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Article

DNA-PK and ATM phosphorylation sites in XLF/Cernunnos are not required for repair of DNA double strand breaks

4 Aug 2008

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Identifiers

PMID: 18644470
DOI: 10.1016/j.dnarep.2008.06.015

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Related research

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DNA-PK and ATM phosphorylation sites in XLF/Cernunnos are not required for repair of DNA double strand breaksPMID 18644470Read ↗

Optimal function of the DNA repair enzyme TDP1 requires its phosphorylation by ATM and/or DNA‐PKSemantic proximity Read ↗

Repair of ionizing radiation-induced DNA double-strand breaks by non-homologous end-joiningSemantic proximity Read ↗

Defective DNA repair and increased genomic instability in Cernunnos-XLF-deficient murine ES cells.Semantic proximity Read ↗

XLF interacts with the XRCC4-DNA ligase IV complex to promote DNA nonhomologous end-joining.Semantic proximity Read ↗

Cernunnos Interacts with the XRCC4·DNA-ligase IV Complex and Is Homologous to the Yeast Nonhomologous End-joining Factor Nej1Semantic proximity Read ↗

Interplay between Cernunnos-XLF and Nonhomologous End-joining Proteins at DNA Ends in the CellSemantic proximity Read ↗

ATM‐mediated phosphorylation of polynucleotide kinase/phosphatase is required for effective DNA double‐strand break repairSemantic proximity Read ↗

Functional significance of the interaction with Ku in DNA double-strand break recognition of XLF.Semantic proximity Read ↗

Evolutionary and functional conservation of the DNA non-homologous end-joining protein, XLF/Cernunnos.Semantic proximity Read ↗

Lymphocyte-specific compensation for XLF/cernunnos end-joining functions in V(D)J recombination.Semantic proximity Read ↗

ATM-dependent phosphorylation and accumulation of endogenous BLM protein in response to ionizing radiationSemantic proximity Read ↗

Cernunnos, a novel nonhomologous end-joining factor, is mutated in human immunodeficiency with microcephaly.Semantic proximity Read ↗

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