Evidence map›Paper›PMID 25124555›Full record

ArticleCell death and differentiation2014

KMTase Set7/9 is a critical regulator of E2F1 activity upon genotoxic stress.

L Lezina, V Aksenova, T Ivanova, N Purmessur, A V Antonov, D Tentler, O Fedorova, A V Garabadgiu, I Talianidis, G Melino and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell death and differentiation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. [Research Progress of Role and Mechanism of SETD7 in Tumor Occurrence 
and Progression].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2023
    Article
  5. Methyltransferase Set7/9 as a Multifaceted Regulator of ROS Response.International journal of biological sciences · 2023
    Review
  6. Article
  7. Review
  8. Review
  9. ZKSCAN5 ActivatesFrontiers in oncology · 2022
    Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  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

11 authors at 2 institutions in 1 country.

L Lezina1] Department of Biochemistry, University of Leicester, Leicester LE1 9HN, UK [2] Molecular Pharmacology Laboratory, Saint-Petersburg Institute of Technology, Saint-Petersburg 190013, Russia.
V AksenovaMolecular Pharmacology Laboratory, Saint-Petersburg Institute of Technology, Saint-Petersburg 190013, Russia.
T IvanovaDepartment of Biochemistry, University of Leicester, Leicester LE1 9HN, UK.
N PurmessurDepartment of Biochemistry, University of Leicester, Leicester LE1 9HN, UK.
A V AntonovMRC Toxicology Unit, Leicester LE1 9HN, UK.
D TentlerMolecular Pharmacology Laboratory, Saint-Petersburg Institute of Technology, Saint-Petersburg 190013, Russia.
O FedorovaMolecular Pharmacology Laboratory, Saint-Petersburg Institute of Technology, Saint-Petersburg 190013, Russia.
A V GarabadgiuMolecular Pharmacology Laboratory, Saint-Petersburg Institute of Technology, Saint-Petersburg 190013, Russia.
I TalianidisB.S.R.C. 'Alexander Fleming', Varkiza 16602, Greece.
G Melino1] Molecular Pharmacology Laboratory, Saint-Petersburg Institute of Technology, Saint-Petersburg 190013, Russia [2] MRC Toxicology Unit, Leicester LE1 9HN, UK [3] Faculty of Medicine, University of Rome 'Tor Vergata', Rome 00133, Italy.
N A Barlev1] Department of Biochemistry, University of Leicester, Leicester LE1 9HN, UK [2] Molecular Pharmacology Laboratory, Saint-Petersburg Institute of Technology, Saint-Petersburg 190013, Russia [3] Gene Expression Laboratory, Institute of Cytology, Saint-Petersburg 194064, Russia.
University of Leicester · GBMRC Toxicology Unit · GB

Funding

Medical Research Council MC_U132670600
6 · The paper itself

Abstract

During the recent years lysine methyltransferase Set7/9 ((Su(var)-3-9, Enhancer-of-Zeste, Trithorax) domain containing protein 7/9) has emerged as an important regulator of different transcription factors. In this study, we report a novel function for Set7/9 as a critical co-activator of E2 promoter-binding factor 1 (E2F1)-dependent transcription in response to DNA damage. By means of various biochemical, cell biology, and bioinformatics approaches, we uncovered that cell-cycle progression through the G1/S checkpoint of tumour cells upon DNA damage is defined by the threshold of expression of both E2F1 and Set7/9. The latter affects the activity of E2F1 by indirectly modulating histone modifications in the promoters of E2F1-dependent genes. Moreover, Set7/9 differentially affects E2F1 transcription targets: it promotes cell proliferation via expression of the CCNE1 gene and represses apoptosis by inhibiting the TP73 gene. Our biochemical screening of the panel of lung tumour cell lines suggests that these two factors are critically important for transcriptional upregulation of the CCNE1 gene product and hence successful progression through cell cycle. These findings identify Set7/9 as a potential biomarker in tumour cells with overexpressed E2F1 activity.

Indexed as

Cell Line, TumorCyclin-Dependent Kinase 2Cyclin EDNA DamageE2F1 Transcription FactorEpigenesis, GeneticG1 Phase Cell Cycle CheckpointsGene ExpressionGene Expression Regulation, NeoplasticHistone-Lysine N-MethyltransferaseHumansLung NeoplasmsPromoter Regions, GeneticProtein BindingTranscription, GeneticCDK2 protein, humanCyclin-Dependent Kinase 2Cyclin EE2F1 protein, humanE2F1 Transcription FactorHistone-Lysine N-MethyltransferaseSETD7 protein, human

Identifiers

PMID25124555
PMCPMC4227146
OpenAlexW2091596849

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.