2010 Fiscal Year Final Research Report
Analysis of X11 proteins functions in vivo
Project/Area Number |
21890002
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Research Category |
Grant-in-Aid for Research Activity Start-up
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Allocation Type | Single-year Grants |
Research Field |
Biological pharmacy
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Research Institution | Hokkaido University |
Principal Investigator |
SAITO Yuhki Hokkaido University, 大学院・薬学研究院, 助教 (70548180)
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Project Period (FY) |
2009 – 2010
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Keywords | アルツハイマー病 / てんかん / X11 |
Research Abstract |
X11/X11L doubly-deficient mice suffered from spontaneous epileptic seizures and hyperpolarization-activated cyclic nucleotide gated (HCN) channels function were reduced in X11/X11L doubly-deficient mice brain. The number of amyloid deposits in X11L-KO/APP23 Tg mice brains were significantly increased. The functional domains of X11 proteins to suppress the metabolism of amyloid precursore protein (APP) were carboxy-terminal PDZ domains.
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[Journal Article] Increased amyloidogenic processing of transgenic human APP in X11-like deficient mouse brain.2010
Author(s)
Maho Kondo, Maki Shiono, Genzo Ito, Norio Takei, Takahide Matsushima, Masahiro Maeda, Hidenori Taru, Saori Hata, Tohru Yamamoto, Yuhki Saito, Toshiharu Suzuki
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Journal Title
Mol.Neurodegener. 5
Pages: 35
Peer Reviewed
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