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.
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