Bromodomains: Translating the words of lysine acetylation into myelin injury and repair

NEUROSCIENCE LETTERS

卷:625

Review

Ntranos, Achilles¹  Casaccia, Patrizia^2,3,4 

[1] Icahn Sch Med Mt Sinai, Dept Neurol, 1428 Madison Ave, New York, NY 10029 USA

[2] Icahn Sch Med Mt Sinai, Dept Neurosci, 1428 Madison Ave, New York, NY 10029 USA

[3] Icahn Sch Med Mt Sinai, Dept Genet & Genom Sci, 1428 Madison Ave, New York, NY 10029 USA

[4] Icahn Sch Med Mt Sinai, Corinne Goldsmith Dickinson Ctr Multiple Sclerosi, 1428 Madison Ave, New York, NY 10029 USA

关键词: Bromodomains;    Lysine acetylation;    Multiple sclerosis;    Remyelination;    Myelin injury;   

DOI  :  10.1016/j.neulet.2015.10.015

来源: Elsevier

【 摘 要 】

Bromodomains are evolutionarily highly conserved alpha-helical structural motifs that recognize and bind acetylated lysine residues. Lysine acetylation is being increasingly recognized as a major posttranslational modification involved in diverse cellular processes and protein interactions and its deregulation has been implicated in the pathophysiology of various human diseases, such as multiple sclerosis and cancer. Bromodomain-containing proteins can have a wide variety of functions, ranging from histone acetyltransferase activity and chromatin remodeling to transcriptional mediation and co-activation. The role of bromodomains in translating a deregulated cell acetylome into disease phenotypes was recently unveiled by the development of small molecule bromodomain inhibitors. This breakthrough discovery highlighted bromodomain-containing proteins as key players of inflammatory pathways responsible for myelin injury and also demonstrated their role in several aspects of myelin repair including oligodendrocyte differentiation and axonal regeneration. (C) 2015 Elsevier Ireland Ltd. All rights reserved.

【 授权许可】

Free