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genetic association/pharmacogenetic studies in population in India: Data suggest that need for (and dose required of) fertility agent recombinant LH in addition to fertility agent recombinant FSH (show BRD2 Proteins) is associated with SNP in LHCGR in women undergoing ovarian stimulation in conjunction with in vitro fertilization. (LH = luteinizing hormone; FSH (show BRD2 Proteins) = follicle stimulating hormone)
hCG (show CGA Proteins) and its receptor, LH/CGR, are expressed in numerous sites of the reproductive tract, both in gonadal and extra-goanadal tissues, promoting oocyte maturation, fertilization, implantation and early embryo development
The reduced fertilisation and pregnancy rate was associated with a lower LH receptor density and a lack of essential down-regulation of the FSH (show BRD2 Proteins) and LH receptor.
This work demonstrates that the expression of FSHR (show FSHR Proteins) and LHCGR can be induced in hGL5 cells but that the FSHR (show FSHR Proteins)-dependent cAMP/PKA pathway is constitutively silenced, possibly to protect cells from FSHR (show FSHR Proteins)-cAMP-PKA-induced apoptosis.
Inactivating mutations of the LHCGR gene may be a common cause of 46,XY primary amenorrhea.
data demonstrate that the majority of LHR mutations lead to intracellular retention and highlight the potential for novel pharmacological chaperone therapeutics that can "rescue" expression/function of retained mutant GPCRs.
expression and activation of LHCGR and ARF6 (show ARF6 Proteins) are up-regulated in GC from PCOS women but the mechanism of agonist-induced LHCGR internalization is unaltered
We showed that GNRHR and LHCGR were highly expressed in some wildtype aldosterone-producing adenoma samples, and that they positively correlated with GnRH-stimulated aldosterone production.
Mutation in the LHCGR gene is associated with Testotoxicosis.
The luteinizing hormone/human chorionic gonadotrophin receptor (LHCGR) variant N312S and the follicle-stimulating hormone receptor (FSHR (show FSHR Proteins)) variant N680S can be utilized for the prediction of pregnancy chances in women undergoing IVF (show SCN5A Proteins).
Activating mutations in LHCGR cause familial male-limited precocious puberty
Study tested for the first time a role of ZFP36L2 (show ZFP36L2 Proteins) in the decay of LHR mRNA, when transcription was inhibited; results of our cell-based assay support the conclusion that LHR mRNA expression is controlled post-transcriptionally by ZFP36L2 (show ZFP36L2 Proteins).
FSHR (show FSHR Proteins) and LHR proteins are significantly upregulated in CCs (show CCS Proteins) surrounding oocytes arrested at the 2-cell stage, reflecting their developmental incompetence.
Triptorelin and cetrorelix induce immune responses and affect uterine development and expressions of genes and proteins of ESR1 (show ESR1 Proteins), LHR, and FSHR (show FSHR Proteins)
Data suggest that persistent cAMP signals from internalized luteinizing hormone receptor (LH receptors) contribute to transmitting LH effects inside follicle cells and ultimately to the oocyte.
Demonstrate the presence of LH receptors. Activation resulted in a dose-dependent increase in glucose-induced release of insulin (show INS Proteins).
LHCGR signaling in regulating the Ahr (show AHR Proteins) message involves protein kinase A pathway and is attributable to decreased transcription rate.
Data from mutant mouse strain (gain-of-function mutation in LHR, D578G; most common mutation found in familial male-limited precocious puberty) confirm that LHR is critical for male steroidogenesis, gametogenesis, and Leydig cell development.
LH/hCG (show CGA Proteins) tightly up-regulates MKP-3 (show DUSP6 Proteins) which in turn, dephosphorylates ERK1/2 and drives p21 expression.
Data suggest that Lhcgr in endometrium and luteinizing hormone in blastocyst are involved in embryo/blastocyst implantation; expression of Lhcgr is up-regulated in endometrial epithelium in estrus cycle at time of implantation readiness (estrus).
The outcomes of the present study support a dynamic multi-facetted regulation of LHR during pre-translation.
expression of LHR mRNA in bovine granulosa cells is established after follicle deviation, and the lower abundance of LRBP (show MVK Proteins) mRNA after the expected time of deviation may contribute to greater expression of LHR in the bovine dominant follicle
These results suggested an acute regulation of INSL3 (show INSL3 Proteins) by luteinizing hormone (LH) because INSL3 (show INSL3 Proteins) concentrations increased immediately after endogenous and exogenous LH stimulation.
INVESTIGATION OF STAT5A (show STAT5A Proteins), FSHR (show FSHR Proteins) AND LHR GENE POLYMORPHISMS IN TURKISH INDIGENOUS CATTLE BREEDS
These findings strongly support the concept that IGF-1 (show IGF1 Proteins) upregulates LHR expression in granulosa cells and that IGF-1 (show IGF1 Proteins) is required for determining which follicle becomes dominant and acquires ovulatory capacity.
LHCGR mRNA expression in granulosa cells was significantly higher in large antral follicles than in cysts, and not detected in granulosa cells of small and medium antral follicles.
The luteinizing hormone receptor [LHR] splicing pattern is complex in bovine Leydig cells, and expression of full-length LHR and isoforms A and B changes when induced with LH.
The LHCGR gene is a potential marker for superovulation response and can be used to predict the most appropriate dose of FSH (show BRD2 Proteins) for superovulation in Chinese Holstein cows.
Dominant follicles experience a reduction in FSH (show BRD2 Proteins) dependence (diminished expression of FSHR (show FSHR Proteins)), but acquire increased LH dependence (enhanced expression of LHCGR) as they grow during the low FSH (show BRD2 Proteins) milieu of follicular waves.
Three single nucleotide polymorphisms in LHCGR were significantly associated with variations in cattle fertility and production traits.
Data show that double mutation of follicle-stimulating hormone receptor (fshr (show FSHR Proteins)) and luteinizing hormone receptor (lhcgr) resulted in infertile males
Data show for the first time in a vertebrate species that Leydig cells as well as Sertoli cells express the mRNAs for both fshr (show FSHR Proteins) and lhcgr.
In porcine 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.
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.
, lutropin-choriogonadotropic hormone receptor
, lutropin/choriogonadotropin receptor
, luteinizing hormone receptor
, LH receptor
, luteinizing hormone receptor 2 protein
, luteinizing hormone receptor precursor variant 1
, luteinizing hormone receptor precursor variant 2
, lutropin-choriogonadotropin receptor
, luteinizing hormone/choriogonadotropin receptor
, lutropin-choriogonadotropic hormone receptor-like