasts and osteoclast function in vitro and in vivo, by altering the activity rather than the number of osteoclasts. Glucocorticoid-induced bone mass reduction is not only mediated by directly inhibiting osteoblasts, but also by inhibiting osteoclast activity, which in turn disrupts the remodelling cycle and suppresses osteoblast activity . [11]
    • atherosclerosis
      • Atherosclerosis is a progressive disease characterised by an inflammatory event in which monocyte-derived macrophages play a central role. [12]
      • Glucocorticoid treatment has been shown to reduce macrophage accumulation in a model of cholesterol-induced atherosclerosis. [13]
      • Glucocorticoid treatment has been shown to decrease neointimal proliferation following balloon angioplasty. [14]
      • Effects of glucocorticoids on etiology and progression of atherosclerosis are only partially mediated through GR. [7]

  • skeleton_muscle

  • neutrophil_granulocyte

  • nasal_mucosa

  • eosinophil_granulocyte

  • peripheral blood mononuclear cell (PBMC)

  • hepatocyte

    Influences

    • positive IGF-1
      • IGF-1 is synthesized in hepatocytes upon GH stimulation. [15]
    • negative CBG
      • Levels of CBG are decreased by glucocorticoids. The effects of glucocorticoids on CBG synthesis are glucocorticoid receptor dependent. [16]

  • hypothalamus

    Influences

    • negative CRH
      • Glucocorticoid/Cortisol binding to GR in the hypothalamus inhibits secretion of CRH [17]
    • negative orexin-A
      • Glucose inhibits the orexin neurons in the hypothalamus
    • negative CRH
      • The reduction in CRF mRNA expression in the parvocellular PVN in uncontrolled diabetes most probably depends on the levels of plasma corticosterone. Increased corticosterone levels were accompanied with a decrease in parvocellular CRF expression. [18]

  • thymus

    • The thymus contains one of the highest concentrations of GR in the body, whereas it does not express MR. [19]

  • spleen

  • microglial_cell_in_central_nervous_system

    Induced phenotypes

    • negative regulation of immune response
      • Corticosterone exerts its effects via both corticosteroid receptors in a concentration dependent manner in microglial cells. [20]
Reference