2022 Fiscal Year Final Research Report
Elucidation of the function of BRINP protein that regulates neuronal excitation and inhibition
Project/Area Number |
20K07748
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 51030:Pathophysiologic neuroscience-related
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Research Institution | Matsuyama University |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
松岡 一郎 松山大学, 薬学部, 客員教員 (40157269)
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Project Period (FY) |
2020-04-01 – 2023-03-31
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Keywords | BRINP / 精神疾患 / 欠損マウス / 大脳皮質 |
Outline of Final Research Achievements |
Neural-specific family gene, BRINP, exhibits abnormal behaviors analogous to symptoms of human psychiatric disorders due to its deficiency. The BRINP genes were expressed in both excitatory and most inhibitory neurons in the adult mouse cortex. In the brain of BRINP1 or BRINP3-deficient mice, mRNA and protein expressions of neurotransmitter receptors, synapse-associated proteins, protein-associated axonal outgrowth were altered, which may lead to the behavioral abnormalities exhibited by deficient mice. We also found that all BRINPs interact with Rab3 and Rab11, its binding preference differ by combination of BRINP member and G protein activation state of Rab.
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Free Research Field |
分子神経生物学
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Academic Significance and Societal Importance of the Research Achievements |
脳の機能性障害である精神疾患は,変性疾患を含む器質性精神障害とは異なり,治療法がある程度確立されているものの,発症の原因についてはよくわかっていない。神経特異的に発現するBRINPファミリー遺伝子を欠損させたマウスはヒト精神疾患の症状と似た行動異常を示し,神経細胞および神経細胞がつくる神経回路の正常な機能に必要な遺伝子やタンパク質の発現が変化していた。今回得られた知見をもとにBRINPタンパク質の分子機能を明らかにすることにより,精神疾患の発症メカニズムの解明,新たな治療法の開発につなげることが期待される。
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