An unorthodox partnership in DNA repair pathway choice

TY - JOUR

T1 - An unorthodox partnership in DNA repair pathway choice

AU - Typas, Dimitris

AU - Mailand, Niels

PY - 2019/11/5

Y1 - 2019/11/5

N2 - 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.

AB - 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.

U2 - 10.15252/embr.201949105

DO - 10.15252/embr.201949105

M3 - Editorial

C2 - 31544332

SN - 1469-221X

VL - 20

JO - E M B O Reports

JF - E M B O Reports

IS - 11

M1 - e49105

ER -