Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Comment
. 2013 Aug;14(8):665-6.
doi: 10.1038/embor.2013.99. Epub 2013 Jul 12.

DNA repair pathway choice--a PTIP of the hat to 53BP1

Cristina Escribano-Diaz  1 , Daniel Durocher
Affiliations
Comment

DNA repair pathway choice--a PTIP of the hat to 53BP1

Cristina Escribano-Diaz et al. EMBO Rep. 2013 Aug.
No abstract available

PubMed Disclaimer

Conflict of interest statement

The authors declare that they have no conflict of interest.

Figures

Figure 1
Figure 1
53BP1 phospho-dependent interactions involved in DSB repair. PTIP and RIF1 interact with chromatin-bound and ATM-phosphorylated 53BP1 at DSB sites. PTIP binds directly to 53BP1 phosphorylated on Ser 14;25 (within the first eight Ser/Thr-Q sites). RIF1 binds to phosphorylated 53BP1 either directly or through an intermediate factor (X). The carboxy-terminal seven Ser/Thr-Q sites (9–15 Ser/Thr-Q sites) are involved in the interaction of RIF1–53BP1, although the amino-terminal eight Ser/Thr-Q sites might stabilize the binding. It is unknown whether PTIP and RIF1 can associate simultaneously with 53BP1 (left side of the figure), or if the binding is exclusive, due to either differential phosphorylation of the Ser/Thr-Q sites or steric hindrance (right side of the figure). 53BP1, PTIP and RIF1 block DNA end-resection and promote NHEJ repair. Although both PTIP and RIF1 contribute to dysfunctional telomere fusions, they also have distinct functions downstream from 53BP1. While RIF1 is essential for CSR and has a milder effect on toxic NHEJ events, PTIP is dispensable for CSR and has a more prominent role in toxic NHEJ events that lead to genome instability in BRCA1-deficient cells. ATM, ataxia telangiectasia-mutated; CSR, class switch recombination; DSB, double-stranded break; NHEJ, non-homologous end-joining.
See this image and copyright information in PMC

Comment on

References

    1. Callen E et al. (2013) Cell 153: 1266–1280 - PMC - PubMed
    1. Chapman JR et al. (2012) Mol Cell 47: 497–510 - PubMed
    1. Zimmermann M et al. (2013) Science 339: 700–704 - PMC - PubMed
    1. Escribano-Diaz C et al. (2013) Mol Cell 49: 872–883 - PubMed
    1. Di Virgilio M et al. (2013) Science 339: 711–715 - PMC - PubMed

MeSH terms