Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

XLF deficiency results in reduced N-nucleotide addition during V(D)J recombination

9 Jun 2016

Abstract excerpt

Repair of DNA double-strand breaks (DSBs) by the nonhomologous end-joining pathway (NHEJ) is important not only for repair of spontaneous breaks but also for breaks induced in developing lymphocytes during V(D)J (variable [V], diversity [D], and joining [J] genes) recombination of their antigen receptor loci to create a diverse repertoire. Mutations in the NHEJ factor XLF result in extreme sensitivity for...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to DNA Repair Mechanisms
Share to Immune Cell Function and Interaction
Share to PARP inhibition in cancer therapy

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Source

Identifiers

PMID: 27281794
DOI: 10.1182/blood-2016-02-701029

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 24 Oct 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

XLF deficiency results in reduced N-nucleotide addition during V(D)J recombinationPMID 27281794Read ↗

Novel XLF/Cernunnos mutation linked to severe combined immunodeficiency, microcephaly and abnormal T and B cell receptor repertoiresSemantic proximity Read ↗

Functional redundancy between repair factor XLF and damage response mediator 53BP1 in V(D)J recombination and DNA repairSemantic proximity Read ↗

XRCC4 deficiency in human subjects causes a marked neurological phenotype but no overt immunodeficiency.Semantic proximity Read ↗

Deficiency of XLF and PAXX prevents DNA double-strand break repair by non-homologous end joining in lymphocytesSemantic proximity Read ↗

Update on DNA-Double Strand Break Repair Defects in Combined Primary ImmunodeficiencySemantic proximity Read ↗

Primary immunodeficiency syndromes associated with defective DNA double-strand break repairSemantic proximity Read ↗

Clinical spectrum of LIG4 deficiency is broadened with severe dysmaturity, primordial dwarfism, and neurological abnormalities.Semantic proximity Read ↗

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

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

The spatial organization of non-homologous end joining: From bridging to end joiningSemantic proximity Read ↗

Ligase IV syndrome.Semantic proximity Read ↗

Leaky severe combined immunodeficiency in mice lacking non-homologous end joining factors XLF and MRI.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.