Loss of mammalian Sprouty2 leads to enteric neuronal hyperplasia and esophageal achalasia

Takaharu Taketomi, Daigo Yoshiga, Koji Taniguchi, Takashi Kobayashi, Atsushi Nonami, Reiko Kato, Mika Sasaki, Atsuo Sasaki, Hitoshi Ishibashi, Maiko Moriyama, Kei Ichiro Nakamura, Junji Nishimura, Akihiko Yoshimura

研究成果: Article

104 引用 (Scopus)

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We report here that loss of the Sprouty2 gene (also known as Spry2) in mice resulted in enteric nerve hyperplasia, which led to esophageal achalasia and intestinal pseudo-obstruction. Glial cell line-derived neurotrophic factor (GDNF) induced hyperactivation of ERK and Akt in enteric nerve cells. Anti-GDNF antibody administration corrected nerve hyperplasia in Sprouty2-deficient mice. We show Sprouty2 to be a negative regulator of GDNF for the neonatal development or survival of enteric nerve cells.

元の言語English
ページ(範囲)855-857
ページ数3
ジャーナルNature Neuroscience
8
発行部数7
DOI
出版物ステータスPublished - 2005 7 25
外部発表Yes

ASJC Scopus subject areas

  • Neuroscience(all)

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    Taketomi, T., Yoshiga, D., Taniguchi, K., Kobayashi, T., Nonami, A., Kato, R., Sasaki, M., Sasaki, A., Ishibashi, H., Moriyama, M., Nakamura, K. I., Nishimura, J., & Yoshimura, A. (2005). Loss of mammalian Sprouty2 leads to enteric neuronal hyperplasia and esophageal achalasia. Nature Neuroscience, 8(7), 855-857. https://doi.org/10.1038/nn1485