USP17- and SCF-regulated degradation of DEC1 controls the DNA damage response
Molecular and Cellular Biology, ISSN: 1098-5549, Vol: 34, Issue: 22, Page: 4177-4185
2014
- 28Citations
- 49Captures
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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.
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Metrics Details
- Citations28
- Citation Indexes28
- 28
- CrossRef22
- Captures49
- Readers49
- 49
Article Description
In response to genotoxic stress, DNA damage checkpoints maintain the integrity of the genome by delaying cell cycle progression to allow for DNA repair. Here we show that the degradation of the basic helix-loop-helix (bHLH) transcription factor DEC1, a critical regulator of cell fate and circadian rhythms, controls the DNA damage response. During unperturbed cell cycles, DEC1 is a highly unstable protein that is targeted for proteasome-dependent degradation by the SCF ubiquitin ligase in cooperation with CK1. Upon DNA damage, DEC1 is rapidly induced in an ATM/ATR-dependent manner. DEC1 induction results from protein stabilization via a mechanism that requires the USP17 ubiquitin protease. USP17 binds and deubiquitylates DEC1, markedly extending its half-life. Subsequently, during checkpoint recovery, DEC1 proteolysis is reestablished through βTrCP-dependent ubiquitylation. Expression of a degradation-resistant DEC1 mutant prevents checkpoint recovery by inhibiting the downregulation of p53. These results indicate that the regulated degradation of DEC1 is a key factor controlling the DNA damage response.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84908868445&origin=inward; http://dx.doi.org/10.1128/mcb.00530-14; http://www.ncbi.nlm.nih.gov/pubmed/25202122; https://www.tandfonline.com/doi/full/10.1128/MCB.00530-14; http://mcb.asm.org/cgi/doi/10.1128/MCB.00530-14; https://syndication.highwire.org/content/doi/10.1128/MCB.00530-14; https://dx.doi.org/10.1128/mcb.00530-14; http://europepmc.org/abstract/med/25202122; http://europepmc.org/articles/PMC4248718; https://mcb.asm.org/content/34/22/4177; https://mcb.asm.org/content/34/22/4177.abstract; https://mcb.asm.org/content/mcb/34/22/4177.full.pdf; http://mcb.asm.org/content/34/22/4177; https://mcb.asm.org/content/34/22/4177.full.pdf; https://journals.asm.org/doi/10.1128/MCB.00530-14; https://journals.asm.org/doi/abs/10.1128/MCB.00530-14
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