This is a preview of subscription content, access via your institution
Relevant articles
Open Access articles citing this article.
-
Mechanisms of synthetic lethality between BRCA1/2 and 53BP1 deficiencies and DNA polymerase theta targeting
Nature Communications Open Access 29 November 2023
Access options
Access Nature and 54 other Nature Portfolio journals
Get Nature+, our best-value online-access subscription
$29.99 /Â 30Â days
cancel any time
Subscribe to this journal
Receive 12 print issues and online access
$189.00 per year
only $15.75 per issue
Rent or buy this article
Prices vary by article type
from$1.95
to$39.95
Prices may be subject to local taxes which are calculated during checkout
References
Original article
Gupta, R. et al. DNA repair network analysis reveals shieldin as a key regulator of NHEJ and PARP inhibitor sensitivity. Cell https://doi.org/10.1016/j.cell.2018.03.050 (2018)
Further reading
Chang, H.H.Y. et al. Non-homologous DNA end joining and alternative pathways to double-strand break repair. Nat. Rev. Mol. Cell Biol. 18, 495–506 (2017)
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Zlotorynski, E. Shieldin the ends for 53BP1. Nat Rev Mol Cell Biol 19, 346–347 (2018). https://doi.org/10.1038/s41580-018-0019-9
Published:
Issue Date:
DOI: https://doi.org/10.1038/s41580-018-0019-9
This article is cited by
-
Mechanisms of synthetic lethality between BRCA1/2 and 53BP1 deficiencies and DNA polymerase theta targeting
Nature Communications (2023)
-
DNA double-strand break repair pathway choice: the fork in the road
Genome Instability & Disease (2020)