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

By Dietke Buck, Laurent Malivert, R. de Chasseval, Anne Barraud, M. Fondanèche, O. Sanal, A. Plebani, J. Stéphan, M. Hufnagel, F. Le Deist and 4 more. Cell, 2006

747 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/74e94527d5007d8dce88878654f5bf96fe7ea07a

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. L. Marácz
2. M. Lieber
3. F. Grin
4. N. Pokorn

In Molecular Biology

1. L. Marácz
2. G. Iliakis
3. Wenqi Wu
4. M. Lieber
5. F. Grin
6. N. Pokorn

In Oncology

1. L. Marácz
2. M. Lieber
3. F. Grin
4. N. Pokorn

Citations in the corpus

• 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).”
• Chapter 1. General introduction (2015, positive): “Cernunnos), which stimulates the activity of Lig4 and is required for NHEJ and V(D)J recombination (50;51).”
• 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).”