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The 5-methylcytosine (m5C) RNA methylation process refers to the enzymatic addition of a methyl group to the fifth carbon of cytosine in RNA molecules, a key epitranscriptomic mark that affects both coding (mRNA) and non-coding (tRNA, rRNA, miRNA) RNAs[1][3][5][7][9]. This reversible process is catalyzed by "writer" enzymes (NSUN family, DNMT2/TRDMT1), removed by "erasers" (TET family, ALKBH1), and interpreted by "reader" proteins (ALYREF, YBX1, etc.)[1][3][7][9]. m5C RNA methylation participates in regulating RNA structure, stability, export, translation, and cellular stress responses. Dysregulation of m5C methylation or its effectors is implicated in cancer, autoimmune disease, cardiovascular disease, and neurological disorders[1][3][5][7][9]. m5C methylation is an active area of research in epitranscriptomics but is not itself considered a direct therapeutic target; rather, the individual proteins mediating the addition, removal, or recognition of m5C are the true molecular drug targets. Note: This entry describes a process, not a targetable molecule, so most structured target fields such as "mechanism of action", "interacting drugs", etc., are not directly applicable except when considering specific proteins (e.g., NSUN2 methyltransferase) rather than the process as a whole.
At the process level, not applicable—individual enzymes (writers/erasers) could be inhibited or activated to alter m5C levels, but the process itself is not a drug target
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