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Article

Genetic separation of Brca1 functions reveal mutation-dependent Polθ vulnerabilities.

Nature communications - 24 Nov 2023

Krais John J, Glass David J, Chudoba Ilse, Wang Yifan, Feng Wanjuan, Simpson Dennis, Patel Pooja, Liu Zemin, Neumann-Domer Ryan, Betsch Robert G, Bernhardy Andrea J, Bradbury Alice M, Conger Jason, Yueh Wei-Ting, Nacson Joseph, Pomerantz Richard T, Gupta Gaorav P, Testa Joseph R, Johnson Neil

Abstract excerpt

Homologous recombination (HR)-deficiency induces a dependency on DNA polymerase theta (Polθ/Polq)-mediated end joining, and Polθ inhibitors (Polθi) are in development for cancer therapy. BRCA1 and BRCA2 deficient cells are thought to be synthetic lethal with Polθ, but whether distinct HR gene mutations give rise to equivalent Polθ-dependence, and the events that drive lethality, are unclear. In this study, we...

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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: 38001070
DOI: 10.1038/s41467-023-43446-1
PMCID: PMC10673838

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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