LHCGR Membrane Protein Introduction

Introduction of LHCGR

LHCGR, encoded by LHCGR gene, is a member of G-protein coupled receptor 1 family and its activity is regulated by G proteins. The receptor is about 85-95 KD and consists of 674 amino acids. It has seven transmembrane α-helixes, heavily glycosylated extracellular domain, and is rich in serine and threonine residues in intracellular region. LHCGR is found not only in the ovary and testis but in many extragonadal organs such as the uterus and breasts. It plays an essential role in normal reproduction.

Function of LHCGR Membrane Protein

LHCGR is the receptor for both luteinizing hormone (LH) and chorionic gonadotropins (such as hCG in humans). When LH binds to the external part of LHCGR, LHCGR will be activated via shift conformation and mechanically activate the G protein releasing from the receptor. Then G protein promotes the activation of adenylate cyclase resulting in the increase of intracellular second messengers cAMP, transducing the signal. In the female, the receptor is required for follicular maturation and ovulation, as well as luteal function. LH interacting with the receptor stimulates ovulation. Chorionic gonadotropin binding with the receptor can maintain conditions necessary for the pregnancy to continue. In the male, chorionic gonadotropin interacting with LHCGR promotes the development of Leydig cells in the testes and LH binding to LHCGR stimulates Leydig cells to produce androgens and spermatogenesis. The testosterone produced by Leydig cells is very important for male sexual development. Lacking LHCGR will lead to infertility and disorders of male secondary sexual character development.

Fig.1 The seven transmembrane α-helix structure of G protein-coupled receptor such as LHCGR.

Application of LHCGR Membrane Protein in Literature

1. G.R.A., et al. Role of Lh polymorphisms and r-hLh supplementation in GnRh agonist treated ART cycles: A cross sectional study. European Journal of Obstetrics & Gynecology & Reproductive Biology. 2018, 222:119-125. PubMed ID: 29408742
   
   

   The findings reveal that N312S polymorphism in the LHCGR gene is associated with the doses of r-hLH supplementation in patients undergoing ART treatment. Patients with heterozygous (N/S) or homozygous (S/S) require higher doses of r-hLH supplementation and show higher clinical pregnancy rates.

2. Kawai T., et al. The cell type-specific expression of Lhcgr in mouse ovarian cells: evidence for a DNA-demethylation-dependent mechanism. Endocrinology. 2018, 159(5):2062-2074. PubMed ID: 29579175
   
   

   The study indicates that the demethylation of the Lhcgr-promoter region is mediated, at least in part, by retinoic acid synthesis and is a key mechanism regulating the cell type-specific differentiation during follicular development.

3. Plöckinger U., et al. Functional implications of LH/hCG receptors in pregnancy-induced cushing syndrome. Journal of the Endocrine Society. 2017, 1(1):57-71. PubMed ID: 29264446
   
   

   The authors describe a patient with reversible, somatic mutation-independent pregnancy-induced Cushing syndrome (CS), which is caused by human choriogonadotropin (hCG)-activated LHCGR-associated mechanism.

4. Robles-Fernandez I., et al. Association between polymorphisms in sex hormones synthesis and metabolism and prostate cancer aggressiveness. Plos One. 2017, 12(10):e0185447. PubMed ID: 28981526
   
   

   The variants in CYP17A1, LHCGR and ESR2 genes associated with a poor progression of prostate cancer are identified in this study. Hence, these variants may be regarded as biomarkers for prostate cancer management.

5. Doroszko M., et al. Luteinizing hormone and GATA4 action in the adrenocortical tumorigenesis of gonadectomized female mice. Cellular Physiology & Biochemistry. 2017, 43(3):1064-1076. PubMed ID: 28977799
   
   

   The study shows that LH/LHCGR signaling is critical for the adrenal cell reprogramming by GATA4 induction, prompting adenoma formation and gonadal-like phenotype of the adrenocortical tumors in inhα/Tag mice.

LHCGR Preparation Options

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