2012 Fiscal Year Final Research Report
The pathophysiological function of Helicobacter pylori CagA oncoprotein that is processed in gastric epithelial cells
| Project/Area Number |
23890037
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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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 |
SAITO Yasuhiro 東京大学, 大学院・医学系研究科, 助教 (30613004)
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| Project Period (FY) |
2011 – 2012
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| Keywords | 胃がん / ピロリ菌 / CagA |
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| Research Abstract |
Infection of the cagA-positive Helicobacter pylori relates to the induction of gastric cancer. The cagA-positive H. pylori produces CagA protein in the bacterial cells and injects it into gastric epithelial cells. The translocated CagA targets SHP2 oncoprotein and deregulates the function of SHP2. The subcellular distribution of CagA in gastric epithelial cells was investigated in this study and CagA was observed in the nucleus as well as cytoplasmic membrane. Since nuclear SHP2 activates Wnt signaling, the results implicate that nuclear CagA aberrantly activates the Wnt pathway via deregulation of nuclear SHP2.
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