GHR

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GHR

A gene on chromosome 5p13-p12 that encodes growth hormone receptor, a type-I cytokine receptor which, once GH is bound, dimerizes and activates the JAK2/STAT5 transduction pathway, leading to growth.

Molecular pathology
Defects in GHR cause Laron type dwarfism.
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After GH binding to growth hormone receptor (GHR), tyrosine kinase janus kinase 2 (JAK2) is activated, which in turn phosphorylates multiple tyrosines within both itself and the GH receptor, as well as multiple signalling pathways.
GH measurements are subject to interference by a number of factors, including GH-binding protein (GHBP), which corresponds to the circulating extracellular domain of the GH receptor (15).
Regulation of endocrine and paracrine sources of Igfs and Gh receptor during compensatory growth in hybrid striped bass (Morone chrysops X Morone saxatilis).
examined efficacy of the GH receptor antagonist pegvisomant, to control gsp oncogene-mediated GH excess and skeletal disease (fibrous dysplasia of bone) associated with MAS.
Poor growth can result from deficiency of GH, the GH molecule being biologically inert, GH receptor problems or downstream defects in the GH signal-transduction pathway, abnormalities of IGF generation, or end-organ unresponsiveness.
In children with this disorder, low IGF-1 levels may be due to growth-hormone resistance or insensitivity associated with mutations in GH receptors, post-GH receptor signaling pathways, or to defects in the IGF-1 gene.
Insulin restores GH responsiveness during lactation-induced negative energy balance in dairy cattle: effects on expression of IGF-I and GH receptor 1A.
Another potential factor is a polymorphism in the human GH receptor (GHR) gene resulting from a genomic deletion of exon 3 (d3-GHR) (8).
In children with this disorder, low IGF-1 levels are due to growth-hormone resistance associated with mutations in GH receptors, post-GH receptor signaling pathways, or to defects in IGF-1 gene expression.
Indirectly, GH binds GH receptor (GHR) on the membrane of liver and then activates hepatic insulin-like growth factor-I (IGF-I) secretion, which stimulates the differentiation and proliferation of bone and muscle cells (McMurtry et al.
In children with this disorder, low IGF-1 levels are due to growth hormone resistance associated with mutations in GH receptors, post-GH receptor signalling pathways, or to defects in IGF-1 gene expression.