Evidence map›Paper›PMID 25806049›Full record

ReviewFrontiers in genetics2015

Regulation of the DNA damage response by ubiquitin conjugation.

Kerstin Brinkmann, Michael Schell, Thorsten Hoppe, Hamid Kashkar

Abstract readReview
In one paragraph

Review in Frontiers in genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
–field-weighted citation impact
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

42 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Targeting the ribosome to treat multiple myeloma.Molecular therapy. Oncology · 2024
    Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Protein homeostasis in the aged and diseased heart.The journal of cardiovascular aging · 2023
    Article
  14. Review
  15. CDK4/6 inhibitors downregulate the ubiquitin-conjugating enzymes UBE2C/S/T involved in the ubiquitin-proteasome pathway in ER + breast cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022
    Article
  16. Article
  17. Article
  18. The Deubiquitinating EnzymeFrontiers in fungal biology · 2022
    Article
  19. The Ubiquitin System: An Emerging Therapeutic Target for Lung Cancer.International journal of molecular sciences · 2021
    Review
  20. Review
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

4 authors.

Kerstin BrinkmannCentre for Molecular Medicine Cologne and Institute for Medical Microbiology, Immunology and Hygiene, University Hospital of Cologne Cologne, Germany ; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University Hospital of Cologne Cologne, Germany.
Michael SchellCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University Hospital of Cologne Cologne, Germany ; Institute for Genetics, University of Cologne Cologne, Germany.
Thorsten HoppeCologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University Hospital of Cologne Cologne, Germany ; Institute for Genetics, University of Cologne Cologne, Germany.
Hamid KashkarCentre for Molecular Medicine Cologne and Institute for Medical Microbiology, Immunology and Hygiene, University Hospital of Cologne Cologne, Germany ; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University Hospital of Cologne Cologne, Germany.

Funding

European Research Council 616499
6 · The paper itself

Abstract

In response to DNA damage, cells activate a highly conserved and complex kinase-based signaling network, commonly referred to as the DNA damage response (DDR), to safeguard genomic integrity. The DDR consists of a set of tightly regulated events, including detection of DNA damage, accumulation of DNA repair factors at the site of damage, and finally physical repair of the lesion. Upon overwhelming damage the DDR provokes detrimental cellular actions by involving the apoptotic machinery and inducing a coordinated demise of the damaged cells (DNA damage-induced apoptosis, DDIA). These diverse actions involve transcriptional activation of several genes that govern the DDR. Moreover, recent observations highlighted the role of ubiquitylation in orchestrating the DDR, providing a dynamic cellular regulatory circuit helping to guarantee genomic stability and cellular homeostasis (Popovic et al., 2014). One of the hallmarks of human cancer is genomic instability (Hanahan and Weinberg, 2011). Not surprisingly, deregulation of the DDR can lead to human diseases, including cancer, and can induce resistance to genotoxic anti-cancer therapy (Lord and Ashworth, 2012). Here, we summarize the role of ubiquitin-signaling in the DDR with special emphasis on its role in cancer and highlight the therapeutic value of the ubiquitin-conjugation machinery as a target in anti-cancer treatment strategy.

Indexed as

apoptosisBcl-2DNA damagegenotoxic anti-cancer therapyp53ubiquitylation

Identifiers

PMID25806049
PMCPMC4354423

What OpenQuestion holds

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Registered trials

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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.