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Article

Alternative end joining during switch recombination in patients with ataxia-telangiectasia.

European journal of immunology - 1 May 2002

Pan Qiang, Petit-Frére Corinne, Lähdesmäki Aleksi, Gregorek Hanna, Chrzanowska Krystyna H, Hammarström Lennart

Abstract excerpt

Ataxia-Telangiectasia (A-T) and Nijmegen breakage syndrome (NBS) are recessive genetic diseases with similar cellular phenotypes that are caused by mutations in the recently described ATM (encoding ATM) and NBS1 (encoding p95) genes, respectively. Both disorders are accompanied by immunodeficienc...

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Source

Identifiers

PMID: 11981817
DOI: 10.1002/1521-4141(200205)32:5<1300::AID-IMMU1300>3.0.CO;2-L

Genes

ATM

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026. Prepared record publication-11981817-2026-09-01.1. Manifest publication-graph-cohort-2026-09-01.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 1 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Alternative end joining during switch recombination in patients with ataxia-telangiectasia.PMID 11981817Read ↗

Alternative end-joining catalyzes robust IgH locus deletions and translocations in the combined absence of ligase 4 and Ku70Semantic proximity Read ↗

Disparate roles of ATR and ATM in immunoglobulin class switch recombination and somatic hypermutation.Semantic proximity Read ↗

Delineation of the role of the Mre11 complex in class switch recombination.Semantic proximity Read ↗

ATM Is Required for Efficient Recombination between Immunoglobulin Switch RegionsSemantic proximity Read ↗

Involvement of Artemis in nonhomologous end-joining during immunoglobulin class switch recombination.Semantic proximity Read ↗

Causative mechanisms and clinical impact of immunoglobulin deficiencies in ataxia telangiectasiaSemantic proximity Read ↗

Impact of DNA ligase IV on nonhomologous end joining pathways during class switch recombination in human cells.Semantic proximity Read ↗

Splitting the ATM: distinct repair and checkpoint defects in ataxia-telangiectasia.Semantic proximity Read ↗

ATM Is Not Required in Somatic Hypermutation of VH, but Is Involved in the Introduction of Mutations in the Switch μ RegionSemantic proximity Read ↗

ATM Expression and Activation in Ataxia Telangiectasia Patients with and without Class Switch Recombination Defects.Semantic proximity Read ↗

Rag mutations reveal robust alternative end joining.Semantic proximity Read ↗

Genetic Risk Variants for Class Switching Recombination Defects in Ataxia-Telangiectasia Patients.Semantic proximity Read ↗

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