Zeb2 is essential for Schwann cell differentiation, myelination and nerve repair

被引：0
作者：
Susanne Quintes
Bastian G Brinkmann
Madlen Ebert
Franziska Fröb
Theresa Kungl
Friederike A Arlt
Victor Tarabykin
Danny Huylebroeck
Dies Meijer
Ueli Suter
Michael Wegner
Michael W Sereda
Klaus-Armin Nave
机构：
[1] Max Planck Institute of Experimental Medicine,Department of Neurogenetics
[2] University Medical Center Göttingen (UMG),Department of Clinical Neurophysiology
[3] Institut für Biochemie,Department of Development and Regeneration
[4] Emil-Fischer-Zentrum,Department of Cell Biology
[5] Friedrich-Alexander Universität Erlangen-Nürnberg,Department of Biology
[6] Institute for Cell and Neurobiology,undefined
[7] Center for Anatomy,undefined
[8] Charité Universitätsmedizin Berlin,undefined
[9] Laboratory of Molecular Biology (Celgen),undefined
[10] KU Leuven,undefined
[11] Erasmus University Medical Center,undefined
[12] Centre for Neuroregeneration,undefined
[13] University of Edinburgh,undefined
[14] Institute of Molecular Health Sciences,undefined
[15] ETH Zu¨rich,undefined
来源：
Nature Neuroscience | 2016年 / 19卷
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摘要：
By studying a severe neuropathy in mice, Quintes, Brinkmann et al. demonstrate that the nuclear zinc-finger protein Zeb2 (Sip1) is essential for Schwann cell differentiation and myelin synthesis. Since Zeb2-deficient Schwann cells continuously express repressors of lineage progression, ‘inhibiting the inhibitors’ emerges as a new principle of peripheral myelination control.
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页码：1050 / 1059
页数：9
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