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Vol. 14, No. 8, pp. 907-912, April 15, 2000
1 Laboratory of Molecular Genetics, National
Institute on Aging, National Institutes of Health, Baltimore,
Maryland 21224 USA; 2 Department of Medicine, Johns Hopkins
University School of Medicine, and 3 Lineberger Comprehensive
Cancer Center, University of North Carolina, Chapel Hill, North
Carolina 27599 USA
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.
[Key Words: Werner syndrome; Ku proteins; WRNp; exonuclease activity]
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