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G protein-coupled receptor 98, also known as GPR98, is a human protein and gene.[1]

This gene encodes a member of the G-protein coupled receptor superfamily. The protein binds calcium and is expressed in the central nervous system. It is also known as very large G-protein coupled receptor 1 because it is 6300 residues long. It contains a C-terminal 7-transmembrane receptor domain, whereas the large N-terminal segment (5900 residues) includes 35 calcium binding Calx-beta domains, and 6 EAR domains. Mutations in this gene are associated with Usher syndrome 2 and familial febrile seizures. Several alternatively spliced transcripts have been described.[1] }}

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  • Nakajima D, Okazaki N, Yamakawa H, et al. (2003). Construction of expression-ready cDNA clones for KIAA genes: manual curation of 330 KIAA cDNA clones.. DNA Res. 9 (3): 99-106.
  • Staub E, Pérez-Tur J, Siebert R, et al. (2002). The novel EPTP repeat defines a superfamily of proteins implicated in epileptic disorders.. Trends Biochem. Sci. 27 (9): 441-4.
  • Ishikawa K, Nagase T, Suyama M, et al. (1998). Prediction of the coding sequences of unidentified human genes. X. The complete sequences of 100 new cDNA clones from brain which can code for large proteins in vitro.. DNA Res. 5 (3): 169-76.
  • Nakayama J, Hamano K, Iwasaki N, et al. (2000). Significant evidence for linkage of febrile seizures to chromosome 5q14-q15.. Hum. Mol. Genet. 9 (1): 87-91.
  • Pieke-Dahl S, Möller CG, Kelley PM, et al. (2000). Genetic heterogeneity of Usher syndrome type II: localisation to chromosome 5q.. J. Med. Genet. 37 (4): 256-62.
  • Nikkila H, McMillan DR, Nunez BS, et al. (2001). Sequence similarities between a novel putative G protein-coupled receptor and Na+/Ca2+ exchangers define a cation binding domain.. Mol. Endocrinol. 14 (9): 1351-64.
  • Wiemann S, Weil B, Wellenreuther R, et al. (2001). Toward a catalog of human genes and proteins: sequencing and analysis of 500 novel complete protein coding human cDNAs.. Genome Res. 11 (3): 422-35.
  • Skradski SL, Clark AM, Jiang H, et al. (2001). A novel gene causing a mendelian audiogenic mouse epilepsy.. Neuron 31 (4): 537-44.
  • McMillan DR, Kayes-Wandover KM, Richardson JA, White PC (2002). Very large G protein-coupled receptor-1, the largest known cell surface protein, is highly expressed in the developing central nervous system.. J. Biol. Chem. 277 (1): 785-92.
  • Nagase T, Kikuno R, Ohara O (2002). Prediction of the coding sequences of unidentified human genes. XXII. The complete sequences of 50 new cDNA clones which code for large proteins.. DNA Res. 8 (6): 319-27.
  • Nakayama J, Fu YH, Clark AM, et al. (2002). A nonsense mutation of the MASS1 gene in a family with febrile and afebrile seizures.. Ann. Neurol. 52 (5): 654-7.
  • Strausberg RL, Feingold EA, Grouse LH, et al. (2003). Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences.. Proc. Natl. Acad. Sci. U.S.A. 99 (26): 16899-903.
  • Ota T, Suzuki Y, Nishikawa T, et al. (2004). Complete sequencing and characterization of 21,243 full-length human cDNAs.. Nat. Genet. 36 (1): 40-5.
  • Weston MD, Luijendijk MW, Humphrey KD, et al. (2004). Mutations in the VLGR1 gene implicate G-protein signaling in the pathogenesis of Usher syndrome type II.. Am. J. Hum. Genet. 74 (2): 357-66.
  • Bjarnadóttir TK, Fredriksson R, Höglund PJ, et al. (2005). The human and mouse repertoire of the adhesion family of G-protein-coupled receptors.. Genomics 84 (1): 23-33.
  • Fu GK, Wang JT, Yang J, et al. (2005). Circular rapid amplification of cDNA ends for high-throughput extension cloning of partial genes.. Genomics 84 (1): 205-10.
  • Schwartz SB, Aleman TS, Cideciyan AV, et al. (2005). Disease expression in Usher syndrome caused by VLGR1 gene mutation (USH2C) and comparison with USH2A phenotype.. Invest. Ophthalmol. Vis. Sci. 46 (2): 734-43.
  • Kimura K, Wakamatsu A, Suzuki Y, et al. (2006). Diversification of transcriptional modulation: large-scale identification and characterization of putative alternative promoters of human genes.. Genome Res. 16 (1): 55-65.



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