Translesion DNA Synthesis and Hsp90

Abstract

Translesion DNA synthesis (TLS) is an essential mechanism for DNA damage tolerance during genome duplication by bypassing DNA lesions with use of specialized low-fidelity polymerases. Thus, TLS is inherently mutagenic, which is presumed to be involved in cancer initiation and progression. Increasing attention has focused on post-translational regulatory mechanisms of TLS polymerases, including covalent modification (e.g., phosphorylation) and proteasomal degradation. In this review article, we focus on our findings on Hsp90-mediated regulation of TLS polymerases and discuss potential pharmacological effects of Hsp90 inhibitors in cancer therapy.