Investigation of the medical/biological roles of the parafibromin functions regulated by SHP2 oncoprotein
Project/Area Number |
15K18399
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Multi-year Fund |
Research Field |
Tumor biology
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Research Institution | The University of Tokyo |
Principal Investigator |
TAKAHASHI Atsushi 東京大学, 大学院医学系研究科(医学部), 助教 (00624496)
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Project Period (FY) |
2015-04-01 – 2017-03-31
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Project Status |
Completed (Fiscal Year 2016)
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Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2016: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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Keywords | Parafibromin / チロシン脱リン酸化酵素SHP2 / Wntシグナル伝達経路 / YAP / 選択的スプライシング / SHP2 / PTK6 / YAP/TAZ |
Outline of Final Research Achievements |
(1) It was suggested that deregulated tyrosine-dephosphorylation of Parafibromin caused lethal defects in embryogenesis of mice. We reported that tyrosine-dephosphorylated form of Parafibromin acts as a coactivator of the Wnt/Hedgehog/Notch signaling pathways, which play crucial roles in morphogenesis. (2) Loss of function of the leucine-zipper motif lost the SHP2-binding ability of the YAP isoform that possesses the exon 6-encoded γ-segment. The YAP isoform lacking the γ-segment was incapable in binding to SHP2, collectively indicated that YAP requires the leucine-zipper motif, which is encoded in the exon 5 and 7, for the complex formation with SHP2.
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Report
(3 results)
Research Products
(7 results)
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[Journal Article] Dephosphorylated parafibromin is a transcriptional coactivator of the Wnt/Hedgehog/Notch pathways.2016
Author(s)
Kikuchi I, Takahashi-Kanemitsu A, Sakiyama N, Tang C, Tang PJ, Noda S, Nakao K, Kassai H, Sato T, Aiba A, and Hatakeyama M.
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Journal Title
Nat Commun
Volume: 7
Issue: 1
Pages: 12887-12887
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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