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N6-methyladenosine-modified messenger RNA refers to **mRNA molecules that have been post-transcriptionally modified by the addition of a methyl group at the nitrogen-6 position of adenosine residues**, known as the m6A modification. This is the most prevalent internal modification in eukaryotic mRNA and affects various aspects of mRNA metabolism, including splicing, export, translation, and decay. The modification is installed by a multi-protein complex called the m6A methyltransferase (primarily METTL3, METTL14, and cofactors), removed by demethylases (e.g., FTO, ALKBH5), and interpreted by “reader” proteins such as members of the YTH domain family. m6A modifications play key regulatory roles in **gene expression, cell differentiation, stress responses, and disease processes** including cancer and metabolic disorders. Therapeutically, drugs target the enzymes responsible for adding or removing m6A but not the modified mRNA molecules themselves[1][2][3][4][5][7]. **Important clarification:** - "N6-methyladenosine-modified mRNA" is **not a drug target or receptor**; it is a class of mRNA molecules marked by a specific chemical modification. *The relevant drug targets are the enzymes ("writers," "erasers," and "readers") that control the deposition, removal, or recognition of the m6A modification* (e.g., METTL3, FTO, ALKBH5, YTHDF proteins)[3][5][7]. - There are no direct drugs, mechanisms of action, biomarkers, or safety concerns for m6A-modified mRNA itself since it is not a protein or functional target, but manipulating the enzymes that regulate m6A is under therapeutic investigation[3][5]. **Summary of corrections and notes:** - **is_incorrect** is set to true because the molecule is not a canonical drug target, receptor, enzyme, transporter, or transcription factor, but a modified product (substrate) of various RNA-modifying enzymes. - When seeking therapeutic or mechanistic information, refer to specific proteins in the m6A regulatory machinery (e.g., METTL3 for writers, FTO/ALKBH5 for erasers, or YTHDF1/2/3 for readers)[3][5][7].
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