Elucidation of the molecular mechanisms of STAT3-alternative splicing and the physiological functions of STAT3-splicing isoforms
| Project/Area Number |
26870308
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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 |
Biological pharmacy
Pathological medical chemistry
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| Research Institution | Kyoto University |
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Principal Investigator |
Masaki So 京都大学, 医学(系)研究科(研究院), 研究員 (70711977)
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| Co-Investigator(Renkei-kenkyūsha) |
KATAOKA Naoyuki 京都大学, 大学院医学研究科, 特定准教授 (60346062)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | スプライシング / シグナル伝達 / スクリーニング / 化合物ライブラリー |
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| Outline of Final Research Achievements |
STAT3 has been recognized as a modulator related various biological responses. STAT3 is known to undergo alternative splicing, and their “alpha” and “beta” splicing isoforms likely have different roles. However, the mechanism of STAT3-alternative splicing remains unclear.
In this study, to unveil the molecular mechanisms of alternative splicing of STAT3 and identification of the chemical compounds that control the balance of splicing isoforms, we established the methodology of elucidation of splicing mechanisms based on the screening to identify small chemical compounds that switch STAT3-alternative splicing patterns. As results, we obtained drug candidates of β-type-inducing factors and a stir, directly or indirectly, to “splicing black box”.
Regarding the difference of physiological functions between STAT3α and β in cells, we found out that STAT3β is regulated in a different manner from STAT3α.
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Report
(3 results)
Research Products
(3 results)
