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Validated All-in-One™ qPCR Primer for LHCGR(NM_000233.3) Search again
Product ID:
HQP101794
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
HHG, LCGR, LGR2, LH/CG-R, LH/CGR, LHR, LHRHR, LSH-R, ULG5
Gene Description:
luteinizing hormone/choriogonadotropin receptor
Target Gene Accession:
NM_000233.3(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:
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| A | B |
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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. |
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Summary
This gene encodes the receptor for both luteinizing hormone and choriogonadotropin. This receptor belongs to the G-protein coupled receptor 1 family, and its activity is mediated by G proteins which activate adenylate cyclase. Mutations in this gene result in disorders of male secondary sexual character development, including familial male precocious puberty, also known as testotoxicosis, hypogonadotropic hypogonadism, Leydig cell adenoma with precocious puberty, and male pseudohermaphtoditism with Leydig cell hypoplasia. [provided by RefSeq].
Gene References into function
- Results confirm the fact that somatic activating mutations of gonadotropin receptors are involved in gonadal tumorigenesis.
- structure, functions, and regulation of this important receptor. review. (lutropin receptor)
- review of the mechanism of desensitization to LH mediated by extensive clustering and internalization of the LH hormone-receptor complex
- Cis- and trans-activation of hormone receptors: the LH receptor
- Evidence that luteinising hormone receptor polymorphisms may contribute to male undermasculinisation.
- HDAC-Sin3A complex regulates LHR Gene transcription
- study of the conformations of the active and inactive states of the hLHR
- LH receptor gene expresses in normal endometrium at very low levels, and at increased levels in endometrial cancerous tissues compared with surrounding microscopically normal tissues
- Homozygous mutation within the conserved Ala-Phe-Asn-Glu-Thr motif of exon 7 of the LH receptor causes male pseudohermaphroditism.
- Structure of LH receptor based on molecular modeling and the supporting experimental data from engineered and naturally occurring mutations. (review)
- LH-responsive Cushing's syndrome, associated with bilateral adrenal hyperplasia, may result from aberrant (or possibly increased) adrenal LH receptor expression.
- findings suggest that the luteinizing hormone receptor 18insLQ gene polymorphism determines an earlier age of disease onset and is prognostic for poor outcome of breast cancer
- although exon 10 of the luteinizing hormone receptor plays no role in ligand binding, it is important for receptor activation by LH by a mechanism probably involving extracellular conformational changes
- Point mutations in the hinge region or ligand binding could cause conformational changes in the transmembrane region that result in Gs activation.
- In human ovaries, MAb found 6 distinct LHR bands migrating at approximately 92, 80, 68, 59, 52 & 48 kDa. There is a possible role for LHR in the development of abnormal pregnancy, pelvic floor disorders & Alzheimer's disease.
- human cervix contains functional LH/hCG receptors, which suggests that LH during the menstrual cycle and hCG during pregnancy may regulate cervical functions.
- results of mutagenesis and buffer studies suggest that electrostatic effects contribute to ligand binding and/or that the LHR ectodomain may exist in two conformations, one being more accessible to ligand at reduced ionic strength.
- the G proteins activated by constitutively active mutants of the hLHR associated with Leydig cell hyperplasia or tumors are identical and are the same as those activated by the agonist-engaged hLHR-wt.
- The LHR gene promoter is repressed by cross talk among the transcription factors EAR3, SP1 and TFIIB.
- characterization of interaction with GAIP-interacting protein C terminus
- cell surface human lutropin receptor self-associates
- a novel, noncontiguous, transferable motif that participates in the sorting of internalized G protein-coupled receptors
- Fetal kidney, liver, pancreas, lung, small and large intestines, and adrenals contained hCG/LH receptors. May mediate pleiotropic actions of hCG in growing human fetus.
- analysis of mutations in human luteinizing hormone receptor
- splice variant of the human luteinizing hormone (LH) receptor modulates the expression of wild-type human LH receptor
- H295R cells contain LH/hCG receptors, which are coupled to increasing DHEAS secretion through upregulating the dhea sulfotransferase enzyme mRNA level
- These data do not support the hypothesis that qualitative changes in LH receptor splicing have a role in luteolysis or that a naturally occurring LH receptor lacking exon 10 has a role in maternal recognition of pregnancy.
- demonstrated the presence of LH/hCG receptor mRNA and protein in normal male breast tissue obtained at autopsy and archival samples of benign gynecomastia and male breast carcinoma
- characterization of the position of conserved alpha-subunit regions in lutropin receptor complexes
- contacts between the small seatbelt loop of alpha-human choriogonadotropin and the lutropin receptor involve its backbone atoms and possibly the side chain of residue betaAsp-99
- palmitoylation of cysteine residues 643 and 644 of the human LHR is a determinant of recycling
- Leydig cell hypoplasia due to inactivation of luteinizing hormone receptor by a novel homozygous nonsense truncation mutation in the seventh transmembrane domain
- SP factors play an intimate part in transcriptional regulation of the this receptor gene.
- activation of the LHR results from subtle modifications of intramolecular interactions between the two domains and low-affinity binding of hCG to the extracellular loops or residues preceding the first transmembrane segment
- Lutropin receptors form homo- and heterodimers, via interactions involving primarily their heptahelical domains. The large hormone-binding ectodomains were dispensable for dimerization but modulated protomer interaction. The dimers show allosterism.
- human follitropin (FSH) receptor association with splicing variant of human lutropin/choriogonadotropin receptor negatively controls the expression of human FSH receptor
- the structural trigger of the constitutive activity of the L457R mutant of the lutropin receptor may also be responsible for its lack of hormone responsiveness
- Epigenetic silencing and activation of the LHR gene is achieved through coordinated histone acetylation and promoter DNA methylation.
- LH receptor expression is elevated in aldosterone-producing adenomas, which makes LH a potential cause of the excessive production of aldosterone in a subset of these adrenal tumors.
- LHR I114F mutation reduces ligand binding and signal transduction, and is partially responsible for Leydig cell hypoplasia
- Decidualization results in the downregulation of LHCGR.
- These studies have revealed a novel mechanism of Trichostatin A action through derecruitment of a repressor from the Luteinizing hormone receptor gene promoter in a PI3K/PKCzeta-induced Sp1 phosphorylation-dependent manner.
- In the absence of ligand, constitutively active receptors are self-associated and located in high buoyancy membrane fractions, both characteristics of the hormone-treated wild type receptor.
- The data presented here support the model of glycoprotein hormone-receptor interaction in which the hormone binds to the extracellular domain through the beta subunit and then the alpha subunit is brought in contact with the transmembrane domain.
- Molecular dynamics simulations on the isolated receptor and computational modeling of LHR homodimerization suggest that mutation-induced LHR activation favors H4-H4 contacts involving the highly conserved W491 from both the receptors monomers.
- REVIEW: novel insights into the properties of target cells expressing activating hLHR mutants and into the structural basis for hLHR activation
- These results reveal a novel mechanism of regulation for gonadotropin receptor expression.
- Ectodomain has major function apart from hormone binding, also interacts with transmembrane domain.
- This study characterized the human trophoblastic luteinizing hormone/chorionic gonadotropin receptor and investigated its expression using the in vitro model of human cytotrophoblast differentiation into syncytiotrophoblast.
- In Ishikawa cells LH/hCG does not utilize its conventional receptor.
- Rhes inhibits functional activity (cyclic AMP production) of LHR.
- study shows FSHR constitutively activating mutants (CAMs) not as active as LHR CAMs with comparable mutation; all FSHR CAMs showed strong promiscuous activation by high concentration of other glycoprotein hormone receptors; LHR CAMs showed little or none
- Although functional changes of the LHR 291Ser candidate allele were observed, no associations with breast cancer were found, while the LHR 312Asn allele can be regarded as a weak breast cancer risk allele.
- An intracellular loop (IL2) residue confers different basal constitutive activities to the human lutropin receptor and human thyrotropin receptor through structural communication between IL2 and helix 6, via helix 3.
- LH/hCGR, coexpressed with hCGbeta, may act as a potential mediator of hCG action in nontrophoblastic gynecological cancers
- The S312N SNP in exon 10 (rs2293275) was significantly less frequent in men with maldescended testes than in controls.
- Data show that mutations of the lutropin/choriogonadotropin receptor that do not activate the phosphoinositide cascade allow hCG to induce aromatase expression in immature rat granulosa cells.
- A novel regulatory signaling mechanism of transcriptional control in which the LHR is derepressed through PKCalpha/ERK-mediated Sp1 phosphorylation, causing the release of HDAC1/mSin3A complex from the promoter.
- Co-expression of LH/hCGR and hCG protein in individual cancer cells may point to an autocrine or paracrine mechanism of _hCG activity in the tumor microenvironment.
- findings identify a new, functional exon in the LHCGR gene and show that mutations in this exon cause some cases of Leydig cell hypoplasia
- We report the discovery of a genetic interaction between APOE and LHCGR alleles that is associated with a significantly decreased risk for Alzheimer's disease in males
- LHR mutations may represent an underestimated cause of infertility in women, in addition to being responsible for male hypogonadism with reduced spermatogenesis
- dissociation of serine/threonine protein phosphatases PP2A and PP1 from the LHR promoter mediates TSA-induced activation of LHR gene transcription in a cell-specific manner
- Asp(330) and Tyr(331) are key amino acids in LH/hCG mediated signaling
- These results show that, in MA-10 cells, the hLHR activates Fyn through an arrestin-3-dependent pathway and that this pathway is a mediator of the hLHR-provoked release of EGF-like growth factors.
- Sexual pseudo-precocity caused by a somatic activating mutation of the LH receptor preceding true sexual precocity.
- These results suggest that the extracellular domain of the LHR is one of the determinants that confer its ability for proper maturation and cell surface expression.
- study showed in ovarian cancer cells LHR expression & activation upregulate ErbB-2 expression; data establish role for LH & LHR in regulation of ErbB-2 expression & suggest ErbB-2 upregulation alone is insufficient in producing aggressive phenotype