Evidence map›Paper›PMID 25202122›Full record

ArticleMolecular and cellular biology2014

USP17- and SCFβTrCP--regulated degradation of DEC1 controls the DNA damage response.

Jihoon Kim, Sara D'Annibale, Roberto Magliozzi, Teck Yew Low, Petra Jansen, Indra A Shaltiel, Shabaz Mohammed, Albert J R Heck, Rene H Medema, Daniele Guardavaccaro

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.7field-weighted citation impact, top 29% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
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  4. SCFCell death & disease · 2023
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  6. Approach to Functions ofInternational journal of molecular sciences · 2023
    Review
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  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. The role of circadian clock genes in tumors.OncoTargets and therapy · 2019
    Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 5 institutions in 1 country.

Jihoon KimHubrecht Institute-KNAW and University Medical Center Utrecht, Utrecht, The Netherlands.
Sara D'AnnibaleHubrecht Institute-KNAW and University Medical Center Utrecht, Utrecht, The Netherlands.
Roberto MagliozziHubrecht Institute-KNAW and University Medical Center Utrecht, Utrecht, The Netherlands.
Teck Yew LowBiomolecular Mass Spectrometry and Proteomics, Bijvoet Center for Biomolecular Research and Utrecht Institute for Pharmaceutical Sciences, Utrecht University, Utrecht, The Netherlands The Netherlands Proteomics Center, Utrecht, The Netherlands.
Petra JansenHubrecht Institute-KNAW and University Medical Center Utrecht, Utrecht, The Netherlands.
Indra A ShaltielDepartment of Cell Biology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Shabaz MohammedBiomolecular Mass Spectrometry and Proteomics, Bijvoet Center for Biomolecular Research and Utrecht Institute for Pharmaceutical Sciences, Utrecht University, Utrecht, The Netherlands The Netherlands Proteomics Center, Utrecht, The Netherlands.
Albert J R HeckBiomolecular Mass Spectrometry and Proteomics, Bijvoet Center for Biomolecular Research and Utrecht Institute for Pharmaceutical Sciences, Utrecht University, Utrecht, The Netherlands The Netherlands Proteomics Center, Utrecht, The Netherlands.
Rene H MedemaDepartment of Cell Biology, The Netherlands Cancer Institute, Amsterdam, The Netherlands.
Daniele GuardavaccaroHubrecht Institute-KNAW and University Medical Center Utrecht, Utrecht, The Netherlands d.guardavaccaro@hubrecht.eu.
University Medical Center Utrecht · NLNetherlands Metabolomics Centre · NLThe Netherlands Cancer Institute · NLHubrecht Institute for Developmental Biology and Stem Cell Research · NLUtrecht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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(βTrCP) 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.

Indexed as

DNA DamageProteolysisAtaxia Telangiectasia Mutated Proteinsbeta-Transducin Repeat-Containing ProteinsCell CycleCell LineDown-RegulationEndopeptidasesHumansMutationProteasome Endopeptidase ComplexTumor Suppressor Protein p53Tumor Suppressor ProteinsUbiquitinationAtaxia Telangiectasia Mutated ProteinsATR protein, humanbeta-Transducin Repeat-Containing ProteinsDELEC1 protein, humanEndopeptidasesProteasome Endopeptidase ComplexTumor Suppressor Protein p53Tumor Suppressor ProteinsUSP17L2 protein, human

Identifiers

PMID25202122
PMCPMC4248718
OpenAlexW2147709272

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.