着色性干皮病基因p48的表达依赖于p53，并参与全基因组修复。
Expression of the p48 xeroderma pigmentosum gene is p53-dependent and is involved in global genomic repair.
作者信息
Hwang B J, Ford J M, Hanawalt P C, Chu G
机构信息
Departments of Medicine and Biochemistry, Stanford University School of Medicine, Stanford, CA 94305-5115, USA.
出版信息
Proc Natl Acad Sci U S A. 1999 Jan 19;96(2):424-8. doi: 10.1073/pnas.96.2.424.
Abstract
In human cells, efficient global genomic repair of DNA damage induced by ultraviolet radiation requires the p53 tumor suppressor, but the mechanism has been unclear. The p48 gene is required for expression of an ultraviolet radiation-damaged DNA binding activity and is disrupted by mutations in the subset of xeroderma pigmentosum group E cells that lack this activity. Here, we show that p48 mRNA levels strongly depend on basal p53 expression and increase further after DNA damage in a p53-dependent manner. Furthermore, like p53(-/-) cells, xeroderma pigmentosum group E cells are deficient in global genomic repair. These results identify p48 as the link between p53 and the nucleotide excision repair apparatus.
摘要
在人类细胞中，由紫外线辐射诱导的DNA损伤的高效全基因组修复需要p53肿瘤抑制因子，但具体机制尚不清楚。p48基因是紫外线辐射损伤的DNA结合活性表达所必需的，并且在缺乏这种活性的着色性干皮病E组细胞亚群中会因突变而被破坏。在这里，我们表明p48 mRNA水平强烈依赖于基础p53表达，并在DNA损伤后以p53依赖的方式进一步增加。此外，与p53(-/-)细胞一样，着色性干皮病E组细胞在全基因组修复方面存在缺陷。这些结果确定p48是p53与核苷酸切除修复机制之间的联系。
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本文引用的文献
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p48 Activates a UV-damaged-DNA binding factor and is defective in xeroderma pigmentosum group E cells that lack binding activity.p48激活一种紫外线损伤DNA结合因子，并且在缺乏结合活性的着色性干皮病E组细胞中存在缺陷。
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