紫外线照射会诱导产生“大量”DNA 光二聚体，例如 (6-4)-光产物和环丁烷嘧啶二聚体，这些光二聚体可通过核苷酸切除修复去除，这是一种在阳光敏感且易患癌症的着色性干皮病中存在缺陷的复杂过程。一些细菌和低等真核生物也可以通过更简单的酶促机制修复光二聚体，但在正常人类细胞中尚未报道这种途径。在这里，我们已经确定了这样一个机制。我们证明，正常人类细胞可以利用涉及 NTH1、APE1、PARP1、XRCC1 和 FEN1 的 DNA 碱基切除修复过程，在 UVC 照射后的早期快速去除光二聚体的子集。这些蛋白质的丢失会减慢正常细胞中光二聚体的早期修复速度，消除色素性干皮病细胞中的残余修复，并使 UVC 敏感性增加约 2 倍。这些数据表明，人类细胞可以使用长补丁碱基切除修复过程切除光二聚体，该过程可附加但独立于核苷酸切除修复。版权所有 © 2023 作者。由爱思唯尔公司出版。保留所有权利。

UV irradiation induces "bulky" DNA photodimers such as (6-4)-photoproducts and cyclobutane pyrimidine dimers that are removed by nucleotide excision repair, a complex process defective in the sunlight-sensitive and cancer-prone disease xeroderma pigmentosum. Some bacteria and lower eukaryotes can also repair photodimers by enzymatically simpler mechanisms, but such pathways have not been reported in normal human cells. Here, we have identified such a mechanism. We show that normal human cells can employ a DNA base excision repair process involving NTH1, APE1, PARP1, XRCC1, and FEN1 to rapidly remove a subset of photodimers at early times following UVC irradiation. Loss of these proteins slows the early rate of repair of photodimers in normal cells, ablates their residual repair in xeroderma pigmentosum cells, and increases UVC sensitivity ∼2-fold. These data reveal that human cells can excise photodimers using a long-patch base excision repair process that functions additively but independently of nucleotide excision repair.Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.