|
ORF cDNA clones
|
CRISPR / TALEN
|
Lentivirus
|
AAV
|
TALE-TF
|
ORF knockin clones
|
|
Antibody
|
Proteins
|
miRNA target clones
|
qPCR primers
|
shRNA clones
|
miRNA products
|
Promoter clones
|
Validated All-in-One™ qPCR Primer for GNRHR(NM_000406.2) Search again
Product ID:
HQP007781
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
GNRHR1, GRHR, HH7, LHRHR, LRHR
Gene Description:
gonadotropin releasing hormone receptor
Target Gene Accession:
NM_000406.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
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.
Validated result:
|
|
| A | B |
|
Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
|
Summary
This gene encodes the receptor for type 1 gonadotropin-releasing hormone. This receptor is a member of the seven-transmembrane, G-protein coupled receptor (GPCR) family. It is expressed on the surface of pituitary gonadotrope cells as well as lymphocytes, breast, ovary, and prostate. Following binding of gonadotropin-releasing hormone, the receptor associates with G-proteins that activate a phosphatidylinositol-calcium second messenger system. Activation of the receptor ultimately causes the release of gonadotropic luteinizing hormone (LH) and follicle stimulating hormone (FSH). Defects in this gene are a cause of hypogonadotropic hypogonadism (HH). Alternative splicing results in multiple transcript variants encoding different isoforms. More than 18 transcription initiation sites in the 5' region and multiple polyA signals in the 3' region have been identified for this gene.
Gene References into function
- Reports complete structure of human gonadotropin-releasing hormone receptor gene with figure 2 showing multiple promoters, transcription sites, and polyadenylation signals.
- This paper reported that a total of 18 transcriptional start sites were identified for the GNRHR gene in the pituitary, which were different from those 5 transcriptional start sites identified in the brain by Fan et al (PMID7768323).
- Site-directed mutagenesis of the C-terminal domain of extracellular loop 2 of the human GnRH receptor showed that a minimum of two mutations is needed in this region for agonist activity of antagonist 135-18
- the E(90)K mutation impairs hGnRHR-effector coupling; sequence modifications that enhance surface expression of the receptor restore function
- Coupling of GnRH concentration and the GnRH receptor-activated gene program
- Novel homozygous splice acceptor site GnRH receptor (GnRHR) mutation: human GnRHR "knockout". amenorrhea and absent thelarche and pubarche
- conserved physical linkage in medaka and human genomes
- our results strongly indicate a role of the C/EBP and GATA motifs in regulating GnRHR gene transcription in human granulosa-luteal cells
- Locally expressed LHRH receptors mediate the oncostatic and antimetastatic activity of LHRH agonists on melanoma cells.
- results clearly indicate a role of octamer transcription factor-1 in the transcriptional repression of the human gonadotropin-releasing hormone receptor gene
- A missense mutation in this gene is found in a case of complete hypogonadotropic hypogonadism.
- Genetic analysis has excluded sequence variations in GNRH1 and GNRHR in four families with recessive IHH, suggesting the existence of a novel, as-yet-undiscovered gene for this condition.
- The dominant-negative effect of the naturally occurring receptor mutants for the WT hGnRHR, which has intrinsic low maturation efficiency suggesting that this effect and the diminished plasma membrane expression is a recent evolutionary event.
- Estrogen receptor-alpha represses human GnRH receptor gene transcription via an indirect mechanism involving Creb-binding protein.
- direct role for the GnRHR in mediating antiproliferative events in two cell systems, neither of which was derived from extrapituitary reproductive tumors.
- Neurons express GnRH receptor and responded to GnRH with time- and dose-dependent increases in GnRH gene expression and protein release.
- In hormone-related tumors, type I GnRH receptors are coupled to the Gi-cAMP signal transduction pathway. In melanoma cells, GnRH-I behaves as a negative regulator of tumor growth and progression.
- the dominant-negative effect, which occurs for human GnRHR mutants isolated from patients with hypogonadotropic hypogonadism , results from receptor retention in the endoplasmic reticulum by mislocalized mutants.
- Pro7.33(303) of the human GnRH receptor is required for selective high affinity binding of mammalian GnRH.
- Expression of gonadotropin-releasing hormone receptor in endometrial stromal sarcomas may provide a rationale for a clinical study of gonadotropin-releasing hormone analogs in the treatment of women with endometrial stromal sarcomas.
- Genetic variation in GNRHR is not likely to be a substantial modulator of pubertal timing in the general population.
- the HFRK motif in the membrane-proximal region confers the differential signal transduction pathways between mammalian and nonmammalian GnRHRs
- the GnRHR-II-reliquum plays a modulatory role in GnRHR-I expression
- there are species-specific dominant negative receptor trafficking effects of the GnRHR between human, rat and mouse
- GNRHR mutations account for approximately 3.5% of all normosmic and 7%-11% of presumed autosomal recessive idiopathic hypogonadotropic hypogonadism, suggesting that additional genes play an important role in normal puberty.
- Cryostat and paraffin sections of prostate biopsy samples of 10 untreated patients with prostate carcinoma (T2-T3, Gleason score 5-8) were investigated for Gn-RH receptors (Gn-RHR) and androgen receptors
- No mutations were identified in the male, whereas in the females the mutation Pro146Ser in the GnRHR was identified in heterozygosity in idiopathic hypogonadotropic hypogonadism
- Activation of the GnRHR by interacting with GnRH may transcriptionally down-regulate itself via the protein kinase C pathway in human neuronal cells.
- data suggest the occurrence of a specific LIM-HD pituitary code and designate the GnRH-R gene as the first identified transcriptional target of Isl-1 in the anterior pituitary
- A homozygous R262Q mutation in the gonadotropin-releasing hormone receptor presenting as constitutional delay of growth and puberty with subsequent borderline oligospermia.
- proportion of the human and the rat WT GnRHR appears to be retained in the endoplasmic reticulum by calnexin, an effect that decreases GnRHR signaling capacity
- The R139C mutation almost completely abolished plasma membrane expression while having little effect on GnRH-binding affinity in hypogonadotropic hypoganadism-related mutant.
- These results reveal GnRH ligand and receptor structural elements for conformational selection, and support co-evolution of GnRH ligand and receptor conformations.
- Summarizes the overall structure-function relationships of the human GnRH receptor, with an emphasis on the impact of naturally occurring mutations.
- Arg(38(1.35)) of the GnRH receptor is essential for high-affinity binding of GnRH agonists and stabilizing the receptor active conformation
- We have defined the proportion of GnRHRs at the cell surface.
- Two endogenous forms of GnRH ligand but only one functional form of full-length GnRH receptor in humans elecits specific functions of the receptor.
- 12% of Kallman syndrome males have KAL1 deletions, but intragenic deletions of the FGFR1, GNRH1, GNRHR, GPR54 and NELF genes are uncommon in Idiopathic hypogonadotropic hypogonadism/Kallman syndrome.
- Transient co-transfection of HEK293 cells with human WT GnRHR and with stimulatory and inhibitory G proteins led to either production or inhibition of total inositol phosphate production, depending on the G protein that was over-expressed
- Data show that over half of meningiomas may be regulated by GnRH-GnRH-R expression in an autocrine fashion.
- Results reveal important pharmacophoric features of the GnRH receptor, and then identify a novel chemical ligand, able to rescue a D(98) mutant of the human GnRHR that could not be rescued as effectively by previously known pharmacoperones.