The role of non-G protein coupled receptor related signal transduction in the pathology of polycystic kidney disease
| Project/Area Number |
17K16278
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pediatrics
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| Research Institution | Wakayama Medical University |
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Principal Investigator |
Hama Taketsugu 和歌山県立医科大学, 医学部, 助教 (00508020)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2019: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2018: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2017: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | TRIP13 / AGS7 / アクセサリータンパク / 多発性嚢胞腎 / GPCR / Gβγ / subcellular fraction / Gタンパク / Gタンパク受容体 / シグナル伝達 |
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| Outline of Final Research Achievements |
Gα and Gβγ are dissociated from G protein. These two molecules are involved in signal transduction. In polycystic kidney disease (PKD), there are many reports that Gα and G protein coupled receptor (GPCR) are involved in the pathopysiology, whereas, there are few about Gβγ through non-GPCR. TRIP13, binding protein with Gβγ, is recentlry focused. In this study, we detected that TRIP13 bound with Gβγ were less in the kidney of PKD than in normal. Non-GPCR signal transduction may also be involved in the pathopysiology of PKD.
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| Academic Significance and Societal Importance of the Research Achievements |
多発性嚢胞腎(PKD)は、常染色体優性遺伝型(ADPKD)と常染色体劣性遺伝型(ARPKD)とがある。ともに腎不全や高血圧、多くの合併症があり、その早期診断や治療の重要性が認識されている。PKDの研究には、GαおよびGタンパク受容体(GPCR)に注目したものが多く、トルバプタンなどGPCR受容体阻害薬がPKDの治療として開発されてきた。しかし、GタンパクはGαとGβγに分かれ、Gβγもシグナル伝達に関与することが分かっている。これまでのGPCRに依存しないGβγとGPCR非依存性のシグナル伝達の役割が判明すれば、PKDの新たな治療を開く可能性がある。
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Report
(4 results)
Research Products
(4 results)
