Biomol Ther (Seoul)  
Altered Translational Control of FMRP on Myelin Proteins in Neuropsychiatric Disorders
Se Jin Jeon1, Jong Hoon Ryu1,*, and Geon Ho Bahn2,*
1Department of Life and Nanopharmaceutical Science, College of Pharmacy, 2Department of Neuropsychiatry, School of Medicine, Kyung Hee University, Seoul 02447, Republic of Korea
E-mail: jhryu63@khu.ac.kr (Ryu JH), mompeian@khu.ac.kr (Bahn GH)
Tel: +82-2-961-9230 (Ryu JH), +82-2-958-8556 (Bahn GH)
Fax: +82-2-966-3885 (Ryu JH), +82-2-966-3885 (Bahn GH)
Received: February 21, 2016; Revised: June 28, 2016; Accepted: July 28, 2016; Published online: November 8, 2016.
© The Korean Society of Applied Pharmacology. All rights reserved.

Abstract
Myelin is a specialized structure of the nervous system that both enhances electrical conductance and insulates neurons from external risk factors. In the central nervous system, polarized oligodendrocytes form myelin by wrapping processes in a spiral pattern around neuronal axons through myelin-related gene regulation. Since these events occur at a distance from the cell body, post-transcriptional control of gene expression has strategic advantage to fine-tune the overall regulation of protein contents in situ. Therefore, many research interests have been focused to identify RNA binding proteins and their regulatory mechanism in myelinating compartments. Fragile X mental retardation protein (FMRP) is one such RNA binding protein, regulating its target expression by translational control. Although the majority of works on FMRP have been performed in neurons, it is also found in the developing or mature glial cells including oligodendrocytes, where its function is not well understood. Here, we will review evidences suggesting abnormal translational regulation of myelin proteins with accompanying white matter problem and neurological deficits in fragile X syndrome, which can have wider mechanistic and pathological implication in many other neurological and psychiatric disorders.
Keywords: Myelin, Fragile x mental retardation protein, Translational control, Oligodendrocyte


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