JH-RE-06 is a potent and selective inhibitor of REV1-REV7 interaction that induces REV1 dimerization blocking the REV1-REV7 interaction and POL ϲ recruitment. JH-RE-06 potently inhibits translesion synthesis (TLS) and augments cisplatin effectiveness in cultured human and mouse cell lines. It improves effectiveness of cisplatin in A375 tumor xenograft mouse model.
potent and selective inhibitor of REV1-REV7 interaction blocking the REV1-REV7 interaction and POL ϲ recruitment
5-Hydroxymethylcytosine (5hmC) binding, ES-cell-specific (HMCES) crosslinks to apurinic or apyrimidinic (AP, abasic) sites in single-strand DNA (ssDNA). To determine whether HMCES responds to the ssDNA abasic site in cells, we exploited the activity of apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like
Intrinsic and acquired drug resistance and induction of secondary malignancies limit successful chemotherapy. Because mutagenic translesion synthesis (TLS) contributes to chemoresistance as well as treatment-induced mutations, targeting TLS is an attractive avenue for improving chemotherapeutics. However, development of small molecules with
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