2011 Fiscal Year Final Research Report
Tumorigenicity by TGF-βsignaling
| Project/Area Number |
21590328
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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 | Showa Pharmaceutical University (2010-2011)
University of Tsukuba (2009) |
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Principal Investigator |
ITOH Susumu 昭和薬科大学, 薬学部, 教授 (70223154)
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| Project Period (FY) |
2009 – 2011
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| Keywords | TGF-β / Smad / がん / 血管新生 / ノックアウトマウス / TMEPAI |
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| Research Abstract |
TMEPAI gene is synergistically activated by both wnt and TGF-β signaling.
C18Orf1, one of TMEPAI family, can inhibit TGF-β signaling like TMEPAI.
Both TMEPAI and C18Orf1 knockout mice were generated. However, no phenotypes for both mice have been observed.
The structure of blood vessels from endothelial cell-specific Smad2/3 double knockout mice seems to be fragile because the expressions of claudin 5, S1PR1 and N-cadherin are reduced in the endothelial cells from those mice.
Endothelial cells from endothelial cell-specific Smad2/3 double knockout mice reveal morphological change when cells receive shear stress.
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[Journal Article] TMEPAI, a transmembrane TGF-β-inducible protein, sequesters from active participation in TGF-β signaling2010
Author(s)
Watanabe Y., Itoh S., Goto T., Ohnishi, E., Inamitsu M., Itoh F., Satoh K., Wiercinska E., Yang W., Shi L., Tanaka A., Nakano N., Mommaas A. M., Shibuya H., ten Dijke P., Kato M
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Journal Title
Mol. Cell
Volume: 37
Pages: 123-134
DOI
Peer Reviewed
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[Journal Article] Poor vessel formation in embryos from knock-in mice expressing ALK5 with L45 loop mutation defective in Smad activation2009
Author(s)
Itoh F., Itoh S., Carvalho R. L. C., Adachi T., Ema M., Goumans M.-J., Larsson J., Karlsson S., Takahashi S., Mummery C. L., ten Dijke P., Kato M
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Journal Title
Lab. Invest
Volume: 89
Pages: 800-810
DOI
Peer Reviewed
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