Xeroderma Pigmentosa Group A (XPA), Nucleotide Excision Repair and Regulation by ATR in Response to Ultraviolet Irradiation.
Xeroderma Pigmentosa Group A (XPA), Nucleotide Excision Repair and Regulation by ATR in Response to Ultraviolet Irradiation.
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DOI：
10.1007/978-3-319-56017-5_4
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发表时间：
2017
影响因子：
--
通讯作者：
Zou Y
中科院分区：
文献类型：
--
作者：
Musich PR;Li Z;Zou Y
色素性干皮病 (XP) 患者对阳光的敏感性促使人们对导致这种情况的八种 XP 基因产物（XPA-XPG 加 XPV）进行了发现和遗传和生化分析。这些研究还阐明了核苷酸切除修复 (NER) 过程，特别是 XPA 蛋白所起的关键作用。最近的研究表明，NER 还涉及许多通常用于 DNA 代谢和细胞周期调节的其他蛋白质。其中最重要的是毛细血管扩张共济失调和 Rad3 相关 (ATR)，这是一种蛋白激酶，参与响应 DNA 损伤（尤其是复制和转录应激）的细胞内信号传导。这篇综述总结了 ATR 作为 DNA 损伤信号激酶和作为内在细胞死亡蛋白的新型配体以延迟损伤诱导的细胞凋亡之间相互作用的最新发现，以及 ATR 对 XPA 的调节和修复 UV 诱导的 DNA 加合物的 NER 过程。我们将讨论 ATR 在 XPA 胞质至核易位中的调节作用。此外，最近的研究结果阐明了 XPA 在 ds-ssDNA 连接处的 DNA 代谢和基因组稳定中的非 NER 作用，如过早衰老的早衰细胞中的例子，也将进行综述。
The sensitivity of Xeroderma pigmentosa (XP) patients to sunlight has spurred the discovery and genetic and biochemical analysis of the eight XP gene products (XPA-XPG plus XPV) responsible for this condition. These studies also have served to elucidate the nucleotide excision repair (NER) process, especially the critical role played by the XPA protein. More recent studies have shown that NER also involves numerous other proteins normally employed in DNA metabolism and cell cycle regulation. Central among these is ataxia telangiectasia and Rad3-related (ATR), a protein kinase involved in intracellular signaling in response to DNA damage, especially replicative and transcription stresses. This review summarizes recent findings on the interplay between ATR as a DNA damage signaling kinase and as a novel ligand for intrinsic cell death proteins to delay damage-induced apoptosis, and on ATR’s regulation of XPA and the NER process for repair of UV-induced DNA adducts. ATR’s regulatory role in the cytosolic-to-nuclear translocation of XPA will be discussed. In addition, recent findings elucidating a non-NER role for XPA in DNA metabolism and genome stabilization at ds-ssDNA junctions, as exemplified in prematurely aging progeroid cells, also will be reviewed.
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影响因子：
16
作者：
Buisson R;Boisvert JL;Benes CH;Zou L
通讯作者：
Zou L
影响因子：
13.3
作者：
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作者：
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通讯作者：
Cortez D
影响因子：
3.8
作者：
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通讯作者：
Drobetsky, Elliot A.
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作者：
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