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Gene Review

Ghr  -  growth hormone receptor

Mus musculus

Synonyms: AA986417, GH receptor, GHBP, GHR/BP, Growth hormone receptor, ...
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Disease relevance of Ghr


High impact information on Ghr


Chemical compound and disease context of Ghr

  • GHR(-/-) mice exhibited 50% reduction in the ratio of islet cell mass to body weight and increased insulin sensitivity but impaired glucose tolerance [9].
  • To establish that these mammary cancers were estrogen-independent, 12-week-old TAg/Ghr(+/+) mice, which lack visible hyperplasia, were either ovariectomized (ovx) or sham operated (sham) [10].

Biological context of Ghr

  • In 10-month-old animals, GH-induced phosphorylation of the GHR complex was maximal 10 min after the addition of hormone, whereas GH-induced MAP kinase activity was maximal at 15 min [11].
  • In this study, the effects of aging on GHR signal transduction were assessed in hepatic tissue to determine whether alterations in the response to GH contribute to the decline in IGF-I [11].
  • The major effect on reproductive function seen in GHR/GHBP knockout (KO) compared with wild-type animals is a dramatic decrease in litter size; this defect is due to a reduction of the ovulation rate [12].
  • Expression of the hGHRH transgene in 2-month-old GHR intact (GHR(+)) mice resulted in the doubling of pituitary weight that was largely attributed to an increase in the number of GH-immunopositive cells [4].
  • GH resistance due to downregulation of GHR expression may be attributed primarily to the obstructive cholestasis; therapies that specifically increase GHR expression may restore GH signaling in this setting [13].

Anatomical context of Ghr

  • These experiments demonstrated that the GHR in the epithelium is not required for functional mammary development [14].
  • Plasma IGF-I is regulated by GH released from the pituitary gland, and although data demonstrate a decline in GH secretion with age, GH receptor (GHR) density in liver tissue has been reported to increase [11].
  • Growth hormone receptor gene deficiency causes delayed insulin responsiveness in skeletal muscles without affecting compensatory islet cell overgrowth in obese mice [15].
  • To assess the relevance of the GH and PRLRs in the mammary gland development, GHR and PRLR null epithelia were transplanted into cleared fat pads of wild-type mice [16].
  • Developmental aspects of adipose tissue in GH receptor and prolactin receptor gene disrupted mice: site-specific effects upon proliferation, differentiation and hormone sensitivity [17].

Associations of Ghr with chemical compounds

  • Female diabetic (nonketotic) NOD mice treated with a polyethylene glycol-treated GHR antagonist (2 mg/kg, every other day) (DA group) or saline (D group) and their nonhyperglycemic age-matched littermates (control animals) were euthanized 3 wk after the onset of diabetes [3].
  • Materials and Methods: Dihydrotestosterone (DHT) or testosterone (T) were administered to orchidectomized (ORX) male GH receptor gene knockout (GHRKO) and corresponding wildtype (WT) mice during late puberty (6-10 weeks of age) [18].
  • Disruption of the GHR gene altered neither prostate androgen receptor expression nor serum testosterone titers [1].
  • TNFalpha down-regulated GHR abundance and prevented GH-induced tyrosine phosphorylation of STAT5 in rat hepatocytes in culture [8].
  • Compared with GHR(-/-) alone, IGF-I overexpression on a GHR(-/-) background caused no change in the diminished blood glucose and serum insulin levels, pancreatic insulin contents, and insulin tolerance but improved glucose tolerance and insulin secretion [9].

Physical interactions of Ghr

  • GHR expression was reduced in BDL mice; in liver, this was associated with reduced Sp3 binding to a GHR gene promoter cis element [13].
  • Liver GH receptor (GHR) and GH binding protein (GHBP) mRNA levels, as well as liver membrane GH binding assays were deeply decreased in the 30d DM group in comparison to controls [19].
  • Ames dwarf mice that do not express growth hormone (GH) or prolactin (PRL) genes were used to study the effects of GH deficiency on the presence and the characteristics of GH-binding protein (GHBP) in serum [20].

Enzymatic interactions of Ghr

  • Like JAK2, HMW JAK2 is tyrosine phosphorylated in response to GH treatment of cells and is coimmunoprecipitated with anti-GHR serum [21].

Regulatory relationships of Ghr


Other interactions of Ghr


Analytical, diagnostic and therapeutic context of Ghr


  1. Disruption of growth hormone signaling retards early stages of prostate carcinogenesis in the C3(1)/T antigen mouse. Wang, Z., Prins, G.S., Coschigano, K.T., Kopchick, J.J., Green, J.E., Ray, V.H., Hedayat, S., Christov, K.T., Unterman, T.G., Swanson, S.M. Endocrinology (2005) [Pubmed]
  2. Inhibitory effect of a growth hormone receptor antagonist (G120K-PEG) on renal enlargement, glomerular hypertrophy, and urinary albumin excretion in experimental diabetes in mice. Flyvbjerg, A., Bennett, W.F., Rasch, R., Kopchick, J.J., Scarlett, J.A. Diabetes (1999) [Pubmed]
  3. Growth hormone receptor antagonism prevents early renal changes in nonobese diabetic mice. Segev, Y., Landau, D., Rasch, R., Flyvbjerg, A., Phillip, M. J. Am. Soc. Nephrol. (1999) [Pubmed]
  4. The effect of GHRH on somatotrope hyperplasia and tumor formation in the presence and absence of GH signaling. Kineman, R.D., Teixeira, L.T., Amargo, G.V., Coschigano, K.T., Kopchick, J.J., Frohman, L.A. Endocrinology (2001) [Pubmed]
  5. Identification of JAK2 as a growth hormone receptor-associated tyrosine kinase. Argetsinger, L.S., Campbell, G.S., Yang, X., Witthuhn, B.A., Silvennoinen, O., Ihle, J.N., Carter-Su, C. Cell (1993) [Pubmed]
  6. SOCS2 negatively regulates growth hormone action in vitro and in vivo. Greenhalgh, C.J., Rico-Bautista, E., Lorentzon, M., Thaus, A.L., Morgan, P.O., Willson, T.A., Zervoudakis, P., Metcalf, D., Street, I., Nicola, N.A., Nash, A.D., Fabri, L.J., Norstedt, G., Ohlsson, C., Flores-Morales, A., Alexander, W.S., Hilton, D.J. J. Clin. Invest. (2005) [Pubmed]
  7. Bone homeostasis in growth hormone receptor-null mice is restored by IGF-I but independent of Stat5. Sims, N.A., Clément-Lacroix, P., Da Ponte, F., Bouali, Y., Binart, N., Moriggl, R., Goffin, V., Coschigano, K., Gaillard-Kelly, M., Kopchick, J., Baron, R., Kelly, P.A. J. Clin. Invest. (2000) [Pubmed]
  8. Tumor necrosis factor alpha blockade restores growth hormone signaling in murine colitis. DiFedele, L.M., He, J., Bonkowski, E.L., Han, X., Held, M.A., Bohan, A., Menon, R.K., Denson, L.A. Gastroenterology (2005) [Pubmed]
  9. Pancreatic islet-specific expression of an insulin-like growth factor-I transgene compensates islet cell growth in growth hormone receptor gene-deficient mice. Guo, Y., Lu, Y., Houle, D., Robertson, K., Tang, Z., Kopchick, J.J., Liu, Y.L., Liu, J.L. Endocrinology (2005) [Pubmed]
  10. Inhibition of estrogen-independent mammary carcinogenesis by disruption of growth hormone signaling. Zhang, X., Mehta, R.G., Lantvit, D.D., Coschigano, K.T., Kopchick, J.J., Green, J.E., Hedayat, S., Christov, K.T., Ray, V.H., Unterman, T.G., Swanson, S.M. Carcinogenesis (2007) [Pubmed]
  11. Decreases in growth hormone receptor signal transduction contribute to the decline in insulin-like growth factor I gene expression with age. Xu, X., Bennett, S.A., Ingram, R.L., Sonntag, W.E. Endocrinology (1995) [Pubmed]
  12. Growth hormone is required for ovarian follicular growth. Bachelot, A., Monget, P., Imbert-Bolloré, P., Coshigano, K., Kopchick, J.J., Kelly, P.A., Binart, N. Endocrinology (2002) [Pubmed]
  13. Alterations in growth hormone receptor abundance regulate growth hormone signaling in murine obstructive cholestasis. Held, M.A., Cosme-Blanco, W., Difedele, L.M., Bonkowski, E.L., Menon, R.K., Denson, L.A. Am. J. Physiol. Gastrointest. Liver Physiol. (2005) [Pubmed]
  14. Prolactin, growth hormone, and epidermal growth factor activate Stat5 in different compartments of mammary tissue and exert different and overlapping developmental effects. Gallego, M.I., Binart, N., Robinson, G.W., Okagaki, R., Coschigano, K.T., Perry, J., Kopchick, J.J., Oka, T., Kelly, P.A., Hennighausen, L. Dev. Biol. (2001) [Pubmed]
  15. Growth hormone receptor gene deficiency causes delayed insulin responsiveness in skeletal muscles without affecting compensatory islet cell overgrowth in obese mice. Robertson, K., Kopchick, J.J., Liu, J.L. Am. J. Physiol. Endocrinol. Metab. (2006) [Pubmed]
  16. The role of prolactin and growth hormone in mammary gland development. Kelly, P.A., Bachelot, A., Kedzia, C., Hennighausen, L., Ormandy, C.J., Kopchick, J.J., Binart, N. Mol. Cell. Endocrinol. (2002) [Pubmed]
  17. Developmental aspects of adipose tissue in GH receptor and prolactin receptor gene disrupted mice: site-specific effects upon proliferation, differentiation and hormone sensitivity. Flint, D.J., Binart, N., Boumard, S., Kopchick, J.J., Kelly, P. J. Endocrinol. (2006) [Pubmed]
  18. Impact of androgens, growth hormone, and igf-I on bone and muscle in male mice during puberty. Venken, K., Mov??rare-Skrtic, S., Kopchick, J.J., Coschigano, K.T., Ohlsson, C., Boonen, S., Bouillon, R., Vanderschueren, D. J. Bone Miner. Res. (2007) [Pubmed]
  19. Changes in the growth hormone-IGF-I axis in non-obese diabetic mice. Landau, D., Segev, Y., Eshet, R., Flyvbjerg, A., Phillip, M. Int. J. Exp. Diabetes Res. (2000) [Pubmed]
  20. Concentration of free growth hormone-binding protein in the serum of mice is not regulated by growth hormone. Sotelo, A.I., Dominici, F.P., Bartke, A., Turyn, D. J. Endocrinol. (1997) [Pubmed]
  21. Growth hormone-dependent tyrosine phosphorylation of a GH receptor-associated high molecular WEIGHT protein immunologically related to JAK2. Jiang, J., Liang, L., Kim, S.O., Zhang, Y., Mandler, R., Frank, S.J. Biochem. Biophys. Res. Commun. (1998) [Pubmed]
  22. Growth hormone and epidermal growth factor in salivary glands of giant and dwarf transgenic mice. Young, W.G., Ramirez-Yañez, G.O., Daley, T.J., Smid, J.R., Coshigano, K.T., Kopchick, J.J., Waters, M.J. J. Histochem. Cytochem. (2004) [Pubmed]
  23. Elevation of growth hormone (GH) and prolactin receptors in transgenic mice expressing ovine GH. Orian, J.M., Snibson, K., Stevenson, J.L., Brandon, M.R., Herington, A.C. Endocrinology (1991) [Pubmed]
  24. Aryl hydrocarbon receptor-mediated suppression of GH receptor and Janus kinase 2 expression in mice. Nukaya, M., Takahashi, Y., Gonzalez, F.J., Kamataki, T. FEBS Lett. (2004) [Pubmed]
  25. Growth hormone alters epidermal growth factor receptor binding affinity via activation of extracellular signal-regulated kinases in 3T3-F442A cells. Huang, Y., Chang, Y., Wang, X., Jiang, J., Frank, S.J. Endocrinology (2004) [Pubmed]
  26. A mammalian model for Laron syndrome produced by targeted disruption of the mouse growth hormone receptor/binding protein gene (the Laron mouse). Zhou, Y., Xu, B.C., Maheshwari, H.G., He, L., Reed, M., Lozykowski, M., Okada, S., Cataldo, L., Coschigamo, K., Wagner, T.E., Baumann, G., Kopchick, J.J. Proc. Natl. Acad. Sci. U.S.A. (1997) [Pubmed]
  27. Effect of metabolic acidosis on the growth hormone/IGF-I endocrine axis in skeletal growth centers. Green, J., Maor, G. Kidney Int. (2000) [Pubmed]
  28. A GH receptor antisense oligonucleotide inhibits hepatic GH receptor expression, IGF-I production and body weight gain in normal mice. Tachas, G., Lofthouse, S., Wraight, C.J., Baker, B.F., Sioufi, N.B., Jarres, R.A., Berdeja, A., Rao, A.M., Kerr, L.M., d'Aniello, E.M., Waters, M.J. J. Endocrinol. (2006) [Pubmed]
  29. Diurnal variation in growth hormone receptor messenger ribonucleic acid in liver and skeletal muscle of lit/+ and lit/lit mice. Itoh, E., Iida, K., del Rincon, J.P., Kim, D.S., Thorner, M.O. Endocr. J. (2004) [Pubmed]
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