| Project/Area Number |
24790319
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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 |
Pathological medical chemistry
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| Research Institution | Kyushu University |
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Principal Investigator |
NISHIO Miki 九州大学, 生体防御医学研究所, 助教 (10467897)
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| Co-Investigator(Renkei-kenkyūsha) |
SUZUKI Akira 九州大学, 生体防御医学研究所, 教授 (10311565)
ITAMI Satoshi 大阪大学, 大学院医学系研究科, 教授 (30136791)
MIZUNO Kensaku 東北大学, 大学院生命科学研究科, 教授 (70128396)
CHIBA Syuhei 大阪大学, 大学院生命科学研究科, 特任助教 (60572493)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 発癌 / Mob1 / シグナル伝達 / 発生 / 発がん / Mob |
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| Research Abstract |
The Hippo pathway is evolutionarily conserved, and the vertebrate Hippo pathway has been implicated in regulating cell contact inhibition, organ size, and tumorigenesis. The Mob1A/1B are the binding partners and strong co-activators of Lats kinases family, and the members of the Hippo pathway.However, the normal functions of Mob1A/1B proteins in vivo had been unknown.To define the functions of mammarian Mob1A/1B, we generated Mob1A and 1B null mutant mice. We showed Mob1A/1B double homozygous mutant mice died at gastrulation.Thus, Mob1A/B is essential for murine embryogenesis. Partially mutants developed a variety of tumors. Moreover, half of human trichilemmal carcinoma samples showed Mob1A/1B inactivation and YAP activation.These observations suggest that the loss of Hippo signaling molecules can be an important driver of cancer progression.
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