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Translesion DNA Synthesis and Hsp90

机译:跨病变DNA合成和Hsp90

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References(55) 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.
机译:参考文献(55)Translesion DNA合成(TLS)是在基因组复制过程中通过使用专门的低保真聚合酶绕过DNA损伤而对DNA损伤耐受的重要机制。因此,TLS具有内在的诱变性,据推测与癌症的发生和发展有关。 TLS聚合酶的翻译后调节机制越来越受到关注,包括共价修饰(例如磷酸化)和蛋白酶体降解。在这篇综述文章中,我们将重点放在有关Hsp90介导的TLS聚合酶调控的研究中,并讨论Hsp90抑制剂在癌症治疗中的潜在药理作用。

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