N1-methyladenosine formation, gene regulation, biological functions, and clinical relevance
N1-methyladenosine (m1A) is an adenosine moiety whose N1-position is methylated. m1A methylation is a prevalent, abundant, and conserved internal post-transcriptional modification among prokaryotic and eukaryotic RNAs, especially in higher eukaryotic cells. Numerous studies have revealed that m1A me...
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Published in | Molecular therapy Vol. 31; no. 2; pp. 308 - 330 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Elsevier Inc
01.02.2023
American Society of Gene & Cell Therapy |
Subjects | |
Online Access | Get full text |
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Summary: | N1-methyladenosine (m1A) is an adenosine moiety whose N1-position is methylated. m1A methylation is a prevalent, abundant, and conserved internal post-transcriptional modification among prokaryotic and eukaryotic RNAs, especially in higher eukaryotic cells. Numerous studies have revealed that m1A methylation plays a critical role in the biogenesis of various RNAs, thereby regulating different biological functions and pathogenesis. In this review, we systematically and comprehensively summarize the installation, removal, and recognition of m1A and highlight the critical effects of m1A on the post-transcriptional metabolism of various RNAs. We emphasize the importance of m1A both in the growth of organisms and pathogenesis of various diseases, particularly cancers. Finally, we also focused on the fact that excretion of m1A in human urine is strongly associated with the progression of a variety of diseases, and we suggest that m1A levels in urine can be quantified for early diagnosis of some diseases as well as for monitoring during disease evolution.
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m1A methylation plays a critical role in the biogenesis of various RNAs. In this review, Xiong et al. systematically and comprehensively summarize the installation, removal, and recognition of m1A and emphasize the importance of m1A both in the growth of organisms and pathogenesis of various diseases, particularly cancers. |
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Bibliography: | These authors contributed equally |
ISSN: | 1525-0016 1525-0024 |
DOI: | 10.1016/j.ymthe.2022.10.015 |