Ku complex interacts with and stimulates the Werner protein
AUTOR(ES)
Cooper, Marcus P.
FONTE
Cold Spring Harbor Laboratory Press
RESUMO
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.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=316545Documentos Relacionados
- Werner syndrome protein interacts with human flap endonuclease 1 and stimulates its cleavage activity
- Ku heterodimer binds to both ends of the Werner protein and functional interaction occurs at the Werner N-terminus
- The Ku Protein Complex Interacts with YY1, Is Up-Regulated in Human Heart Failure, and Represses α Myosin Heavy-Chain Gene Expression
- The membrane form of the DNA repair protein Ku interacts at the cell surface with metalloproteinase 9
- A class of activation domains interacts directly with TFIIA and stimulates TFIIA-TFIID-promoter complex assembly.