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Gene Review

GPR98  -  G protein-coupled receptor 98

Homo sapiens

Synonyms: DKFZp761P0710, FEB4, G-protein coupled receptor 98, KIAA0686, KIAA1943, ...
 
 
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Disease relevance of GPR98

  • The identification of additional VLGR1 mutations to test whether a phenotype/genotype correlation exists, akin to that shown for other Usher syndrome disease genes, is warranted [1].
  • We screened for MASS1 mutations in individuals from 48 families with familial febrile seizures and found 25 DNA alterations [2].
  • The molecular basis and pathophysiology of hearing loss suggest BUB/BnJ and Frings mice as models to study cellular and molecular mechanisms underlying USH2C auditory pathology [3].
 

High impact information on GPR98

  • Mutations in the VLGR1 gene implicate G-protein signaling in the pathogenesis of Usher syndrome type II [1].
  • VLGR1 mutations have been previously identified in both humans and mice and are associated with a reflex-seizure phenotype in both species [1].
  • The VLGR1 (MASS1) gene in the 5q14.3-q21.1 USH2C locus was considered a likely candidate on the basis of its protein motif structure and expressed-sequence-tag representation from both cochlear and retinal subtracted libraries [1].
  • These findings indicate that there is a gene on chromosome 5q14-q15 that confers susceptibility to FSs and we call this gene FEB4 [4].
  • Our results suggest that a loss-of-function mutation in MASS1 might be responsible for the seizure phenotypes, though it is not likely that MASS1 contributed to the cause of febrile seizures in most of our families [2].
 

Biological context of GPR98

  • The human orthologous gene, MASS1, was mapped to chromosome 5q14, for which we previously have reported significant evidence of linkage to febrile seizures (FEB4) [2].
  • Mutation analysis of the exons and exon-intron boundaries of MASS1 in our family did not reveal a disease causing mutation [5].
  • It is 51% identical to human VLGR1 in amino acid sequence, but is 64% identical in the 7-transmembrane and cytoplasmic domains [6].
 

Anatomical context of GPR98

  • CONCLUSIONS: USH2C and USH2A manifest photoreceptor disease with rod- and cone-mediated visual losses and thinning of the outer nuclear layer [7].
 

Other interactions of GPR98

References

  1. Mutations in the VLGR1 gene implicate G-protein signaling in the pathogenesis of Usher syndrome type II. Weston, M.D., Luijendijk, M.W., Humphrey, K.D., Möller, C., Kimberling, W.J. Am. J. Hum. Genet. (2004) [Pubmed]
  2. A nonsense mutation of the MASS1 gene in a family with febrile and afebrile seizures. Nakayama, J., Fu, Y.H., Clark, A.M., Nakahara, S., Hamano, K., Iwasaki, N., Matsui, A., Arinami, T., Ptácek, L.J. Ann. Neurol. (2002) [Pubmed]
  3. The Mass1frings mutation underlies early onset hearing impairment in BUB/BnJ mice, a model for the auditory pathology of Usher syndrome IIC. Johnson, K.R., Zheng, Q.Y., Weston, M.D., Ptacek, L.J., Noben-Trauth, K. Genomics (2005) [Pubmed]
  4. Significant evidence for linkage of febrile seizures to chromosome 5q14-q15. Nakayama, J., Hamano, K., Iwasaki, N., Nakahara, S., Horigome, Y., Saitoh, H., Aoki, T., Maki, T., Kikuchi, M., Migita, T., Ohto, T., Yokouchi, Y., Tanaka, R., Hasegawa, M., Matsui, A., Hamaguchi, H., Arinami, T. Hum. Mol. Genet. (2000) [Pubmed]
  5. Genome-wide linkage of febrile seizures and epilepsy to the FEB4 locus at 5q14.3-q23.1 and no MASS1 mutation. Deprez, L., Claes, L.R., Claeys, K.G., Audenaert, D., Van Dyck, T., Goossens, D., Van Paesschen, W., Del-Favero, J., Van Broeckhoven, C., De Jonghe, P. Hum. Genet. (2006) [Pubmed]
  6. Analysis of the very large G-protein coupled receptor gene (Vlgr1/Mass1/USH2C) in zebrafish. Gibert, Y., McMillan, D.R., Kayes-Wandover, K., Meyer, A., Begemann, G., White, P.C. Gene (2005) [Pubmed]
  7. Disease expression in Usher syndrome caused by VLGR1 gene mutation (USH2C) and comparison with USH2A phenotype. Schwartz, S.B., Aleman, T.S., Cideciyan, A.V., Windsor, E.A., Sumaroka, A., Roman, A.J., Rane, T., Smilko, E.E., Bennett, J., Stone, E.M., Kimberling, W.J., Liu, X.Z., Jacobson, S.G. Invest. Ophthalmol. Vis. Sci. (2005) [Pubmed]
 
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