Smad2 protein disruption in the central nervous system leads to aberrant cerebellar development and early postnatal ataxia in mice

Lixiang Wang, Masatoshi Nomura, Yutaka Goto, Kimitaka Tanaka, Ryuichi Sakamoto, Ichiro Abe, Shohei Sakamoto, Atsushi Shibata, Patricio L.M. Enciso, Masahiro Adachi, Keizo Ohnaka, Hisaya Kawate, Ryoichi Takayanagi

研究成果: ジャーナルへの寄稿学術誌査読

17 被引用数 (Scopus)

抄録

Smad2 is a critical mediator of TGF-β signals that are known to play an important role in a wide range of biological processes in various cell types. Its role in the development of the CNS, however, is largely unknown. Mice lacking Smad2 in the CNS (Smad2-CNS-KO) were generated by a Cre-loxP approach. These mice exhibited behavioral abnormalities in motor coordination from an early postnatal stage and mortality at approximately 3 weeks of age, suggestive of severe cerebellar dysfunction. Gross observation of Smad2-CNS-KO cerebella demonstrated aberrant foliations in lobule IX and X. Further analyses revealed increased apoptotic cell death, delayed migration and maturation of granule cells, and retardation of dendritic arborization of Purkinje cells. These findings indicate that Smad2 plays a key role in cerebellar development and motor function control.

本文言語英語
ページ(範囲)18766-18774
ページ数9
ジャーナルJournal of Biological Chemistry
286
21
DOI
出版ステータス出版済み - 5月 27 2011

!!!All Science Journal Classification (ASJC) codes

  • 生化学
  • 分子生物学
  • 細胞生物学

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