CTBS inhibitors, classified by their influence on related cellular pathways, primarily target the processes of RNA synthesis, RNA modification, and protein translation. Agents like Actinomycin D, α-Amanitin, DRB, and Ribavirin hinder RNA synthesis by distinct mechanisms. For instance, Actinomycin D binds specifically to guanosine-cytosine rich DNA sequences, inhibiting RNA synthesis, while α-Amanitin selectively obstructs RNA polymerase II. The reduced synthesis of RNA can indirectly impede CTBS's RNA modification activity, given that it operates within this cellular context.
Additionally, compounds such as 5-Azacytidine and Mycophenolic acid can influence gene expression and RNA synthesis, respectively. By doing so, they have potential implications for CTBS's functional role in RNA modification. Compounds affecting protein translation, including Puromycin, Cycloheximide, and Rapamycin, exert their effects on ribosomal function or broader translation regulatory pathways. Given that CTBS's role intertwines with RNA processes that are precursors to protein translation, altering translation dynamics can indirectly influence CTBS. Lastly, inhibitors of glycolysis and cellular energy pathways, such as 2-Deoxyglucose and Oxamate, provide an indirect avenue to modulate CTBS. Disturbances in cellular energetics can have cascading effects on enzymatic functions, including those related to RNA, where CTBS operates.
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