Expression of CagA in polarized epithelial cells elicits forced mitogenesis
| Project/Area Number |
21790412
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Bacteriology (including Mycology)
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| Research Institution | The University of Tokyo |
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Principal Investigator |
KAMIYA Naoko The University of Tokyo, 大学院・医学系研究科, 助教 (40279352)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | ヘリコバクター・ピロリ / 胃がん / cagA遺伝子 / 上皮細胞極性 / 細胞増殖 / 胃癌 |
|---|
| Research Abstract |
Infection with Helicobacter pylori cagA-positive strains is associated with gastric carcinoma. CagA-deregulated SHP2 elicits sustained Erk-MAPK activation. CagA also interacts and inhibits PAR1, resulting in induction of junctional and polarity defects. In polarized epithelial cells, CagA-driven Erk-MAPK signal prevents p21 expression by activating RhoA, thereby inducing forced mitogenesis.
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Report
(3 results)
Research Products
(24 results)
