Evidence map›Paper›PMID 28854356›Full record

ArticleCell reports2017

Multilayered Reprogramming in Response to Persistent DNA Damage in C. elegans.

Diletta Edifizi, Hendrik Nolte, Vipin Babu, Laia Castells-Roca, Michael M Mueller, Susanne Brodesser, Marcus Krüger, Björn Schumacher

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

30 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
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  7. Genomic Instability and Epigenetic Changes during Aging.International journal of molecular sciences · 2023
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  15. Flavonoids-Natural Gifts to Promote Health and Longevity.International journal of molecular sciences · 2022
    Review
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  19. Article
  20. The Keap1-Nrf2 System: A Mediator between Oxidative Stress and Aging.Oxidative medicine and cellular longevity · 2021
    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

8 authors at 2 institutions in 1 country.

Diletta EdifiziInstitute for Genome Stability in Aging and Disease, Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, Cologne 50931, Germany; Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases and Systems Biology of Aging Cologne, University of Cologne, Joseph-Stelzmann-Str. 26, Cologne 50931, Germany.
Hendrik NolteCologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases and Systems Biology of Aging Cologne, University of Cologne, Joseph-Stelzmann-Str. 26, Cologne 50931, Germany.
Vipin BabuInstitute for Genome Stability in Aging and Disease, Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, Cologne 50931, Germany; Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases and Systems Biology of Aging Cologne, University of Cologne, Joseph-Stelzmann-Str. 26, Cologne 50931, Germany.
Laia Castells-RocaInstitute for Genome Stability in Aging and Disease, Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, Cologne 50931, Germany; Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases and Systems Biology of Aging Cologne, University of Cologne, Joseph-Stelzmann-Str. 26, Cologne 50931, Germany.
Michael M MuellerInstitute for Genome Stability in Aging and Disease, Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, Cologne 50931, Germany; Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases and Systems Biology of Aging Cologne, University of Cologne, Joseph-Stelzmann-Str. 26, Cologne 50931, Germany.
Susanne BrodesserCologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases and Systems Biology of Aging Cologne, University of Cologne, Joseph-Stelzmann-Str. 26, Cologne 50931, Germany.
Marcus KrügerCologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases and Systems Biology of Aging Cologne, University of Cologne, Joseph-Stelzmann-Str. 26, Cologne 50931, Germany; Center for Molecular Medicine, University of Cologne, Robert-Koch-Str. 21, 50931 Cologne, Germany.
Björn SchumacherInstitute for Genome Stability in Aging and Disease, Medical Faculty, University of Cologne, Joseph-Stelzmann-Str. 26, Cologne 50931, Germany; Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases and Systems Biology of Aging Cologne, University of Cologne, Joseph-Stelzmann-Str. 26, Cologne 50931, Germany; Center for Molecular Medicine, University of Cologne, Robert-Koch-Str. 21, 50931 Cologne, Germany. Electronic address: bjoern.schumacher@uni-koeln.de.
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEUniversity of Cologne · DE

Funding

European Research Council 260383
6 · The paper itself

Abstract

DNA damage causally contributes to aging and age-related diseases. Mutations in nucleotide excision repair (NER) genes cause highly complex congenital syndromes characterized by growth retardation, cancer susceptibility, and accelerated aging in humans. Orthologous mutations in Caenorhabditis elegans lead to growth delay, genome instability, and accelerated functional decline, thus allowing investigation of the consequences of persistent DNA damage during development and aging in a simple metazoan model. Here, we conducted proteome, lipidome, and phosphoproteome analysis of NER-deficient animals in response to UV treatment to gain comprehensive insights into the full range of physiological adaptations to unrepaired DNA damage. We derive metabolic changes indicative of a tissue maintenance program and implicate an autophagy-mediated proteostatic response. We assign central roles for the insulin-, EGF-, and AMPK-like signaling pathways in orchestrating the adaptive response to DNA damage. Our results provide insights into the DNA damage responses in the organismal context.

Indexed as

Cellular ReprogrammingDNA DamageActive Transport, Cell NucleusAgingAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCell NucleusDNA RepairDown-RegulationIon TransportLipid MetabolismMutationPhosphoproteinsProteolysisProteomeCaenorhabditis elegans ProteinsPhosphoproteinsProteomeagingCaenorhabditis elegansDNA damage responseDNA repairlipidomicsnucleotide excision repairproteomics

Identifiers

PMID28854356
PMCPMC5583510
OpenAlexW2751268777

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.