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Updated: Jan 24, 2026

Non-Viral Engineering of Primary Human T Cells via Homology-Mediated End-Joining Targeted Integration of Large DNA Templates
Published on: May 9, 2025
UBQLN4 promotes non-homologous end joining by repressing DNA end-resection
Ron D Jachimowicz1, H Christian Reinhardt1,2,3,4
1Clinic I of Internal Medicine, Faculty of Medicine and University Hospital Cologne, Cologne, Germany.
Abstract:
Ataxia-telangiectasia-mutated (ATM) promotes homologous recombination (HR)-mediated DNA double-strand break repair. It was recently shown that the proteasomal shuttle factor UBQLN4 facilitates MRE11 degradation to repress HR. Surprisingly, the UBQLN4-MRE11 interaction is ATM-dependent, suggesting that the proximal DNA damage kinase ATM does not only initiate HR, but also limits excessive end resection.
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