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Article

Deletion of individual Ku subunits in mice causes an NHEJ-independent phenotype potentially by altering apurinic/apyrimidinic site repair.

PloS one - 1 Jan 2014

Choi Yong Jun, Li Han, Son Mi Young, Wang Xiao-Hong, Fornsaglio Jamie L, Sobol Robert W, Lee Moonsook, Vijg Jan, Imholz Sandra, Dollé Martijn E T, van Steeg Harry, Reiling Erwin, Hasty Paul

Abstract excerpt

Ku70 and Ku80 form a heterodimer called Ku that forms a holoenzyme with DNA dependent-protein kinase catalytic subunit (DNA-PKCS) to repair DNA double strand breaks (DSBs) through the nonhomologous end joining (NHEJ) pathway. As expected mutating these genes in mice caused a similar DSB repair-defective phenotype. However, ku70(-/-) cells and ku80(-/-) cells also appeared to have a defect in base excision repair...

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Share to Antigens, Nuclear
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 24466051
DOI: 10.1371/journal.pone.0086358
PMCID: PMC3900520

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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