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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Nonhomologous end-joining factor 1

XLF, Cernunnos, XRCC4-like factor, nonhomologous end-joining factor
Double-strand breaks in DNA result from genotoxic stresses and are among the most damaging of DNA lesions. This gene encodes a DNA repair factor essential for the nonhomologous end-joining pathway, which preferentially mediates repair of double-stranded breaks. Mutations in this gene cause different kinds of severe combined immunodeficiency disorders. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: XRCC4, Artemis, DNA-PKcs, CAN, IRBP
Papers on XLF
Invasive oral cancer stem cells display resistance to ionising radiation.
Mackenzie et al., London, United Kingdom. In Oncotarget, Jan 2016
We propose that this is a result of preferential activation of the DNA damagerepair pathway in oral CSC with increased activation of ATM and BRCA1, elevated levels of DNA repair proteins RAD52, XLF, and a significantly faster rate of DNA double-strand-breaks clearance 24 hours following IR.
Synthesis of Biotinylated Inositol Hexakisphosphate To Study DNA Double-Strand Break Repair and Affinity Capture of IP6-Binding Proteins.
Hanakahi et al., Chicago, United States. In Biochemistry, Nov 2015
We found that IP6-biotin could affinity capture Ku and other required NHEJ factors from human cell extracts, including the DNA-dependent protein kinase catalytic subunit (DNA-PKcs), XRCC4, and XLF.
XRCC4 deficiency in human subjects causes a marked neurological phenotype but no overt immunodeficiency.
Ogi et al., Nagoya, Japan. In J Allergy Clin Immunol, Oct 2015
The final rejoining step requires DNA ligase IV (LIG4) together with the partner proteins X-ray repair cross-complementing protein 4 (XRCC4) and XRCC4-like factor.
XRCC4/XLF Interaction Is Variably Required for DNA Repair and Is Not Required for Ligase IV Stimulation.
Meek et al., East Lansing, United States. In Mol Cell Biol, Oct 2015
XLF stimulates the XRCC4/DNA ligase IV complex by an unknown mechanism.
DNA repair. PAXX, a paralog of XRCC4 and XLF, interacts with Ku to promote DNA double-strand break repair.
Jackson et al., Cambridge, United Kingdom. In Science, Feb 2015
XRCC4 and XLF are two structurally related proteins that function in DNA double-strand break (DSB) repair.
Akt promotes tumorigenesis in part through modulating genomic instability via phosphorylating XLF.
Wei et al., Boston, United States. In Nucleus, 2014
To this end, we recently reported that Akt impairs NHEJ by phosphorylating XLF at T181, to trigger its dissociation from the functional DNA ligase IV (LIG4)/XRCC4 complex.
Structural insights into NHEJ: building up an integrated picture of the dynamic DSB repair super complex, one component and interaction at a time.
Tainer et al., Berkeley, United States. In Dna Repair (amst), 2014
X-ray crystal structures, cryo-electron microscopy envelopes, and small angle X-ray scattering (SAXS) solution conformations and assemblies are defining most of the core protein components for NHEJ: Ku70/Ku80 heterodimer; the DNA dependent protein kinase catalytic subunit (DNA-PKcs); the structure-specific endonuclease Artemis along with polynucleotide kinase/phosphatase (PNKP), aprataxin and PNKP related protein (APLF); the scaffolding proteins XRCC4 and XLF (XRCC4-like factor); DNA polymerases, and DNA ligase IV (Lig IV).
The clinical impact of deficiency in DNA non-homologous end-joining.
Jeggo et al., Newcastle upon Tyne, United Kingdom. In Dna Repair (amst), 2014
Mutations in NHEJ genes, defining human syndromes deficient in DNA ligase IV (LIG4 Syndrome), XLF-Cernunnos, Artemis or DNA-PKcs, have been identified in such patients.
Functional overlaps between XLF and the ATM-dependent DNA double strand break response.
Oksenych et al., Boston, United States. In Dna Repair (amst), 2014
Recent studies have shown that the XLF C-NHEJ factor has functional redundancy with several members of the ATM-dependent DSBR pathway in C-NHEJ, highlighting unappreciated major roles for both XLF as well as the DSBR in V(D)J recombination, CSR and C-NHEJ in general.
XRCC4 and XLF form long helical protein filaments suitable for DNA end protection and alignment to facilitate DNA double strand break repair.
Lees-Miller et al., Calgary, Canada. In Biochem Cell Biol, 2013
XRCC4 also interacts with XRCC4-like factor (XLF, also called Cernunnos); yet, XLF has been one of the least mechanistically understood proteins and precisely how XLF functions in NHEJ has been enigmatic.
Overlapping functions between XLF repair protein and 53BP1 DNA damage response factor in end joining and lymphocyte development.
Zha et al., New York City, United States. In Proc Natl Acad Sci U S A, 2012
XLF repair protein and 53BP1 DNA damage response factor have overlapping functions in end joining and lymphocyte development
Functional redundancy between repair factor XLF and damage response mediator 53BP1 in V(D)J recombination and DNA repair.
Guo et al., Boston, United States. In Proc Natl Acad Sci U S A, 2012
find that combined XLF/53BP1 deficiency in mice severely impairs C-NHEJ, V(D)J recombination, and lymphocyte development while also leading to general genomic instability and growth defects
Cernunnos influences human immunoglobulin class switch recombination and may be associated with B cell lymphomagenesis.
Pan-Hammarström et al., Huddinge, Sweden. In J Exp Med, 2012
A suggested link between defects in the Cernunnos-dependent nonhomologous end-joining pathway and aberrant class switch recombination or switch translocations during the development of B cell malignancies.
A human XRCC4-XLF complex bridges DNA.
Junop et al., Hamilton, Canada. In Nucleic Acids Res, 2012
Evidence for how XRCC4-XLF complexes robustly bridge DNA molecules.
Crystallization and preliminary X-ray diffraction analysis of the human XRCC4-XLF complex.
Junop et al., Hamilton, Canada. In Acta Crystallogr Sect F Struct Biol Cryst Commun, 2011
Multiple truncations of the XLF and XRCC4 proteins were cocrystallized, but yielded low-resolution diffraction (~20 A)
More forks on the road to replication stress recovery.
Nickoloff et al., Fort Collins, United States. In J Mol Cell Biol, 2011
In recent years, several proteins involved in DSB repair by non-homologous end joining (NHEJ) have been implicated in the replication stress response, including DNA-PKcs, Ku, DNA Ligase IV-XRCC4, Artemis, XLF and Metnase.
ATM damage response and XLF repair factor are functionally redundant in joining DNA breaks.
Alt et al., Boston, United States. In Nature, 2011
XLF, ATM and H2AX all have fundamental roles in processing and joining DNA ends during V(D)J recombination, but that these roles have been masked by unanticipated functional redundancies
XLF interacts with the XRCC4-DNA ligase IV complex to promote DNA nonhomologous end-joining.
Jackson et al., Cambridge, United Kingdom. In Cell, 2006
The XLF-encoded protein (XRRC4 like factor, FLJ12610) is involved in DNA double-strand break repair via nonhomologous end-joining and associates with the Ligase IV-XRCC4 complex. XLF is mutated in a number of radiosensitive and immuno-deficient patients.
DNA double-strand break repair: a relentless hunt uncovers new prey.
Ferguson et al., Ann Arbor, United States. In Cell, 2006
In this issue of Cell, and report the discovery of a new NHEJ factor called Cernunnos-XLF.
Cernunnos, a novel nonhomologous end-joining factor, is mutated in human immunodeficiency with microcephaly.
Revy et al., Paris, France. In Cell, 2006
Cernunnos-XLF is a new Non-homologous End Joining pathway protein, which if mutated results in several conditions -immunodeficiency and developmental anomalies and other conditions, which likely result from inability to repair spontaneous DNA damage.
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