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Novel missense polymorphism in the regulator of G‐protein signaling 10 gene: analysis of association with schizophrenia
Author(s) -
HISHIMOTO AKITOYO,
SHIRAKAWA OSAMU,
NISHIGUCHI NAOKI,
AOYAMA SHINSUKE,
ONO HISAE,
HASHIMOTO TAKESHI,
MAEDA KIYOSHI
Publication year - 2004
Publication title -
psychiatry and clinical neurosciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.609
H-Index - 74
eISSN - 1440-1819
pISSN - 1323-1316
DOI - 10.1111/j.1440-1819.2004.01303.x
Subject(s) - missense mutation , regulator , genetics , regulator of g protein signaling , gene , polymorphism (computer science) , schizophrenia (object oriented programming) , genetic association , biology , allele , medicine , signal transduction , mutation , single nucleotide polymorphism , genotype , g protein , psychiatry , gtpase activating protein
Dysfunction of neuronal signal transduction via G‐protein has previously been speculated to be involved in the pathophysiology of schizophrenia. Regulator of G‐protein signaling (RGS) is a protein that acts as a GTPase‐activator for Gα protein. A total of 33 Japanese patients with schizophrenia were screened for mutations in the coding region of the RGS10 gene, and a novel missense polymorphism (Val38Met) in the RGS domain was detected. A case‐control study did not reveal a significant association between this polymorphism and schizophrenia. The results do not provide evidence that the RGS10 gene is involved in biological vulnerability to schizophrenia.