Nichols A F, Ong P, Linn S
Division of Biochemistry and Molecular Biology, University of California, Berkeley, California 94720-3202, USA.
J Biol Chem. 1996 Oct 4;271(40):24317-20. doi: 10.1074/jbc.271.40.24317.
The activity of a damage-specific DNA-binding protein (DDB) is absent from a subset, Ddb-, of cell strains from patients with xeroderma pigmentosum group E (XP-E). DDB is a heterodimer of 127-kDa and 48-kDa subunits. We have now identified single-base mutations in the gene of the 48-kDa subunit in cells from the three known Ddb- individuals, but not in XP-E strains that have the activity. An A --> G transition causes a K244E change in XP82TO and a G --> A transition causes an R273H change in XP2RO and XP3RO. No mutations were found in the cDNA of the 127-kDa subunit. Overexpression of p48 in insect cells greatly increases DDB activity in the cells, especially if p127 is jointly overexpressed. These results demonstrate that p48 is required for DNA binding activity, but at the same time necessitate further definition of the genetic basis of XP group E.
在一部分来自着色性干皮病E组(XP - E)患者的细胞株(Ddb -)中,缺乏一种损伤特异性DNA结合蛋白(DDB)的活性。DDB是一种由127 kDa和48 kDa亚基组成的异二聚体。我们现已在来自三名已知Ddb -个体的细胞中,而非具有该活性的XP - E细胞株中,鉴定出48 kDa亚基基因中的单碱基突变。在XP82TO细胞中,一个A→G的转换导致了K244E的变化;在XP2RO和XP3RO细胞中,一个G→A的转换导致了R273H的变化。在127 kDa亚基的cDNA中未发现突变。在昆虫细胞中过表达p48可极大地提高细胞中的DDB活性,尤其是在同时过表达p127的情况下。这些结果表明,p48是DNA结合活性所必需的,但同时也需要进一步明确E组XP的遗传基础。