GHRHR

Official Full Name

growth hormone releasing hormone receptor

Organism

Homo sapiens

GeneID

2692

Background

This gene encodes a receptor for growth hormone-releasing hormone. Binding of this hormone to the receptor leads to synthesis and release of growth hormone. Mutations in this gene have been associated with isolated growth hormone deficiency (IGHD), also known as Dwarfism of Sindh, a disorder characterized by short stature. [provided by RefSeq, Jun 2010]

Synonyms

GRFR; GHRFR; IGHD4; IGHD1B;

Bio Chemical Class

GPCR secretin

Protein Sequence

MDRRMWGAHVFCVLSPLPTVLGHMHPECDFITQLREDESACLQAAEEMPNTTLGCPATWDGLLCWPTAGSGEWVTLPCPDFFSHFSSESGAVKRDCTITGWSEPFPPYPVACPVPLELLAEEESYFSTVKIIYTVGHSISIVALFVAITILVALRRLHCPRNYVHTQLFTTFILKAGAVFLKDAALFHSDDTDHCSFSTVLCKVSVAASHFATMTNFSWLLAEAVYLNCLLASTSPSSRRAFWWLVLAGWGLPVLFTGTWVSCKLAFEDIACWDLDDTSPYWWIIKGPIVLSVGVNFGLFLNIIRILVRKLEPAQGSLHTQSQYWRLSKSTLFLIPLFGIHYIIFNFLPDNAGLGIRLPLELGLGSFQGFIVAILYCFLNQEVRTEISRKWHGHDPELLPAWRTRAKWTTPSRSAAKVLTSMC

Open

Disease

Bone growth disorder, Human immunodeficiency virus disease, Lipoatrophy/lipodystrophy, Pituitary gland disorder

Approved Drug

2 +

Clinical Trial Drug

Discontinued Drug

4 +

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Detailed Information

The GHRHR gene produces a receptor that interacts with growth hormone-releasing hormone (GHRH) to stimulate the production and release of growth hormone. Part of the G protein-coupled receptor family, its activation starts signaling pathways controlling hormone release. Changes in this receptor are intimately connected to growth hormone deficits, such as Sindh dwarfism, which causes low height. The study shows that GHRHR is engaged in many physiological processes and has a major influence on certain kinds of cancer growth.

Role of GHRHR in Growth Hormone Secretion

The hypothalamus releases GHRH, a neuroendocrine hormone that controls growth hormone production by stimulating the GHRHR. Most of these receptors are on the pituitary gland's growth hormone-secreting cells. GHRH activates G proteins when it binds to GHRHR; these G proteins then activate adenylate cyclase, generating cyclic AMP (cAMP), hence promoting the release of growth hormone. Once in circulation, growth hormone encourages liver production and release of insulin-like growth factor I (IGF-I). This mechanism supports the traditional hypothalamus-pituitary-liver axis required for development and weight increase.

Research indicates that GHRH is vital not just for normal development and metabolism but also for disease control. Activation of GHRH receptors, for example, may promote tumor cell growth, therefore making GHRHR a possible target for cancer treatment. Studies have shown that GHRH antagonists not only prevent cancer development but also show antioxidant and anti-inflammatory qualities.

Figure 1 illustrates how GHRH influences Ca2+ and K+ channels through coupling with protein kinase A (PKA) and protein kinase C (PKC) systems, affecting voltage-gated calcium and potassium currents in somatotropes. Figure 1. The mechanism of GHRH action on Ca²⁺ and K⁺ channels involves coupling with the protein kinase A (PKA) and protein kinase C (PKC) systems. (Fridlyand LE, et al., 2016)

GHRHR Gene Mutations and Associated Diseases

GHRHR Gene Mutations and Related Disorders Commonly linked to dwarfism, the p.Glu72 mutation in the GHRHR gene serves as an example. Apart from growth hormone shortages, GHRHR mutations have links to immunological disorders including experimental autoimmune encephalomyelitis (EAE). Dysfunctional GHRH/GHRHR signaling may change immune function, hence affecting the onset and progression of diseases.

GHRHR absence or dysfunction may cause major growth retardation and insensitivity to external GHRH therapy. Examining these mutations gives theoretical bases and possible treatments for linked diseases as well as a better understanding of GHRHR's function in hormone release.

Relationship between GHRHR and Cancer

GHRHR is also rather important in cancer formation outside its function in growth control. GHRH and its receptor are expressed in many cancer forms, therefore enabling a signaling route that promotes tumor cell proliferation. GHRHR activation increases proliferation, especially in malignant tumors, therefore providing a new target for cancer therapy.

Laboratory investigations have shown strong anti-tumor benefits of new GHRH antagonist cancer medications. These antagonists reduce tumor cell growth by either preventing GHRH binding with its receptor or suppressing the mutant receptor SV1. By changing immunological activities, they also increase the anti-tumor ability of the body. Creating more safe, reliable, and strong GHRH antagonists could one day change cancer therapy.

Role of GHRHR in Other Biological Processes

GHRHR is not just important in the pituitary and hormone release; it also has major effects on other tissues and cells. Among others, it is found in the heart, lymphocytes, testes, ovaries, skin, pancreas, and other organs taking part in various biological activities. Especially in pancreatic beta-cells, GHRHR lets GHRH control insulin release. Studies show possible uses of GHRH and its receptors in diabetes therapy, especially in boosting insulin release and β-cell safeguarding.

Apart from its central nervous system function, GHRH release in peripheral tissues shows autocrine or paracrine activities. GHRH, for example, controls growth, survival, and tissue-specific differentiation, hence affecting metabolic and immunological balance. GHRHR also works in tumors and some stem cells, hence possibly affecting stem cell function and tumor development.

References:

Halmos G, Szabo Z, Juhasz E, et al. Signaling mechanism of growth hormone-releasing hormone receptor. Vitam Horm. 2023;123:1-26.
Martari M, Salvatori R. Diseases associated with growth hormone-releasing hormone receptor (GHRHR) mutations. Prog Mol Biol Transl Sci. 2009;88:57-84.
Gesmundo I, Pedrolli F, Cai R, et al. Growth hormone-releasing hormone and cancer. Rev Endocr Metab Disord. Published online October 18, 2024.
Fridlyand LE, Tamarina NA, et al. Growth Hormone-Releasing Hormone in Diabetes. Front Endocrinol (Lausanne). 2016;7:129. Published 2016 Oct 10.

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