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METTL Family in Health and Disease
- Source :
- Molecular Biomedicine, Vol 5, Iss 1, Pp 1-27 (2024)
- Publication Year :
- 2024
- Publisher :
- Springer, 2024.
-
Abstract
- Abstract Transcription, RNA splicing, RNA translation, and post-translational protein modification are fundamental processes of gene expression. Epigenetic modifications, such as DNA methylation, RNA modifications, and protein modifications, play a crucial role in regulating gene expression. The methyltransferase-like protein (METTL) family, a constituent of the 7-β-strand (7BS) methyltransferase subfamily, is broadly distributed across the cell nucleus, cytoplasm, and mitochondria. Members of the METTL family, through their S-adenosyl methionine (SAM) binding domain, can transfer methyl groups to DNA, RNA, or proteins, thereby impacting processes such as DNA replication, transcription, and mRNA translation, to participate in the maintenance of normal function or promote disease development. This review primarily examines the involvement of the METTL family in normal cell differentiation, the maintenance of mitochondrial function, and its association with tumor formation, the nervous system, and cardiovascular diseases. Notably, the METTL family is intricately linked to cellular translation, particularly in its regulation of translation factors. Members represent important molecules in disease development processes and are associated with patient immunity and tolerance to radiotherapy and chemotherapy. Moreover, future research directions could include the development of drugs or antibodies targeting its structural domains, and utilizing nanomaterials to carry miRNA corresponding to METTL family mRNA. Additionally, the precise mechanisms underlying the interactions between the METTL family and cellular translation factors remain to be clarified.
Details
- Language :
- English
- ISSN :
- 26628651
- Volume :
- 5
- Issue :
- 1
- Database :
- Directory of Open Access Journals
- Journal :
- Molecular Biomedicine
- Publication Type :
- Academic Journal
- Accession number :
- edsdoj.8603014ed20b415e85a3eb92f223808e
- Document Type :
- article
- Full Text :
- https://doi.org/10.1186/s43556-024-00194-y