論文

査読有り 筆頭著者
2002年4月1日

Notch pathway molecules are essential for the maintenance, but not the generation, of mammalian neural stem cells

Genes & Development
  • Seiji Hitoshi
  • ,
  • Tania Alexson
  • ,
  • Vincent Tropepe
  • ,
  • Dorit Donoviel
  • ,
  • Andrew J. Elia
  • ,
  • Jeffrey S. Nye
  • ,
  • Ronald A. Conlon
  • ,
  • Tak W. Mak
  • ,
  • Alan Bernstein
  • ,
  • Derek van der Kooy

16
7
開始ページ
846
終了ページ
858
記述言語
掲載種別
研究論文(学術雑誌)
DOI
10.1101/gad.975202
出版者・発行元
Cold Spring Harbor Laboratory

Neural stem cells, which exhibit self-renewal and multipotentiality, are generated in early embryonic brains and maintained throughout the lifespan. The mechanisms of their generation and maintenance are largely unknown. Here, we show that neural stem cells are generated independent of RBP-Jκ, a key molecule in Notch signaling, by using RBP-Jκ−/− embryonic stem cells in an embryonic stem cell-derived neurosphere assay. However, Notch pathway molecules are essential for the maintenance of neural stem cells; they are depleted in the early embryonic brains ofRBP-Jκ−/− or Notch1−/− mice. Neural stem cells also are depleted in embryonic brains deficient for the presenilin1 (PS1) gene, a key regulator in Notch signaling, and are reduced in PS1+/− adult brains. Both neuronal and glial differentiation in vitro were enhanced by attenuation of Notch signaling and suppressed by expressing an active form of Notch1. These data are consistent with a role for Notch signaling in the maintenance of the neural stem cell, and inconsistent with a role in a neuronal/glial fate switch.

リンク情報
DOI
https://doi.org/10.1101/gad.975202
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/11937492
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000174971800009&DestApp=WOS_CPL
URL
https://syndication.highwire.org/content/doi/10.1101/gad.975202
ID情報
  • DOI : 10.1101/gad.975202
  • ISSN : 0890-9369
  • eISSN : 1549-5477
  • PubMed ID : 11937492
  • Web of Science ID : WOS:000174971800009

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