Ku complex interacts with and stimulates the Werner protein.
Werner syndrome (WS) is the hallmark premature aging disorder in which affected humans appear older than their chronological age. The protein WRNp, defective in WS, has helicase function, DNA-dependent ATPase, and exonuclease activity. Although WRNp functions in nucleic acid metabolism, there is little or no information about the pathways or protein interactions in which it participates. Here we identify Ku70 and Ku86 as proteins that interact with WRNp. Although Ku proteins had no effect on ATPase or helicase activity, they strongly stimulated specific exonuclease activity. These results suggest that WRNp and the Ku complex participate in a common DNA metabolic pathway.
Pubmed ID: 10783163 RIS Download
Adenosine Triphosphatases | Animals | Antigens, Nuclear | Base Sequence | Blotting, Western | Cell Line | Cell Nucleus | Chromatography, Affinity | DNA Helicases | DNA-Binding Proteins | Electrophoresis, Polyacrylamide Gel | Enzyme Activation | Exodeoxyribonucleases | Exonucleases | Humans | Molecular Sequence Data | Nuclear Proteins | Precipitin Tests | Protein Binding | RecQ Helicases | Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization