| Project/Area Number |
26860214
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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)
OOTSUBO kohei 九州大学, 呼吸器科, 大学院生
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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 |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | Hippo経路 / 肺形成 / 腫瘍形成 / Hippo / 肺腺がん / 肺がん |
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| Outline of Final Research Achievements |
Hippo signaling is activated when mechanical tension is imposed by the surrounding microenvironment such as high cell density, small cell size, and soft extracellular matrix.Dysregulation of this pathway leads to developmental abnormality, organomegaly, and tumorigenesis.
To clarify the function of MOB1A/1B and Hippo pathway in normal lung development and the tumorigenesis,we generated mice deficient for MOB1A and MOB1B specifically in bronchioalveolar epithelial cells. Our results showed MOB1A/MOB1B is essential for normal alveolar cell maturation and surfactant homeostasis.In addition we showed that MOB1A/MOB1B controls adhesion of bronchiolar cells and BASCs to their niche by downstream Collagen17a1 dependent.
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