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Data suggest that, during follicle maturation, levels of MIR122 determine levels of LHR mRNA expression in the ovary. (LHR = luteinizing hormone receptor; MIR122 = microRNA 122) [REVIEW]
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 (zeige BRD2 Proteine) is associated with SNP in LHCGR in women undergoing ovarian stimulation in conjunction with in vitro fertilization. (LH = luteinizing hormone; FSH (zeige BRD2 Proteine) = follicle stimulating hormone)
hCG (zeige CGA Proteine) 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 (zeige BRD2 Proteine) and LH receptor.
This work demonstrates that the expression of FSHR (zeige FSHR Proteine) and LHCGR can be induced in hGL5 cells but that the FSHR (zeige FSHR Proteine)-dependent cAMP/PKA pathway is constitutively silenced, possibly to protect cells from FSHR (zeige FSHR Proteine)-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 (zeige ARF6 Proteine) 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.
Activating mutations in LHCGR cause familial male-limited precocious puberty
Study tested for the first time a role of ZFP36L2 (zeige ZFP36L2 Proteine) 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 (zeige ZFP36L2 Proteine).
FSHR (zeige FSHR Proteine) and LHR proteins are significantly upregulated in CCs (zeige CCS Proteine) 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 (zeige ESR1 Proteine), LHR, and FSHR (zeige FSHR Proteine)
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 (zeige INS Proteine).
LHCGR signaling in regulating the Ahr (zeige AHR Proteine) 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 (zeige CGA Proteine) tightly up-regulates MKP-3 (zeige DUSP6 Proteine) 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 (zeige MVK Proteine) 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 (zeige INSL3 Proteine) by luteinizing hormone (LH) because INSL3 (zeige INSL3 Proteine) concentrations increased immediately after endogenous and exogenous LH stimulation.
INVESTIGATION OF STAT5A (zeige STAT5A Proteine), FSHR (zeige FSHR Proteine) AND LHR GENE POLYMORPHISMS IN TURKISH INDIGENOUS CATTLE BREEDS
These findings strongly support the concept that IGF-1 (zeige IGF1 Proteine) upregulates LHR expression in granulosa cells and that IGF-1 (zeige IGF1 Proteine) 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 (zeige BRD2 Proteine) for superovulation in Chinese Holstein cows.
Dominant follicles experience a reduction in FSH (zeige BRD2 Proteine) dependence (diminished expression of FSHR (zeige FSHR Proteine)), but acquire increased LH dependence (enhanced expression of LHCGR) as they grow during the low FSH (zeige BRD2 Proteine) 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 (zeige FSHR Proteine)) 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 (zeige FSHR Proteine) 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