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

By Peter Ahnesorg, Philippa Smith, Stephen P. Jackson. Cell, 2006

816 citations recorded by the source corpus.

Subfields: Molecular Biology, Public Health, Environmental and Occupational Health

View Paper: https://www.semanticscholar.org/paper/3514e3bb4ded0b7ec77143852432c45aa56ed0c4

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In Molecular Biology

1. G. Iliakis
2. Wenqi Wu
3. M. Lieber

In Public Health, Environmental and Occupational Health

1. M. Lieber

Citations in the corpus

• Chapter 1. General introduction (2015, neutral): “Cernunnos), which stimulates the activity of Lig4 and is required for NHEJ and V(D)J recombination (50;51).”
• The Mechanism of Double-Strand DNA Break Repair by the Nonhomologous DNA End Joining Pathway (2010, background): “When XLF is missing in humans, patients are IR sensitive and lack V(D)J recombination (120, 121).”
• PARP-1 and Ku compete for repair of DNA double strand breaks by distinct NHEJ pathways (2006, background): “Higher eukaryotes utilize a pathway of nonhomologous end joining (NHEJ) to repair the majority of DSBs that employs the products of DNA-PKcs, KU70, KU80, LIG4, XRCC4 and Artemis (1,2), as well as the recently characterized factor XLF/Cernunos (3,4).”
• Cernunnos, a novel nonhomologous end-joining factor, is mutated in human immunodeficiency with microcephaly. (2006, background): “Moreover, the interaction of Cernunnos/XLF with the XRCC4:DNA-LigaseIV complex in vivo was further documented through coimmunoprecipitation experiments (Ahnesorg et al., 2006 and unpublished data).”