DinB Inhibitors

The class of DinB inhibitors, as represented here, includes chemicals that indirectly affect the activity of DinB (DNA Polymerase IV) by influencing DNA damage, DNA repair pathways, and translesion synthesis (TLS) processes. DinB's primary role in bacteria is to facilitate DNA replication across damaged sites, which is crucial in maintaining genomic integrity under stress conditions, such as those induced by DNA-damaging agents. Fluoroquinolone antibiotics like Ciprofloxacin and Nalidixic Acid work by inducing DNA damage, which can stimulate the SOS response and, consequently, the activity of DinB as part of the TLS mechanism. Mitomycin C, a DNA cross-linking agent, and Aflatoxin B1, which forms DNA adducts, also create DNA lesions that may necessitate the involvement of DinB for replication bypass. The exposure of cells to UVC light and the application of certain agents like Etoposide, Camptothecin, Bleomycin, and Oxaliplatin lead to various forms of DNA damage. These agents induce DNA breaks, interstrand crosslinks, or adducts, potentially triggering the need for TLS and the action of DinB. Novobiocin, affecting DNA gyrase, can alter DNA supercoiling and topology, possibly impacting the conditions under which DinB operates. Hydroxyurea, known to induce replication stress, may also augment the activation of TLS pathways, including those mediated by DinB.