2009 Fiscal Year Final Research Report
Identification of novel AKT regulating molecules.
Project/Area Number |
19770098
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Single-year Grants |
Research Field |
Functional biochemistry
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Research Institution | Hokkaido University |
Principal Investigator |
SUIZU Futoshi Hokkaido University, 遺伝子病制御研究所, 助教 (90431379)
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Project Period (FY) |
2007 – 2009
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Keywords | タンパク分解 / リン酸化 / AKT / ユビキチン / セリンスレオニンキナーゼ / ダウン症 / 21Trisomy / TTC3 |
Research Abstract |
In yeast two-hybrid assays, we found that TTC3, which is located at chromosome 21 within the Down Syndrome Critical Region, specifically interacted with Akt. TTC3 preferentially binds to phosphorylated Akt and facilitates its ubiquitination/degradation predominantly within the nucleus. By confocal microscopy the TTC3 co-localizes with Akt throughout the cell cycle, suggesting that TTC3 regulate cell survival and proliferation by controlling Akt activity within the nucleus. (Suizu et al. Developmental Cell 2009)
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[Journal Article] The E3 Ligase TTC3 Facilitates Ubiquitination and Degragation of Phosphorylated Akt.2009
Author(s)
Suizu, F., Hiramuki, Y., Okumura, F., Matsuda, M., Okumura, A.J., Hirata, N, Narita, M., Kohno, T., Yokota, J., Bohgaki, M., Obuse, C., Hatakeyama, S., Obata, T., Noguchi, M.
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Journal Title
Developmental Cell 17(6)
Pages: 800-810
Peer Reviewed
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[Journal Article] The death effector domain-containing DEDD supports S6K1 activity via preventing Cdk1-dependent inhibitory phosphorylation.2009
Author(s)
Kurabe, N., Arai, S., Nishijima, A., Kubota, N., Suizu, F., Mori, M., Kurokawa, J., Miyazaki, M.K., Ide, T., Murakami, K., Ueki, K., Koga, H., Yatomi, Y., Tashiro, F., Noguchi, M., Kadowaki, T., Miyazaki, T.
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Journal Title
J Biol Chem 284(8)
Pages: 5050-5055
Peer Reviewed
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