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Document Version Version Comment Date Status
18215.0 [No comment] 14.04.2010 11:44 Released

ID: 18215.0, MPI für experimentelle Medizin / Neurogenetics
Notch1 control of oligodendrocyte differentiation in the spinal cord
Authors:Genoud, S.; Lappe-Siefke, Corinna; Goebbels, Sandra; Radtke, F.; Aguet, M.; Scherer, S. S.; Suter, U.; Nave, Klaus-Armin; Mantei, N.
Date of Publication (YYYY-MM-DD):2002-08-19
Title of Journal:Journal of Cell Biology
Journal Abbrev.:J. Cell Biol.
Issue / Number:4
Start Page:709
End Page:718
Review Status:Peer-review
Audience:Experts Only
Abstract / Description:We have selectively inhibited Notch1 signaling in oligodendrocyte precursors (OPCs) using the Cre/loxP system in transgenic mice to investigate the role of Notch1 in oligodendrocyte (OL) development and differentiation. Early development of OPCs appeared normal in the spinal cord. However, at embryonic day 17.5, premature OL differentiation was observed and ectopic immature OLs were present in the gray matter. At birth, OL apoptosis was strongly increased in Notch I mutant animals. Premature OL differentiation was also observed in the cerebrum, indicating that Notch1 is required for the correct spatial and temporal regulation of OL differentiation in various regions of the central nervous system. These findings establish a widespread function of Notch1 in the late steps of mammalian OPC development in vivo.
Free Keywords:ectopic expression; brain; Cre-lox P; newborn; apoptosis
Comment of the Author/Creator:Date: 2002, AUG 19
External Publication Status:published
Document Type:Article
Communicated by:Klaus-Armin Nave
Affiliations:MPI für experimentelle Medizin/Neurogenetics
External Affiliations:ETH Honggerberg, Swiss Fed Inst Technol, Dept Biol, Inst Cell; Biol, CH-8093 Zurich, Switzerland; Swiss Inst Expt Canc Res, CH-1066 Epalinges, Switzerland; Univ Lausanne, Lausanne Branch, Ludwig Inst Canc Res, CH-1066 Epalinges, Switzerland; Univ Penn, Med Ctr, Dept Neurol, Philadelphia, PA 19104 USA
Identifiers:ISI:000177649900011 [ID No:1]
ISSN:0021-9525 [ID No:2]
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