4.6 Review

m6A RNA Methylation Controls Neural Development and Is Involved in Human Diseases

Journal

MOLECULAR NEUROBIOLOGY
Volume 56, Issue 3, Pages 1596-1606

Publisher

SPRINGER
DOI: 10.1007/s12035-018-1138-1

Keywords

N6-methyladenosine (m(6)A); Methyltransferase; Demethylase; METTL3; FTO; Neural development

Categories

Funding

  1. Subsidized Project for Postgraduates' Innovative Fund in Scientific Research of Huaqiao University
  2. NIH/NIMH [R01-MH083680]
  3. National Natural Science Foundation of China [81471152, 31771141, 81701132]

Ask authors/readers for more resources

RNA modifications are involved in many aspects of biological functions. N6-methyladenosine (m(6)A) is one of the most important forms of RNA methylation and plays a vital role in regulating gene expression, protein translation, cell behaviors, and physiological conditions in many species, including humans. The dynamic and reversible modification of m(6)A is conducted by three elements: methyltransferases (writers), such as methyltransferase-like protein 3 (METTL3) and METTL14; m(6)A-binding proteins (readers), such as the YTH domain family proteins (YTHDFs) and YTH domain-containing protein 1 (YTHDC1); and demethylases (erasers), such as fat mass and obesity-associated protein (FTO) and AlkB homolog 5 (ALKBH5). In this review, we summarize the current knowledge on mapping mRNA positions of m(6)A modification and revealing molecular processes of m(6)A. We further highlight the biological significance of m(6)A modification in neural cells during development of the nervous system and its association with human diseases. m(6)A RNA methylation is becoming a new frontier in neuroscience and should help us better understand neural development and neurological diseases from a novel point of view.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.6
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available