KARP-1 is induced by DNA damage in a p53- and ataxia telangiectasia mutated-dependent fashion.
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.
Myung
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K
Department of Molecular Biology, Cell Biology and Biochemistry, Brown University, Providence, RI 02912, USA.
Braastad
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Hendrickson
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D001260:Ataxia Telangiectasia / Q000235:genetics* / Q000378:metabolism; D001665:Binding Sites; D002352:Carrier Proteins / Q000096:biosynthesis / Q000235:genetics*; D004249:DNA Damage; D004265:DNA Helicases; D004260:DNA Repair; D018922:HL-60 Cells; D006367:HeLa Cells; D006801:Humans; D007438:Introns; D000072200:Ku Autoantigen; D016350:Leucine Zippers; D008969:Molecular Sequence Data; D012333:RNA, Messenger / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism*; D015854:Up-Regulation
D002352:Carrier Proteins; D012333:RNA, Messenger; D016159:Tumor Suppressor Protein p53; D004265:DNA Helicases; C106893:XRCC5 protein, human; D000072200:Ku Autoantigen