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SG ID |
SG00001044 |
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UniProt Accession |
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Theoretical PI |
7.83
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Molecular Weight |
78215 Da
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Genbank Nucleotide ID |
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Genbank Protein ID |
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Gene Name |
Lhcgr |
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Gene Synonyms/Alias |
Lhr |
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Protein Name |
Lutropin-choriogonadotropic hormone receptor |
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Protein Synonyms/Alias |
LH/CG-R Luteinizing hormone receptor;LSH-RFlags: Precursor |
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Organism |
Mus musculus (Mouse) |
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NCBI Taxonomy ID |
10090 |
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Chromosome Location |
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Function in Stage |
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Function in Cell Type |
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Description |
Receptor for lutropin-choriogonadotropic hormone. LH actions mediated by testosterone are required for completion of spermatogenesis, and finally, androgen-independent actions of LH are required for the formation of adult-type Leydig cells and recruitment of macrophages into the testes. |
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The information of related literatures |
1. T. Pakarainen, F. P. Zhang, S. Makela, M. Poutanen and I. Huhtaniemi (2005) Testosterone replacement therapy induces spermatogenesis and partially restores fertility in luteinizing hormone receptor knockout mice. Endocrinology 146(2): 596-606. Abstract Testosterone (T) is essential for spermatogenesis, fertility, and maintenance of the male phenotype. We analyzed in hypogonadal LH receptor knockout (LuRKO) male mice whether T treatment can restore their phenotype, spermatogenesis, and fertility. In LuRKO mice, spermatogenesis is arrested at round spermatids, adult-type Leydig cells are absent, T production is dramatically decreased, the animals are cryptorchid, and their accessory sex organs are atrophic. T replacement therapy from 21 d of life for 60 or 120 d in LuRKO mice induced a male phenotype macroscopically indistinguishable from that of wild-type littermates as well as full spermatogenesis and testicular descent. Thus, the absence of LH-dependent prepubertal androgen priming is not necessary for subsequent maturation of the male phenotype. Conspicuously, some abnormalities remained in epididymal histology after T treatment despite normal expression of several epididymis-specific genes in caput epididymis. The mice displayed normal mating behavior, although at lower frequency than wild-type controls. The spermatozoa were able to fertilize oocytes, but their impaired passage from epididymis to uterus was apparent. The mice remained subfertile, because only 9% of all breedings resulted in pregnancy, and only two of 13 mice (15%) were fertile. Moreover, inflammation in epididymides and prostate was found in many T-treated LuRKO mice, which probably impaired sperm transport and contributed to their high rate of subfertility. In conclusion, T replacement initiated prepubertally only partially restores the fertility of LuRKO mice, even though most features of the male phenotype recover. Full fertility may require higher and/or earlier postnatal T exposure or production of other Leydig cell factors lacking in this model. PMID: [15514086] 2. Z. M. Lei, S. Mishra, P. Ponnuru, X. Li, Z. W. Yang and V. Rao Ch (2004) Testicular phenotype in luteinizing hormone receptor knockout animals and the effect of testosterone replacement therapy. Biol Reprod 71(5): 1605-13. Abstract The LH receptor knockout model, developed in our laboratory, was used in determining what FSH alone can do in the absence of LH signaling and whether any of the testicular LH actions are not mediated by androgens. The results revealed that null animals contained smaller seminiferous tubules, which contained the same number of Sertoli cells, spermatogonia, and early spermatocytes as wild-type siblings. The number of late spermatocytes, on the other hand, was moderately decreased, the number of round spermatids was dramatically decreased, and elongated spermatids were completely absent. These changes appear to be due to an increase in apoptosis in spermatocytes. While the number of Leydig cells progressively increased from birth to 60 days of age in wild-type animals, they remained unchanged in null animals. Consequently, 60-day-old null animals contained only a few Leydig cells of fetal type. The age-dependent increase in testicular macrophages lagged behind in null animals compared with wild-type siblings. Orchidopexy indicated that -/- testicular phenotype was not due to abdominal location. Rather, it was mostly due to androgen deficiency, as 21-day testosterone replacement therapy stimulated the growth of seminiferous tubules, decreased apoptosis, and increased the number of late spermatocytes and round spermatids and their subsequent differentiation into mature sperm. The therapy, however, failed to restore adult-type Leydig cells and testicular macrophage numbers to the wild-type levels. In summary, our data support the concept that FSH signaling alone can maintain the proliferation and development of Sertoli cells, spermatogonia, and early spermatocytes. LH actions mediated by testosterone are required for completion of spermatogenesis, and finally, androgen-independent actions of LH are required for the formation of adult-type Leydig cells and recruitment of macrophages into the testes. PMID: [15253923] 3. Z. M. Lei, S. Mishra, W. Zou, B. Xu, M. Foltz, X. Li and C. V. Rao (2001) Targeted disruption of luteinizing hormone/human chorionic gonadotropin receptor gene. Mol Endocrinol 15(1): 184-200. Abstract LH/hCG receptors were disrupted by gene targeting in embryonic stem cells. The disruption resulted in infertility in both sexes. The gonads contained no receptor mRNA or receptor protein. Serum LH levels were greatly elevated, and FSH levels were moderately elevated in both sexes; estradiol and progesterone levels decreased but were not totally suppressed in females; testosterone levels were dramatically decreased and estradiol levels moderately elevated in males. The external and internal genitalia were grossly underdeveloped in both sexes. Abnormalities included ambiguous vaginal opening, abdominal testes, micropenis, dramatically decreased weights of the gonads and reproductive tract, arrested follicular growth beyond antral stage, disarray of seminiferous tubules, diminished number and hypotrophy of Leydig cells, and spermatogenic arrest beyond the round spermatid stage. LH/hCG receptor gene disruption had no effect on FSH receptor mRNA levels in ovaries and testes, progesterone receptor (PR) levels in ovaries and androgen receptor (AR) levels in testes. However, it caused a dramatic decrease in StAR and estrogen receptor-alpha (ERalpha) mRNA levels and an increase in ERbeta mRNA levels in both ovaries and testes. Estradiol and progesterone replacement therapy in females and testosterone replacement in males, to determine whether phenotype and biochemical changes were a consequence of decreased gonadal steroid levels or due to a loss of LH signaling, revealed complete restoration of some and partial restoration of others. Nevertheless, the animals remained infertile. It is anticipated that the LH receptor knockout animals will increase our current understanding of gonadal and nongonadal actions of LH and hCG. PMID: [11145749] 4. C. V. Rao and Z. M. Lei (2002) Consequences of targeted inactivation of LH receptors. Mol Cell Endocrinol 187(1-2): 57-67. Abstract The inactivation of luteinizing hormone (LH) receptors was neither lethal nor it had any effect on sex differentiation. However, it dramatically reduced the growth and development of gonads and the reproductive tract. As a result, both female and male animals were infertile. Serum LH levels were dramatically elevated, follicle stimulating hormone (FSH) levels moderately elevated in both sexes, estradiol and progesterone levels partially decreased in females, testosterone levels dramatically decreased and estradiol levels moderately increased in males. The knockout of LH receptors had no effect on gonadal FSH receptors in both sexes, progesterone receptors in females and androgen receptors in males. However, estrogen receptor ERalpha and steroidogenic acute regulatory protein decreased and ERbeta increased in both sexes. cDNA expression array analyses revealed that testes were affected more than ovaries and more genes showed an increase rather than a decrease in testes. The affected genes came from many unexpected families. Both null females and males had a decreased density of femur and became obese with age. The ovarian failure in knockout animals could not be reversed by estradiol/progesterone replacement therapy or by PMSG and human chorionic gonadotropin (hCG) injections. Although, testosterone replacement therapy of 30-60-day old null males partially improved spermatogenesis, the animals still remained infertile. A single testosterone injection on postnatal day 1 followed by 21-45-day testosterone replacement therapy beginning at 30 days of age, however, restored fertility. Studies showed that uterus of null animals could not initiate pregnancy even though the size and morphology were greatly improved by estradiol and progesterone replacement therapy. In general, non-gonadal phenotypes in null females and males were not completely reversed by hormone replacement therapy, suggesting that LH signaling could be important for their function. Heterozygous animals were indistinguishable from wild-type animals at 60 days of age. However, as they grew to about 1 year of age, they began to stop cycling, some became extremely obese, showed a decreased density of femur and all animals developed endometrial tumors with a cancer histology. LH receptor-knockout animals will be useful in advancing our present understanding on the importance of classical as well as non-classical actions of LH in the body, in advancing novel therapeutic uses of hCG, and in better understanding and rationalizing the consequences of inactivating type human LH receptor mutations. PMID: [11988312] 5. F. P. Zhang, M. Poutanen, J. Wilbertz and I. Huhtaniemi (2001) Normal prenatal but arrested postnatal sexual development of luteinizing hormone receptor knockout (LuRKO) mice. Mol Endocrinol 15(1): 172-83. Abstract To study further the role of gonadotropins in reproductive functions, we generated mice with LH receptor (LHR) knockout (LuRKO) by inactivating, through homologous recombination, exon 11 on the LHR gene. LuRKO males and females were born phenotypically normal, with testes, ovaries, and genital structures indistinguishable from their wild-type (WT) littermates. Postnatally, testicular growth and descent, and external genital and accessory sex organ maturation, were blocked in LuRKO males, and their spermatogenesis was arrested at the round spermatid stage. The number and size of Leydig cells were dramatically reduced. LuRKO females also displayed underdeveloped external genitalia and uteri postnatally, and their age of vaginal opening was delayed by 5-7 days. The (-/-) ovaries were smaller, and histological analysis revealed follicles up to the early antral stage, but no preovulatory follicles or corpora lutea. Reduced gonadal sex hormone production was found in each sex, as was also reflected by the suppressed accessory sex organ weights and elevated gonadotropin levels. Completion of meiosis of testicular germ cells in the LuRKO males differs from other hypogonadotropic/cryptorchid mouse models, suggesting a role for FSH in this process. In females, FSH appears to stimulate developing follicles from the preantral to early antral stage, and LH is the stimulus beyond this stage. Hence, in each sex, the intrauterine sex differentiation is independent of LH action, but it has a crucial role postnatally for attaining sexual maturity. The LuRKO mouse is a close phenocopy of recently characterized human patients with inactivating LHR mutations, although the lack of pseudohermaphroditism in LuRKO males suggests that the intrauterine sex differentiation in this species is not dependent on LH action. PMID: [11145748] Back to Top |
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Figures for illustrating the function of this protein/gene |
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Function |
Receptor for lutropin-choriogonadotropic hormone. Theactivity of this receptor is mediated by G proteins which activateadenylate cyclase. Back to Top |
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Subcellular Location |
Cell membrane; Multi-pass membrane protein. |
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Tissue Specificity |
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Gene Ontology |
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Interpro |
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Pfam |
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SMART |
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PROSITE |
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PRINTS |
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Created Date |
18-Oct-2012 |
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Record Type |
Experiment identified |
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Protein sequence Annotation |
SIGNAL 1 26 By similarity. CHAIN 27 700 Lutropin-choriogonadotropic hormone receptor. /FTId=PRO_0000012781. TOPO_DOM 27 362 Extracellular (Potential). TRANSMEM 363 390 Helical; Name=1; (Potential). TOPO_DOM 391 399 Cytoplasmic (Potential). TRANSMEM 400 422 Helical; Name=2; (Potential). TOPO_DOM 423 443 Extracellular (Potential). TRANSMEM 444 466 Helical; Name=3; (Potential). TOPO_DOM 467 486 Cytoplasmic (Potential). TRANSMEM 487 509 Helical; Name=4; (Potential). TOPO_DOM 510 529 Extracellular (Potential). TRANSMEM 530 551 Helical; Name=5; (Potential). TOPO_DOM 552 574 Cytoplasmic (Potential). TRANSMEM 575 598 Helical; Name=6; (Potential). TOPO_DOM 599 609 Extracellular (Potential). TRANSMEM 610 631 Helical; Name=7; (Potential). TOPO_DOM 632 700 Cytoplasmic (Potential). REPEAT 52 75 LRR 1. REPEAT 126 150 LRR 2. REPEAT 176 200 LRR 3. REPEAT 225 248 LRR 4. LIPID 647 647 S-palmitoyl cysteine (By similarity). LIPID 648 648 S-palmitoyl cysteine (By similarity). CARBOHYD 103 103 N-linked (GlcNAc...) (Potential). CARBOHYD 178 178 N-linked (GlcNAc...) (Potential). CARBOHYD 199 199 N-linked (GlcNAc...) (Potential). CARBOHYD 295 295 N-linked (GlcNAc...) (Potential). CARBOHYD 303 303 N-linked (GlcNAc...) (Potential). CARBOHYD 317 317 N-linked (GlcNAc...) (Potential). DISULFID 443 518 By similarity. Back to Top |
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Nucleotide Sequence |
Length: 2569 bp Go to nucleotide: FASTA |
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Protein Sequence |
Length: 700 bp Go to amino acid: FASTA |
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The verified Protein-Protein interaction information |
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Other Protein-Protein interaction resources |
String database |
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View Microarray data |
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Comments |
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