An unorthodox partnership in DNA repair pathway choice

Research output: Contribution to journal › Editorial › Research › peer-review

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An unorthodox partnership in DNA repair pathway choice. / Typas, Dimitris; Mailand, Niels.

In: EMBO Reports, Vol. 20, No. 11, e49105, 2019.

Research output: Contribution to journal › Editorial › Research › peer-review

Harvard

Typas, D & Mailand, N 2019, 'An unorthodox partnership in DNA repair pathway choice', EMBO Reports, vol. 20, no. 11, e49105. https://doi.org/10.15252/embr.201949105

APA

Typas, D., & Mailand, N. (2019). An unorthodox partnership in DNA repair pathway choice. EMBO Reports, 20(11), [e49105]. https://doi.org/10.15252/embr.201949105

Vancouver

Typas D, Mailand N. An unorthodox partnership in DNA repair pathway choice. EMBO Reports. 2019;20(11). e49105. https://doi.org/10.15252/embr.201949105

Author

Typas, Dimitris ; Mailand, Niels. / An unorthodox partnership in DNA repair pathway choice. In: EMBO Reports. 2019 ; Vol. 20, No. 11.

Bibtex

@article{1a83ddf24b3d4849a2a2b873b5e8928f,
title = "An unorthodox partnership in DNA repair pathway choice",
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.",
author = "Dimitris Typas and Niels Mailand",
year = "2019",
doi = "10.15252/embr.201949105",
language = "English",
volume = "20",
journal = "E M B O Reports",
issn = "1469-221X",
publisher = "Wiley-Blackwell",
number = "11",

}

RIS

TY - JOUR

T1 - An unorthodox partnership in DNA repair pathway choice

AU - Typas, Dimitris

AU - Mailand, Niels

PY - 2019

Y1 - 2019

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

VL - 20

JO - E M B O Reports

JF - E M B O Reports

SN - 1469-221X

IS - 11

M1 - e49105

ER -

ID: 228087145