HDAC1 and HDAC2 regulate oligodendrocyte differentiation by disrupting the β-catenin–TCF interaction

被引：0
|
作者：
Feng Ye
Ying Chen
ThaoNguyen Hoang
Rusty L Montgomery
Xian-hui Zhao
Hong Bu
Tom Hu
Makoto M Taketo
Johan H van Es
Hans Clevers
Jenny Hsieh
Rhonda Bassel-Duby
Eric N Olson
Q Richard Lu
机构：
[1] University of Texas Southwestern Medical Center,Department of Developmental Biology and Kent Waldrep Foundation Center for Basic Neuroscience Research on Nerve Growth and Regeneration
[2] Laboratory of Transplant Engineering and Immunology,Department of Molecular Biology
[3] West China Hospital,Department of Pharmacology
[4] Sichuan University,undefined
[5] University of Texas Southwestern Medical Center,undefined
[6] Graduate School of Medicine,undefined
[7] Kyoto University,undefined
[8] Hubrecht Institute,undefined
[9] West China Second University Hospital,undefined
[10] Sichuan University,undefined
来源：
Nature Neuroscience | 2009年 / 12卷
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摘要：
Previous work has suggested that the histone deacetylase HDAC1 promotes and canonical Wnt signaling antagonizes oligodendrocyte differentiation. Here, Ye et al. show that HDAC1/2 directly interferes with canonical Wnt signaling in oligodendrocyte precursors by competing with β-catenin for interaction with the transcriptional co-factor TCF7L2. TCF7L2 itself is shown to be crucial for oligodendrocyte development.
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页码：829 / 838
页数：9
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