Evidence map›Paper›PMID 29294106›Full record

ArticleNucleic acids research2018

Sp1 phosphorylation by ATM downregulates BER and promotes cell elimination in response to persistent DNA damage.

Sally C Fletcher, Claudia P Grou, Arnaud J Legrand, Xin Chen, Kalle Soderstrom, Mattia Poletto, Grigory L Dianov

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. IncRNA-ZFAS1, an Emerging Gate-Keeper in DNA Damage-Dependent Transcriptional Regulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  3. Role of post-translational modifications of Sp1 in cancer: state of the art.Frontiers in cell and developmental biology · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Activated STAT3 Is a Novel Regulator of theInternational journal of molecular sciences · 2021
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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

7 authors at 3 institutions in 3 countries.

Sally C FletcherDepartment of Oncology, CRUK & MRC Oxford Institute for Radiation Oncology, University of Oxford, Old Road Campus Research Building, Oxford OX3 7DQ, UK.
Claudia P GrouDepartment of Oncology, CRUK & MRC Oxford Institute for Radiation Oncology, University of Oxford, Old Road Campus Research Building, Oxford OX3 7DQ, UK.
Arnaud J LegrandDepartment of Oncology, CRUK & MRC Oxford Institute for Radiation Oncology, University of Oxford, Old Road Campus Research Building, Oxford OX3 7DQ, UK.
Xin ChenDepartment of Oncology, CRUK & MRC Oxford Institute for Radiation Oncology, University of Oxford, Old Road Campus Research Building, Oxford OX3 7DQ, UK.
Kalle SoderstromNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Oxford OX3 7LD, UK.
Mattia PolettoDepartment of Oncology, CRUK & MRC Oxford Institute for Radiation Oncology, University of Oxford, Old Road Campus Research Building, Oxford OX3 7DQ, UK.
Grigory L DianovDepartment of Oncology, CRUK & MRC Oxford Institute for Radiation Oncology, University of Oxford, Old Road Campus Research Building, Oxford OX3 7DQ, UK.
University of Oxford · GBCRUK/MRC Oxford Institute for Radiation Oncology · GBInstitute of Cytology and Genetics · RU

Funding

Medical Research Council MC_PC_12002
6 · The paper itself

Abstract

ATM (ataxia-telangiectasia mutated) is a central molecule for DNA quality control. Its activation by DNA damage promotes cell-cycle delay, which facilitates DNA repair prior to replication. On the other hand, persistent DNA damage has been implicated in ATM-dependent cell death via apoptosis; however, the mechanisms underlying this process remain elusive. Here we find that, in response to persistent DNA strand breaks, ATM phosphorylates transcription factor Sp1 and initiates its degradation. We show that Sp1 controls expression of the key base excision repair gene XRCC1, essential for DNA strand break repair. Therefore, degradation of Sp1 leads to a vicious cycle that involves suppression of DNA repair and further aggravation of the load of DNA damage. This activates transcription of pro-apoptotic genes and renders cells susceptible to elimination via both apoptosis and natural killer cells. These findings constitute a previously unrecognized 'gatekeeper' function of ATM as a detector of cells with persistent DNA damage.

Indexed as

DNA RepairApoptosisAtaxia Telangiectasia Mutated ProteinsCells, CulturedDNA DamageDown-RegulationHumansKiller Cells, NaturalMalePhosphorylationSerineSp1 Transcription FactorX-ray Repair Cross Complementing Protein 1Ataxia Telangiectasia Mutated ProteinsATM protein, humanSerineSP1 protein, humanSp1 Transcription FactorX-ray Repair Cross Complementing Protein 1XRCC1 protein, human

Identifiers

PMID29294106
PMCPMC5829641
OpenAlexW2781323229

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.