A nucleotide excision repair master-switch: p53 regulated coordinate induction of global genomic repair genes
A nucleotide excision repair master-switch: p53 regulated coordinate induction of global genomic repair genes
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DOI：
10.4161/cbt.59
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发表时间：
2002-03-01
影响因子：
3.6
通讯作者：
Fornace, AJ
中科院分区：
文献类型：
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作者：
Amundson, SA;Patterson, A;Fornace, AJ
肿瘤抑制基因p53在许多人类癌症中发生突变。其主要作用之一是作为转录因子，其许多效应基因控制关键的细胞过程，包括细胞周期检查点和凋亡。在DNA修复中，p53本身及其一些效应基因也发挥了重要作用。目前已知两个p53调控基因GADD45a和DDB2的产物参与核苷酸切除修复（NER）的全局基因组修复（GGR）子途径。我们最近报道了第三GGR基因，XPC，正常人外周血淋巴细胞暴露于γ射线的诱导。我们现在表明，XPC是诱导在各种人类细胞系在响应电离和紫外线（UV）辐射和烷化剂，这种诱导需要野生型p53。
The tumor suppressor gene p53 is mutated in many human cancers. One of its major roles is as a transcription factor, and its many effector genes control key cellular processes including cell cycle checkpoints and apoptosis. An important role in DNA repair is also emerging for both p53 itself and some of its effector genes. The products of two p53-regulated genes, GADD45a and DDB2, are now known to participate in the global genomic repair (GGR) sub-pathway of nucleotide excision repair (NER). We recently reported the induction of a third GGR gene, XPC, following exposure of normal human peripheral blood lymphocytes to gamma-rays. We now show that XPC is induced in a variety of human cell lines in response to both ionizing and ultra-violet (UV) radiation and alkylating agents, and that this induction requires wild-type p53.