KARP-1 由DNA损伤以p53和共济失调毛细血管扩张突变依赖的方式诱导产生。
KARP-1 is induced by DNA damage in a p53- and ataxia telangiectasia mutated-dependent fashion.
作者信息
Myung K, Braastad C, He D M, Hendrickson E A
机构信息
Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI 02912, USA.
出版信息
Proc Natl Acad Sci U S A. 1998 Jun 23;95(13):7664-9. doi: 10.1073/pnas.95.13.7664.
Abstract
The KARP-1 (Ku86 Autoantigen Related Protein-1) gene, which is expressed from the human Ku86 autoantigen locus, appears to play a role in mammalian DNA double-strand break repair as a regulator of the DNA-dependent protein kinase complex. Here we demonstrate that KARP-1 gene expression is significantly up-regulated following exposure of cells to DNA damage. KARP-1 mRNA induction was completely dependent on the ataxia telangiectasia and p53 gene products, consistent with the presence of a p53 binding site within the second intron of the KARP-1 locus. These observations link ataxia telangiectasia, p53, and KARP-1 in a common pathway.
摘要
KARP-1（Ku86自身抗原相关蛋白-1）基因由人类Ku86自身抗原基因座表达，作为DNA依赖性蛋白激酶复合物的调节因子，似乎在哺乳动物DNA双链断裂修复中发挥作用。在此，我们证明细胞暴露于DNA损伤后，KARP-1基因表达显著上调。KARP-1 mRNA的诱导完全依赖于共济失调毛细血管扩张症和p53基因产物，这与KARP-1基因座第二个内含子内存在p53结合位点一致。这些观察结果将共济失调毛细血管扩张症、p53和KARP-1联系在一条共同途径中。
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