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Article

Suppression of non-homologous end joining does not rescue DNA repair defects in Fanconi anemia patient cells.

Cell cycle (Georgetown, Tex.) - 1 Oct 2020

Thongthip Supawat, Conti Brooke A, Lach Francis P, Smogorzewska Agata

Abstract excerpt

Severe cellular sensitivity and aberrant chromosomal rearrangements in response to DNA interstrand crosslink (ICL) inducing agents are hallmarks of Fanconi anemia (FA) deficient cells. These phenotypes have previously been ascribed to inappropriate activity of non-homologous end joining (NHEJ) rather than a direct consequence of DNA ICL repair defects. Here we used chemical inhibitors, RNAi, and Clustered...

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Identifiers

PMID: 32865112
DOI: 10.1080/15384101.2020.1810394
PMCID: PMC7553586

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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