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Validated All-in-One™ qPCR Primer for GHSR(NM_198407.2) Search again
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene encodes a member of the G-protein coupled receptor family. The encoded protein may play a role in energy homeostasis and regulation of body weight. Two identified transcript variants are expressed in several tissues and are evolutionary conserved in fish and swine. One transcript, 1a, excises an intron and encodes the functional protein; this protein is the receptor for the Ghrelin ligand and defines a neuroendocrine pathway for growth hormone release. The second transcript (1b) retains the intron and does not function as a receptor for Ghrelin; however, it may function to attenuate activity of isoform 1a.
Gene References into function
- The 1b variant may not be functional, it only encodes 5 of the 7 transmembrane domains and fails to respond in xenopus oocytes.
- Hypothalamic growth hormone secretagogue receptor regulates growth hormone secretion, feeding, and adiposity
- Review. This review will summarize data regarding the structure of the GHS-R gene and the protein encoded, reports investigating the expression and control of the GHS-R in various tissues, and studies of the underlying transcriptional mechanisms.
- The presence of ligand and receptor of the ghrelin signaling system within the human ovary opens up the possibility of a potential regulatory role of this novel molecule in ovarian function under physiological and pathophysiological conditions.
- Constitutive overexpression of GHSR can up-regulate basal signaling activity in the GHRH/GH axis and reduce adiposity without affecting other GHSR-mediated signals.
- no conclusive evidence for an involvement of the ghrelin receptor gene in body weight regulation or short normal stature
- results demonstrate that ghrelin and the type 1a growth hormone secretagogue receptor are expressed in adult human testis and testicular tumors
- Specific ghrelin (GHS) binding sites, other than GHS-R1a and 1b, are present in human prostatic neoplasms. Ghrelin, in addition to des-acyl ghrelin, exerts different effects on cell proliferation in prostate carcinoma cell lines.
- genetic variations in the GHS-R1a gene are not the main regulators of IGF-I levels
- potential use of ghrelin and GHS-R agonists in the management of disease-associated cachexia.
- ghrelin receptor, neurotensin receptor 2 and GPR39 display an unusually high degree of constitutive activity, determined by an aromatic cluster on the inner face of the extracellular ends of TMs VI and VII
- ovarian surface epithelium and related tumors are potential targets for systemic or locally produced ghrelin because they express the functional type 1a GHS-R
- Single nucleotide polymorphisms and haplotypes within the GHSR region are involved in the pathogenesis of human obesity.
- Downregulation of GHS-R1a and high levels of GHS-R1b transcripts are associated with adrenal tumors
- the 171T/C polymorphism of the ghrelin receptor gene in patients diagnosed with Eating disorders
- Review concludes that selective lack of ghrelin receptor constitutive signaling leads to a syndrome characterized not only by short stature, but also by obesity that apparently develops during puberty.
- A GHSR missense mutation segregates with short stature resulting in decreased cell-surface expression of the receptor and selective impairment of the constitutive activity of GHSR, while preserving its ability to respond to ghrelin.
- Ghrelin and the growth hormone secretagogue receptor have roles in astrocytoma motility
- Variants in ghrelin receptor are associated with parameters of left ventricular mass and geometry independent of blood pressure and body mass in general population and may be involved in pathogenesis of left ventricular hypertrophy.
- ghrelin, through GHSR-1a, activates the Elk1 transcriptional factor and ERK1/2 by a PLC- and PKCepsilon-dependent pathway
- This overview focuses on recent studies of tissue distribution, expression regulation and the multiple actions of the ghrelin receptor (GHS-R) and its involvement in the control of energy homeostasis and its ability to stimulate food intake and adiposity
- NMU & its cancer-specific receptors NTSR1 & GHSR1b, as well as its target genes, are overexpressed in lung cancer and in cell lines, and that those gene products play indispensable roles in the growth and progression of lung cancer cells.
- Investigation of whether the full-length GRLN-R physically interacts with its truncated splice variant GHS-R1b
- Adenosine is not a direct GHSR agonist. In human embryonic kidney 293s (HEK) cells expressing GHSR, adenosine activates endogenously expressed A(2B)R resulting in calcium mobilization.
- This study demonstrates the cyclical expression of GHS-R and ghrelin in human endometrium.
- These findings demonstrate in a defined system that unacylated ghrelin does not antagonize activation of the GHS-R by ghrelin.
- HepG2 cells do not express a GHS-R1a-type ghrelin receptor
- Our results showed that ghrelin receptor was expressed in cancers throughout the gastrointestinal tract, mainly in the cytoplasm of mucosal layer cells.
- A number of GHRL and GHSR polymorphisms were associated with body mass index (BMI) and height.
- Higher GHSR-1a is associated with Crohn's disease.
- higher expression of GHSR-1a in the ACTH-dependent Cushing patients responsive to GHRP-6, suggesting an association between receptor gene expression and in vivo response to the secretagogue
- Data suggest that expression of prostanoid receptors (prostaglandin E2 EP3-I, prostacyclin, and thromboxane A2 receptors) in vascular inflammation could influence cell responses dependent on the constitutive activation of ghrelin receptors.
- Common variation in GHSR is not associated with body size in U.K. adults or children.
- Polymorphisms in the GHSR promoter may modify changes in body weight during long-term lifestyle intervention and affect ghrelin receptor signalling through modulation of GHSR gene expression.
- Variants of the ghrelin and GHSR genes are not major contributors to height variation in a French population.
- The polymorphisms within GHSR might be a genetic risk factor for metabolic syndrome in women.
- GHRH interacts with ghrelin receptor GHS-R1a, and, in consequence, modifies the ghrelin-associated intracellular signaling pathway
