DDX27 inhibitors constitute a group of chemicals that target various aspects of RNA metabolism and cellular stress responses, thereby indirectly affecting the function of the DDX27 protein. These compounds generally do not inhibit the helicase activity of DDX27 directly but instead alter the availability of its substrates or modulate the cellular environment in which DDX27 operates. For example, transcription inhibitors like Actinomycin D, Alpha-amanitin, and DRB reduce the synthesis of RNA, which could limit the availability of RNA substrates necessary for DDX27 function. Other compounds such as Triptolide and BMH-21 exert their effects by inhibiting transcriptional activity and RNA polymerase I, respectively, which can have downstream effects on ribosome biogenesis-a process in which DDX27 is implicated.
Moreover, chemicals that disrupt nucleocytoplasmic transport, such as Leptomycin B, can impact the localization of DDX27, potentially affecting its functional interactions with RNA molecules and other proteins within the cell. DNA-damaging agents like Oxaliplatin form adducts with DNA that can disrupt transcription and, consequently, the role of DDX27 in RNA processing or ribosome assembly. Translation initiation inhibitors, including Rocaglamide, Silvestrol, and Homoharringtonine, can indirectly affect DDX27's role in ribosome biogenesis by interfering with the initiation of protein synthesis. Tunicamycin, which induces stress on the endoplasmic reticulum by inhibiting N-linked glycosylation, could affect DDX27 function during cellular responses to stress.
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