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Increased amyloidogenic processing of transgenic human APP in X11-like deficient mouse brain

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Title: Increased amyloidogenic processing of transgenic human APP in X11-like deficient mouse brain
Authors: Kondo, Maho Browse this author
Shiono, Maki Browse this author
Itoh, Genzo Browse this author
Takei, Norio Browse this author
Matsushima, Takahide Browse this author
Maeda, Masahiro Browse this author
Taru, Hidenori Browse this author →KAKEN DB
Hata, Saori Browse this author →KAKEN DB
Yamamoto, Tohru Browse this author →KAKEN DB
Saito, Yuhki Browse this author →KAKEN DB
Suzuki, Toshiharu Browse this author →KAKEN DB
Issue Date: 15-Sep-2010
Publisher: BIOMED CENTRAL LTD
Journal Title: MOLECULAR NEURODEGENERATION
Volume: 5
Start Page: 35
Publisher DOI: 10.1186/1750-1326-5-35
PMID: 20843325
Abstract: Background: X11-family proteins, including X11, X11-like (X11L) and X11-like 2 (X11L2), bind to the cytoplasmic domain of amyloid beta-protein precursor (APP) and regulate APP metabolism. Both X11 and X11L are expressed specifically in brain, while X11L2 is expressed ubiquitously. X11L is predominantly expressed in excitatory neurons, in contrast to X11, which is strongly expressed in inhibitory neurons. In vivo gene-knockout studies targeting X11, X11L, or both, and studies of X11 or X11L transgenic mice have reported that X11-family proteins suppress the amyloidogenic processing of endogenous mouse APP and ectopic human APP with one exception: knockout of X11, X11L or X11L2 has been found to suppress amyloidogenic metabolism in transgenic mice overexpressing the human Swedish mutant APP (APPswe) and the mutant human PS1, which lacks exon 9 (PS1dE9). Therefore, the data on X11-family protein function in transgenic human APP metabolism in vivo are inconsistent. Results: To confirm the interaction of X11L with human APP ectopically expressed in mouse brain, we examined the amyloidogenic metabolism of human APP in two lines of human APP transgenic mice generated to also lack X11L. In agreement with previous reports from our lab and others, we found that the amyloidogenic metabolism of human APP increased in the absence of X11L. Conclusion: X11L appears to aid in the suppression of amyloidogenic processing of human APP in brain in vivo, as has been demonstrated by previous studies using several human APP transgenic lines with various genetic backgrounds. X11L appears to regulate human APP in a manner similar to that seen in endogenous mouse APP metabolism.
Rights: http://creativecommons.org/licenses/by/3.0/
Type: article
URI: http://hdl.handle.net/2115/51694
Appears in Collections:薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 鈴木 利治

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