Ku regulates the non-homologous end joining pathway choice of DNA double-strand break repair in human somatic cells.

Fattah, Farjana; Lee, Eu Han; Weisensel, Natalie; Wang, Yongbao; Lichter, Natalie; Hendrickson, Eric A

Fattah, Farjana; Lee, Eu Han; Weisensel, Natalie; Wang, Yongbao; Lichter, Natalie; Hendrickson, Eric A.

Affiliation

Fattah F; Department of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota Medical School, Minneapolis, Minnesota, United States of America.

PLoS Genet ; 6(2): e1000855, 2010 Feb 26.

Article in En | MEDLINE | ID: mdl-20195511

Subject(s)

DNA Breaks, Double-Stranded; DNA Helicases/metabolism; DNA Repair; Recombination, Genetic; Animals; Cricetinae; DNA/genetics; DNA Ligase ATP; DNA Ligases/deficiency; DNA Repair Enzymes/deficiency; DNA Repair Enzymes/metabolism; DNA-Activated Protein Kinase/deficiency; DNA-Activated Protein Kinase/metabolism; DNA-Binding Proteins/deficiency; DNA-Binding Proteins/metabolism; HCT116 Cells; Haploidy; Humans; Ku Autoantigen; Mutation/genetics; Nuclear Proteins/deficiency; Nuclear Proteins/metabolism; Plasmids/genetics; Reproducibility of Results

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Full text: 1 Database: MEDLINE Main subject: Recombination, Genetic / DNA Helicases / DNA Repair / DNA Breaks, Double-Stranded Limits: Animals / Humans Language: En Journal: PLoS Genet Journal subject: GENETICA Year: 2010 Type: Article Affiliation country: United States

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