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- Publisher Website: 10.1101/gad.975202
- Scopus: eid_2-s2.0-0036205049
- PMID: 11937492
- WOS: WOS:000174971800009
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Article: Notch pathway molecules are essential for the maintenance, but not the generation, of mammalian neural stem cells
Title | Notch pathway molecules are essential for the maintenance, but not the generation, of mammalian neural stem cells |
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Authors | |
Keywords | Cell cycle time Multipotentiality Embryonic stem cell Presenilin RBP-Jκ Self-renewal |
Issue Date | 2002 |
Citation | Genes and Development, 2002, v. 16, n. 7, p. 846-858 How to Cite? |
Abstract | 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-1- 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 of RBP-Jκ-1- or Notch1-1- 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. |
Persistent Identifier | http://hdl.handle.net/10722/291592 |
ISSN | 2023 Impact Factor: 7.5 2023 SCImago Journal Rankings: 5.015 |
PubMed Central ID | |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Hitoshi, Seiji | - |
dc.contributor.author | Alexson, Tania | - |
dc.contributor.author | Tropepe, Vincent | - |
dc.contributor.author | Donoviel, Dorit | - |
dc.contributor.author | Elia, Andrew J. | - |
dc.contributor.author | Nye, Jeffrey S. | - |
dc.contributor.author | Conlon, Ronald A. | - |
dc.contributor.author | Mak, Tak W. | - |
dc.contributor.author | Bernstein, Alan | - |
dc.contributor.author | Van Der Kooy, Derek | - |
dc.date.accessioned | 2020-11-17T14:54:42Z | - |
dc.date.available | 2020-11-17T14:54:42Z | - |
dc.date.issued | 2002 | - |
dc.identifier.citation | Genes and Development, 2002, v. 16, n. 7, p. 846-858 | - |
dc.identifier.issn | 0890-9369 | - |
dc.identifier.uri | http://hdl.handle.net/10722/291592 | - |
dc.description.abstract | 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-1- 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 of RBP-Jκ-1- or Notch1-1- 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. | - |
dc.language | eng | - |
dc.relation.ispartof | Genes and Development | - |
dc.subject | Cell cycle time | - |
dc.subject | Multipotentiality | - |
dc.subject | Embryonic stem cell | - |
dc.subject | Presenilin | - |
dc.subject | RBP-Jκ | - |
dc.subject | Self-renewal | - |
dc.title | Notch pathway molecules are essential for the maintenance, but not the generation, of mammalian neural stem cells | - |
dc.type | Article | - |
dc.description.nature | link_to_OA_fulltext | - |
dc.identifier.doi | 10.1101/gad.975202 | - |
dc.identifier.pmid | 11937492 | - |
dc.identifier.pmcid | PMC186324 | - |
dc.identifier.scopus | eid_2-s2.0-0036205049 | - |
dc.identifier.volume | 16 | - |
dc.identifier.issue | 7 | - |
dc.identifier.spage | 846 | - |
dc.identifier.epage | 858 | - |
dc.identifier.isi | WOS:000174971800009 | - |
dc.identifier.f1000 | 1006012 | - |
dc.identifier.issnl | 0890-9369 | - |