The potential role of ribonucleic acid methylation in the pathological mechanisms of fragile X syndrome

被引:3
|
作者
Chen, Yu-Shan [1 ,2 ]
Dong, Jing [1 ]
Tan, Wei [2 ]
Liu, Hui [1 ,2 ]
Zhang, Si-Ming [1 ,2 ]
Zou, Jia [1 ,2 ]
Chen, Yi-Qi [1 ,2 ]
Bai, Shu-Yuan [1 ,2 ]
Zeng, Yan [1 ,2 ,3 ]
机构
[1] Wuhan Univ Sci & Technol, Brain Sci & Adv Technol Inst, Sch Med, Hubei Prov Key Lab Occupat Hazard Identificat & Co, Wuhan, Peoples R China
[2] Wuhan Univ Sci & Technol, Geriatr Hosp, Wuhan, Peoples R China
[3] Wuhan Univ Sci & Technol, West Huangjiahu Rd, Wuhan 430065, Peoples R China
基金
中国国家自然科学基金;
关键词
Fragile X syndrome; RNA modification; 5-methylcytosine (m 5 C); RNA -binding protein; Synaptic function; N6-methyladenosine(m6A); MENTAL-RETARDATION PROTEIN; MESSENGER-RNA TRANSLATION; NUCLEAR EXPORT; MOUSE MODEL; M(6)A RNA; BINDING; 5-HYDROXYMETHYLCYTOSINE; IDENTIFICATION; NEURONS; RIBONUCLEOPROTEIN;
D O I
10.1016/j.bbr.2023.114586
中图分类号
B84 [心理学]; C [社会科学总论]; Q98 [人类学];
学科分类号
03 ; 0303 ; 030303 ; 04 ; 0402 ;
摘要
Fragile X syndrome (FXS) is a common inherited cause of intellectual disabilities and single-gene cause of autism spectrum disorder (ASD), resulting from the loss of functional fragile X messenger ribonucleoprotein (FMRP), an RNA-binding protein (RBP) encoded by the fragile X messenger ribonucleoprotein 1 (FMR1) gene. Ribonucleic acid (RNA) methylation can lead to developmental diseases, including FXS, through various mechanisms mediated by 5-hydroxymethylcytosine, 5-methylcytosine, N6-methyladenosine, etc. Emerging evidence suggests that modifications of some RNA species have been linked to FXS. However, the underlying pathological mechanism has yet to be elucidated. In this review, we reviewed the implication of RNA modification in FXS and summarized its specific characteristics for facilitating the identification of new therapeutic targets.
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页数:6
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