Evidence map›Paper›PMID 30196736›Full record

ArticleCell cycle (Georgetown, Tex.)2018

DNA damage-induced dynamic changes in abundance and cytosol-nuclear translocation of proteins involved in translational processes, metabolism, and autophagy.

Martin V Bennetzen, Martin Kosar, Jakob Bunkenborg, Mark Ronald Payne, Jirina Bartkova, Mikael S Lindström, Jiri Lukas, Jens S Andersen, Jiri Bartek, Dorthe Helena Larsen

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 42% 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

4 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Nuclear Organization in Response to Stress: A Special Focus on Nucleoli.Results and problems in cell differentiation · 2022
    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 2 countries.

Martin V Bennetzena Center for Experimental BioInformatics, Department of Biochemistry and Molecular Biology , University of Southern Denmark , Odense M , Denmark.
Martin Kosarb Genome Integrity Unit, Danish Cancer Society Research Center , Danish Cancer Society , Copenhagen , Denmark.
Jakob Bunkenborga Center for Experimental BioInformatics, Department of Biochemistry and Molecular Biology , University of Southern Denmark , Odense M , Denmark.ORCID 0000-0002-2908-9323
Mark Ronald Paynec National Institute of Aquatic Resources , Technical University of Denmark , Lyngby , Denmark.ORCID 0000-0001-5795-2481
Jirina Bartkovab Genome Integrity Unit, Danish Cancer Society Research Center , Danish Cancer Society , Copenhagen , Denmark.
Mikael S Lindströmd Department of Medical Biochemistry and Biophysics, Science for Life Laboratory, Division of Genome Biology , Karolinska Institutet , Solna , Sweden.
Jiri Lukase Protein Signaling Program, The Novo Nordisk Foundation Center for Protein Research , Faculty of Health and Medical Sciences, University of Copenhagen , Copenhagen , Denmark.
Jens S Andersena Center for Experimental BioInformatics, Department of Biochemistry and Molecular Biology , University of Southern Denmark , Odense M , Denmark.
Jiri Bartekb Genome Integrity Unit, Danish Cancer Society Research Center , Danish Cancer Society , Copenhagen , Denmark.
Dorthe Helena Larsenb Genome Integrity Unit, Danish Cancer Society Research Center , Danish Cancer Society , Copenhagen , Denmark.ORCID 0000-0002-8280-1252
Science for Life Laboratory · SEUniversity of Southern Denmark · DKDanish Cancer Society · DKTechnical University of Denmark · DKUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ionizing radiation (IR) causes DNA double-strand breaks (DSBs) and activates a versatile cellular response regulating DNA repair, cell-cycle progression, transcription, DNA replication and other processes. In recent years proteomics has emerged as a powerful tool deepening our understanding of this multifaceted response. In this study we use SILAC-based proteomics to specifically investigate dynamic changes in cytoplasmic protein abundance after ionizing radiation; we present in-depth bioinformatics analysis and show that levels of proteins involved in autophagy (cathepsins and other lysosomal proteins), proteasomal degradation (Ubiquitin-related proteins), energy metabolism (mitochondrial proteins) and particularly translation (ribosomal proteins and translation factors) are regulated after cellular exposure to ionizing radiation. Downregulation of no less than 68 ribosomal proteins shows rapid changes in the translation pattern after IR. Additionally, we provide evidence of compartmental cytosol-nuclear translocation of numerous DNA damage related proteins using protein correlation profiling. In conclusion, these results highlight unexpected cytoplasmic processes actively orchestrated after genotoxic insults and protein translocation from the cytoplasm to the nucleus as a fundamental regulatory mechanism employed to aid cell survival and preservation of genome integrity.

Indexed as

AutophagyCell NucleusCell SurvivalCytosolDNA DamageDNA RepairHumansProteinsProtein TransportRadiation, Ionizinglysosomal proteinsProteinscytoplasmDNA damage response (DDR)ionizing radiation (IR)protein regulationprotein synthesisquantitative proteomics

Identifiers

PMID30196736
PMCPMC6226234
OpenAlexW2890128237

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.