| Project/Area Number |
22590298
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pathological medical chemistry
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| Research Institution | Miyagi Cancer Center Research Institute |
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Principal Investigator |
SHIMA Hiroshi 地方独立行政法人宮城県立病院機構宮城県立がんセンター(研究所), がん薬物療法研究部, 部長 (10196462)
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| Co-Investigator(Kenkyū-buntansha) |
YAMASITA Youzi 地方独立行政法人宮城県立病院機構宮城県立がんセンター(研究所), がん薬物療法研究部, 特任研究員 (30420045)
WATANABE Tosio 奈良女子大学, 自然科学系, 教授 (60201208)
SUGAMURA Kazuo 地方独立行政法人宮城県立病院機構宮城県立がんセンター(研究所), 発がん制御研究部, 特任部長 (20117360)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 分子腫瘍学 / キネシンモーター / KIF3 / ホスファターゼ / ２重基質ホスファターゼ / 2重基質ホスファターゼ / 2重基質ボスファターゼ / 癌 |
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| Research Abstract |
We identified the protein-phosphatase DUSP26 as a novel regulator of the KIF3 motor. Dusp26 is recruited to the KIF3 motor mainly by interaction with Kif3a, and thereby dephosphorylates Kap3. Enzyme activity of the Dusp26 was shown to promote distribution of beta-catenin/N-cadherinto cell-cell junction sites, resulting in increased cell-cell adhesiveness. We also showed that DUSP26 mRNA expression was downregulated in human glioblastoma samples, and a CpG island upstream of the DUSP26 transcrptional start site was heavily methylated in glioma cell lines. These results suggest previously unidentified functions of DUSP26 in intracellular transport and cell-cell adhesion.Downregulation of DUSP26 may contribute to malignant phenotypes of glioma. We showed that DUSP13B inactivated MAPK activation in the order of selectivity, JNK=p38> ERK in cells. Reporter gene analysis showed that DUSP13B had significant inhibitory effect on AP-1 dependent gene expression. DUSP13B is the first identified testis specific phosphatase that inhibits stress-activated MAPKs.
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