Date published: 2025-9-18

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RPA135 Inhibitors

RPA135 inhibitors encompass a variety of chemical compounds that indirectly inhibit the function of RPA135, a subunit of RNA polymerase I, through diverse mechanisms. These inhibitors target different aspects of transcription and DNA processing, thereby influencing the activity of RNA polymerase I, of which RPA135 is an integral part. Compounds like Actinomycin D, BMH-21, CX-5461, and Triptolide directly interact with RNA polymerase I or its transcription process, resulting in reduced functionality of RPA135. Actinomycin D binds to DNA, inhibiting the enzyme, while BMH-21 and CX-5461 disrupt RNA polymerase I, leading to degradation or reduced activity of RPA135. Triptolide inhibits RNA polymerase I transcription, affecting RPA135's role.

Other inhibitors, such as 5-Fluorouracil, Oxaliplatin, Cisplatin, and Aphidicolin, act by interfering with RNA processing or creating DNA adducts. For instance, 5-Fluorouracil's metabolites disrupt RNA processing, impacting RPA135. Oxaliplatin and Cisplatin form DNA adducts, hindering RNA polymerase I's function. Aphidicolin, by inhibiting DNA polymerase, indirectly affects RNA polymerase I and RPA135. Additionally, compounds like DRB, Amatoxin, Leptomycin B, and Cordycepin affect RPA135 by altering the transcriptional environment or chain elongation processes. DRB inhibits transcription elongation, thus affecting RNA polymerase I. Amatoxin, targeting RNA polymerase II, can have indirect consequences on the cellular transcription environment influencing RPA135. Leptomycin B, by inhibiting nuclear export, and Cordycepin, terminating RNA chain elongation, also contribute to the regulation of RNA polymerase I activity and, consequently, RPA135 function.

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