An unorthodox partnership in DNA repair pathway choice

Dimitris Typas, Niels Mailand

Research output: Contribution to journalEditorialResearchpeer-review

2 Citations (Scopus)

Abstract

Complex regulatory circuits determine whether DNA double-strand breaks (DSBs) are repaired by nonhomologous end-joining (NHEJ) or homology-directed repair (HDR) pathways, a carefully balanced equilibrium of which is critical for genome stability. In this issue of EMBO Reports, Deng et al [1] report that a novel p53-suppressed long noncoding RNA (lncRNA), PRLH1, interacts with and stabilizes the E3 ubiquitin ligase RNF169 to stimulate HDR-mediated DSB repair and proliferation of p53-deficient cancer cells. These findings suggest a new regulatory principle in modulating DSB repair pathway selection that may contribute to tumorigenesis.

Original languageEnglish
Article numbere49105
JournalEMBO Reports
Volume20
Issue number11
ISSN1469-221X
DOIs
Publication statusPublished - 2019

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