The demise of a TUDOR under stress opens a chromatin link to 53BP1
EMBO Journal, ISSN: 0261-4189, Vol: 31, Issue: 8, Page: 1847-1849
2012
- 2Citations
- 27Captures
Metric Options: CountsSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations2
- Citation Indexes2
- CrossRef2
- Captures27
- Readers27
- 27
Article Description
The mechanisms that localise 53BP1 to sites of DNA double-strand breaks (DSBs) have remained elusive, despite this protein's key roles in DNA damage response signalling and repair processes. Recent studies, including the work by Mallette et al (2012) in this issue of The EMBO Journal, now provide crucial insights into the roles of ubiquitin-dependent signalling cascades at DNA damage sites required for chromatin-mediated 53BP1 recruitment. © 2012 European Molecular Biology Organization | All Rights Reserved.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84859923056&origin=inward; http://dx.doi.org/10.1038/emboj.2012.78; http://www.ncbi.nlm.nih.gov/pubmed/22453339; http://emboj.embopress.org/cgi/doi/10.1038/emboj.2012.78; https://dx.doi.org/10.1038/emboj.2012.78; https://www.embopress.org/doi/full/10.1038/emboj.2012.78
Springer Science and Business Media LLC
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