HDAC-mediated deacetylation of NF-κB is critical for Schwann cell myelination-Reference-Cited by-同舟云学术

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HDAC-mediated deacetylation of NF-κB is critical for Schwann cell myelination

Published:2011-03-20 Issue:4 Volume:14 Page:437-441
ISSN:1097-6256
Container-title:Nature Neuroscience
language:en
Short-container-title:Nat Neurosci

Author:

Chen Ying,Wang Haibo,Yoon Sung Ok,Xu Xiaomei,Hottiger Michael O,Svaren John,Nave Klaus A,Kim Haesun A,Olson Eric N,Lu Q Richard

Publisher

Springer Science and Business Media LLC

Subject

General Neuroscience

Link

http://www.nature.com/articles/nn.2780.pdf

Reference23 articles.

1. Suter, U. & Scherer, S.S. Disease mechanisms in inherited neuropathies. Nat. Rev. Neurosci. 4, 714–726 (2003).

2. Jessen, K.R. & Mirsky, R. The origin and development of glial cells in peripheral nerves. Nat. Rev. Neurosci. 6, 671–682 (2005).

3. Svaren, J. & Meijer, D. The molecular machinery of myelin gene transcription in Schwann cells. Glia 56, 1541–1551 (2008).

4. Shahbazian, M.D. & Grunstein, M. Functions of site-specific histone acetylation and deacetylation. Annu. Rev. Biochem. 76, 75–100 (2007).

5. Ye, F. et al. HDAC1 and HDAC2 regulate oligodendrocyte differentiation by disrupting the beta-catenin–TCF interaction. Nat. Neurosci. 12, 829–838 (2009).

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