protein

Recombinant Human Lutropin-choriogonadotropic hormone receptor (LHCGR), partial

MBS960675

0.01 mg (E-Coli)

160 USD

Recombinant Protein

Recombinant Human Lutropin-choriogonadotropic hormone receptor (LHCGR), partial

[Lutropin-choriogonadotropic hormone receptor (LHCGR)]

[Luteinizing hormone receptor; LHR; LSH-R]

[lutropin-choriogonadotropic hormone receptor; Lutropin-choriogonadotropic hormone receptor; lutropin-choriogonadotropic hormone receptor; luteinizing hormone/choriogonadotropin receptor; Luteinizing hormone receptor; LHR; LSH-R]

[LHCGR]

[LHCGR; LHCGR; HHG; LHR; LCGR; LGR2; ULG5; LHRHR; LSH-R; LH/CGR; LH/CG-R; LCGR; LGR2; LHRHR; LH/CG-R; LHR; LSH-R]

LSHR_HUMAN

E Coli or Yeast or Baculovirus or Mammalian Cell

[27-363aa; Partial]

EALCPEPCNCVPDGALRCPGPTAGLTRLSLAYLPVKVIP
SQAFRGLNEVIKIEISQIDSLERIEANAFDNLLNLSEIL
IQNTKNLRYIEPGAFINLPRLKYLSICNTGIRKFPDVTK
VFSSESNFILEICDNLHITTIPGNAFQGMNNESVTLKLY
GNGFEEVQSHAFNGTTLTSLELKENVHLEKMHNGAFRGA
TGPKTLDISSTKLQALPSYGLESIQRLIATSSYSLKKLP
SRETFVNLLEATLTYPSHCCAFRNLPTKEQNFSHSISEN
FSKQCESTVRKVNNKTLYSSMLAESELSGWDYEYGFCLP
KTPRCAPEPDAFNPCEDIMGYDFLR

Greater than 90% as determined by SDS-PAGE.

Liquid containing glycerol

Store at -20 degree C, for extended storage, conserve at -20 degree C or -80 degree C.

SDS-PAGE

Production Note: Special Offer: The E Coli host-expressed protein is manufactured from a stock plasmid containing the protein gene. E Colihost-expressed protein is stocked in different unit sizes ranging from as small as 10 ug to as large as 1 mg. Bulk inventory is also available. The E Coli host-expressed protein has been ordered over and over again by researchers and has stood the test of time as both a robust protein and important target for the research community. It is part of our new program to make our most popular protein targets and corresponding hosts available in expanded unit sizes and with a quick processing time. Select E Coli host-expressed protein for the fastest delivery among all hosts. Please contact our technical support team or email to support@mybiosource.com for more details.

Neuroscience

Receptor for lutropin-choriogonadotropic hormone. The activity of this receptor is mediated by G proteins which activate adenylate cyclase.

Cloning and sequencing of human LH/hCG receptor cDNA.Minegish T., Nakamura K., Takakura Y., Miyamoto K., Hasegawa Y., Ibuki Y., Igarashi M.Biochem. Biophys. Res. Commun. 172:1049-1054(1990) Expression of human luteinizing hormone (LH) receptor interaction with LH and chorionic gonadotropin from human but not equine, rat, and ovine species.Jia X.-C., Oikawa M., Bo M., Tanaka T., Ny T., Boime I., Hsueh A.J.W.Mol. Endocrinol. 5:759-768(1991) Isolation of TSH and LH/CG receptor cDNAs from human thyroid regulation by tissue specific splicing.Frazier A.L., Robbins L.S., Stork P.J., Sprengel R., Segaloff D.L., Cone R.D.Mol. Endocrinol. 4:1264-1276(1990) Structure of the human luteinizing hormone-choriogonadotropin receptor gene unusual promoter and 5' non-coding regions.Atger M., Misrahi M., Sar S., Leflem L., Dessen P., Milgrom E.Mol. Cell. Endocrinol. 111:113-123(1995) Generation and annotation of the DNA sequences of human chromosomes 2 and 4.Hillier L.W., Graves T.A., Fulton R.S., Fulton L.A., Pepin K.H., Minx P., Wagner-McPherson C., Layman D., Wylie K., Sekhon M., Becker M.C., Fewell G.A., Delehaunty K.D., Miner T.L., Nash W.E., Kremitzki C., Oddy L., Du H., Sun H., Bradshaw-Cordum H., Ali J., Carter J., Cordes M., Harris A., Isak A., van Brunt A., Nguyen C., Du F., Courtney L., Kalicki J., Ozersky P., Abbott S., Armstrong J., Belter E.A., Caruso L., Cedroni M., Cotton M., Davidson T., Desai A., Elliott G., Erb T., Fronick C., Gaige T., Haakenson W., Haglund K., Holmes A., Harkins R., Kim K., Kruchowski S.S., Strong C.M., Grewal N., Goyea E., Hou S., Levy A., Martinka S., Mead K., McLellan M.D., Meyer R., Randall-Maher J., Tomlinson C., Dauphin-Kohlberg S., Kozlowicz-Reilly A., Shah N., Swearengen-Shahid S., Snider J., Strong J.T., Thompson J., Yoakum M., Leonard S., Pearman C., Trani L., Radionenko M., Waligorski J.E., Wang C., Rock S.M., Tin-Wollam A.-M., Maupin R., Latreille P., Wendl M.C., Yang S.-P., Pohl C., Wallis J.W., Spieth J., Bieri T.A., Berkowicz N., Nelson J.O., Osborne J., Ding L., Meyer R., Sabo A., Shotland Y., Sinha P., Wohldmann P.E., Cook L.L., Hickenbotham M.T., Eldred J., Williams D., Jones T.A., She X., Ciccarelli F.D., Izaurralde E., Taylor J., Schmutz J., Myers R.M., Cox D.R., Huang X., McPherson J.D., Mardis E.R., Clifton S.W., Warren W.C., Chinwalla A.T., Eddy S.R., Marra M.A., Ovcharenko I., Furey T.S., Miller W., Eichler E.E., Bork P., Suyama M., Torrents D., Waterston R.H., Wilson R.K.Nature 434:724-731(2005) Genomic distribution and gonadal mRNA expression of two human luteinizing hormone receptor exon 1 sequences in random populations.Tsai-Morris C.-H., Geng Y., Buczko E., Dehejia A., Dufau M.L.Hum. Hered. 49:48-51(1999) Evidence that palmitoylation of carboxyl terminus cysteine residues of the human luteinizing hormone receptor regulates postendocytic processing.Munshi U.M., Clouser C.L., Peegel H., Menon K.M.Mol. Endocrinol. 19:749-758(2005) Structural predictions for the ligand-binding region of glycoprotein hormone receptors and the nature of hormone-receptor interactions.Jiang X., Dreano M., Buckler D.R., Cheng S., Ythier A., Wu H., Hendrickson W.A., el Tayar N.Structure 3:1341-1353(1995) Gonadotropin-independent precocious puberty due to luteinizing hormone receptor mutations in Brazilian boys a novel constitutively activating mutation in the first transmembrane helix.Latronico A.C., Shinozaki H., Guerra G. Jr., Pereira M.A.A., Lemos Marini S.H.V., Baptista M.T.M., Arnhold I.J.P., Fanelli F., Mendonca B.B., Segaloff D.L.J. Clin. Endocrinol. Metab. 85:4799-4805(2000) Nodular Leydig cell hyperplasia in a boy with familial male-limited precocious puberty.Leschek E.W., Chan W.-Y., Diamond D.A., Kaefer M., Jones J., Barnes K.M., Cutler G.B. Jr.J. Pediatr. 138:949-951(2001) Mutant luteinizing hormone receptors in a compound heterozygous patient with complete Leydig cell hypoplasia abnormal processing causes signaling deficiency.Martens J.W.M., Lumbroso S., Verhoef-Post M., Georget V., Richter-Unruh A., Szarras-Czapnik M., Romer T.E., Brunner H.G., Themmen A.P.N., Sultan C.J. Clin. Endocrinol. Metab. 87:2506-2513(2002) Luteinizing hormone signaling and breast cancer polymorphisms and age of onset.Powell B.L., Piersma D., Kevenaar M.E., van Staveren I.L., Themmen A.P.N., Iacopetta B.J., Berns E.M.J.J.J. Clin. Endocrinol. Metab. 88:1653-1657(2003) A constitutively activating mutation of the luteinizing hormone receptor in familial male precocious puberty.Shenker A., Laue L., Kosugi S., Merendino J.J. Jr., Minegishi T., Cutler G.B. Jr.Nature 365:652-654(1993) Cosegregation of missense mutations of the luteinizing hormone receptor gene with familial male-limited precocious puberty.Kremer H., Mariman E., Otten B.J., Moll G.W. Jr., Stoelinga G.B.A., Wit J.M., Jansen M., Drop S.L., Faas B., Ropers H.-H., Brunner H.G.Hum. Mol. Genet. 2:1779-1783(1993) Characterization of heterogeneous mutations causing constitutive activation of the luteinizing hormone receptor in familial male precocious puberty.Kosugi S., van Dop C., Geffner M.E., Rabl W., Carel J.-C., Chaussain J.-L., Mori T., Merendino J.J. Jr., Shenker A.Hum. Mol. Genet. 4:183-188(1995) A new constitutively activating point mutation in the luteinizing hormone/choriogonadotropin receptor gene in cases of male-limited precocious puberty.Yano K., Saji M., Hidaka A., Moriya N., Okuno A., Kohn L.D., Cutler G.B. Jr.J. Clin. Endocrinol. Metab. 80:1162-1168(1995) A novel mutation of the luteinizing hormone receptor gene causing male gonadotropin-independent precocious puberty.Latronico A.C., Anasti J., Arnhold I.J., Mendonca B.B., Domenice S., Albano M.C., Zachman K., Wajchenberg B.L., Tsigos C.J. Clin. Endocrinol. Metab. 80:2490-2494(1995) Male pseudohermaphroditism due to a homozygous missense mutation of the luteinizing hormone receptor gene.Kremer H., Kraaij R., Toledo S.P.A., Post M., Fridman J.B., Hayashida C.Y., van Reen M., Milgrom E., Ropers H.-H., Mariman E., Themmen A.P.N., Brunner H.G.Nat. Genet. 9:160-164(1995) A missense (T577I) mutation in the luteinizing hormone receptor gene associated with familial male-limited precocious puberty.Cocco S., Meloni A., Marini M.G., Cao A., Moi P.3.3.CO;2-B>Hum. Mutat. 7:164-166(1996) A new point mutation in the luteinising hormone receptor gene in familial and sporadic male limited precocious puberty genotype does not always correlate with phenotype.Evans B.A.J., Bowen D.J., Smith P.J., Clayton P.E., Gregory J.W.J. Med. Genet. 33:143-147(1996) Testicular and ovarian resistance to luteinizing hormone caused by inactivating mutations of the luteinizing hormone-receptor gene.Latronico A.C., Anasti J., Arnhold I.J.P., Rapaport R., Mendonca B.B., Bloise W., Castro M., Tsigos C., Chrousos G.P.N. Engl. J. Med. 334:507-512(1996) Comparison of immunocytochemical and molecular features with the phenotype in a case of incomplete male pseudohermaphroditism associated with a mutation of the luteinizing hormone receptor.Misrahi M., Meduri G., Pissard S., Bouvattier C., Beau I., Loosfelt H., Jolivet A., Rappaport R., Milgrom E., Bougneres P.J. Clin. Endocrinol. Metab. 82:2159-2165(1997) Polymorphisms in the coding exons of the human luteinizing hormone receptor gene.Wu S.-M., Jose M., Hallermeier K., Rennert O.M., Chan W.-Y.3.0.CO;2-D>Hum. Mutat. 11:333-334(1998) A mutation in the first transmembrane domain of the lutropin receptor causes male precocious puberty.Gromoll J., Partsch C.-J., Simoni M., Nordhoff V., Sippell W.G., Nieschlag E., Saxena B.B.J. Clin. Endocrinol. Metab. 83:476-480(1998) A novel mutation of the human luteinizing hormone receptor in 46XY and 46XX sisters.Stavrou S.S., Zhu Y.S., Cai L.Q., Katz M.D., Herrera C., Defillo-Ricart M., Imperato-Mcginley J.J. Clin. Endocrinol. Metab. 83:2091-2098(1998) A unique constitutively activating mutation in third transmembrane helix of luteinizing hormone receptor causes sporadic male gonadotropin-independent precocious puberty.Latronico A.C., Abell A.N., Arnhold I.J., Liu X., Lins T.S., Brito V.N., Billerbeck A.E., Segaloff D.L., Mendonca B.B.J. Clin. Endocrinol. Metab. 83:2435-2440(1998) Evidences for an allelic variant of the human LC/CG receptor rather than a gene duplication functional comparison of wild-type and variant receptors.Rodien P., Cetani F., Costagliola S., Tonacchera M., Duprez L., Minegishi T., Govaerts C., Vassart G.J. Clin. Endocrinol. Metab. 83:4431-4434(1998) A homozygous microdeletion in helix 7 of the luteinizing hormone receptor associated with familial testicular and ovarian resistance is due to both decreased cell surface expression and impaired effector activation by the cell surface receptor.Latronico A.C., Chai Y., Arnhold I.J.P., Liu X., Mendonca B.B., Segaloff D.L.Mol. Endocrinol. 12:442-450(1998) A homozygous mutation in the luteinizing hormone receptor causes partial Leydig cell hypoplasia correlation between receptor activity and phenotype.Martens J.W., Verhoef-Post M., Abelin N., Ezabella M., Toledo S.P., Brunner H.G., Themmen A.P.Mol. Endocrinol. 12:775-784(1998) Leydig-cell tumors caused by an activating mutation of the gene encoding the luteinizing hormone receptor.Liu G., Duranteau L., Carel J.-C., Monroe J., Doyle D.A., Shenker A.N. Engl. J. Med. 341:1731-1736(1999) A novel missense homozygous inactivating mutation in the fourth transmembrane helix of the luteinizing hormone receptor in Leydig cell hypoplasia.Leung M.Y.-K., Al-Muslim O., Wu S.-M., Aziz A., Inam S., Awadh M., Rennert O.M., Chan W.-Y.Am. J. Med. Genet. A 130:146-153(2004) Leydig cell hypoplasia absent luteinizing hormone receptor cell surface expression caused by a novel homozygous mutation in the extracellular domain.Richter-Unruh A., Verhoef-Post M., Malak S., Homoki J., Hauffa B.P., Themmen A.P.N.J. Clin. Endocrinol. Metab. 89:5161-5167(2004) The consensus coding sequences of human breast and colorectal cancers.Sjoeblom T., Jones S., Wood L.D., Parsons D.W., Lin J., Barber T.D., Mandelker D., Leary R.J., Ptak J., Silliman N., Szabo S., Buckhaults P., Farrell C., Meeh P., Markowitz S.D., Willis J., Dawson D., Willson J.K.V., Gazdar A.F., Hartigan J., Wu L., Liu C., Parmigiani G., Park B.H., Bachman K.E., Papadopoulos N., Vogelstein B., Kinzler K.W., Velculescu V.E.Science 314:268-274(2006) A splice site mutation combined with a novel missense mutation of LHCGR cause male pseudohermaphroditism.Qiao J., Han B., Liu B.-L., Chen X., Ru Y., Cheng K.-X., Chen F.-G., Zhao S.-X., Liang J., Lu Y.-L., Tang J.-F., Wu Y.-X., Wu W.-L., Chen J.-L., Chen M.-D., Song H.-D.Hum. Mutat. 30:E855-E865(2009) +Additional computationally mapped references. p>Provides general information on the entry.

106067657

NP_000224.2

NM_000233.3

P22888

41.67kD

Arf6 Signaling Events Pathway (138034); Calcium Signaling Pathway (83050); Calcium Signaling Pathway (459); Class A/1 (Rhodopsin-like Receptors) Pathway (1269545); G Alpha (s) Signalling Events Pathway (1269575); GPCR Downstream Signaling Pathway (1269574); GPCR Ligand Binding Pathway (1269544); GPCRs, Class A Rhodopsin-like Pathway (198886); Hormone Ligand-binding Receptors Pathway (1269559); Neuroactive Ligand-receptor Interaction Pathway (83053)

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, Jul 2008]

LHR: Receptor for lutropin-choriogonadotropic hormone. The activity of this receptor is mediated by G proteins which activate adenylate cyclase. Defects in LHCGR are a cause of familial male precocious puberty (FMPP); also known as testotoxicosis. In FMPP the receptor is constitutively activated. Defects in LHCGR are the cause of luteinizing hormone resistance (LHR); also known as Leydig cell hypoplasia in males. LHR is an autosomal recessive disorder characterized by unresponsiveness to luteinizing hormone, defective sexual development in males, and defective follicular development and ovulation, amenorrhea and infertility in females. Two forms of the disorder have been defined in males. Type 1 is a severe form characterized by complete 46,XY male pseudohermaphroditism, low testosterone and high luteinizing hormone levels, total lack of responsiveness to luteinizing and chorionic gonadotropin hormones, lack of breast development, and absent development of secondary male sex characteristics. Type 2, a milder form, displays a broader range of phenotypic expression ranging from micropenis to severe hypospadias. Belongs to the G-protein coupled receptor 1 family. FSH/LSH/TSH subfamily. 2 isoforms of the human protein are produced by alternative splicing. Protein type: GPCR, family 1; Membrane protein, multi-pass; Receptor, GPCR; Membrane protein, integral. Chromosomal Location of Human Ortholog: 2p21. Cellular Component: endosome; integral to plasma membrane; plasma membrane. Molecular Function: lutropin-choriogonadotropic hormone receptor activity; peptide receptor activity, G-protein coupled. Biological Process: adenylate cyclase activation; cognition; G-protein coupled receptor protein signaling pathway; G-protein signaling, adenylate cyclase activating pathway; G-protein signaling, coupled to cyclic nucleotide second messenger; G-protein signaling, coupled to IP3 second messenger (phospholipase C activating); hormone-mediated signaling; luteinizing hormone signaling pathway; male genitalia development; male gonad development; ovulation cycle process; positive regulation of inositol trisphosphate biosynthetic process. Disease: Leydig Cell Hypoplasia, Type I; Precocious Puberty, Male-limited

0.01 mg (E-Coli)

160 USD

0.05 mg (E-Coli)

200

0.1 mg (E-Coli)

295

0.2 mg (E-Coli)

480

0.5 mg (E-Coli)

790

1 mg (E-Coli)

1215