Evidence map›Paper›PMID 25210580›Full record

ArticleCommunicative & integrative biology2013

The innate immune system as mediator of systemic DNA damage responses.

Maria Ermolaeva, Björn Schumacher

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Communicative & integrative biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

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  8. Genetic and cellular sensitivity ofDisease models & mechanisms · 2018
    Article
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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

2 authors at 2 institutions in 2 countries.

Maria ErmolaevaInstitute for Genome Stability in Aging and Disease, Medical Faculty, University of Cologne; Cologne, Germany.
Björn SchumacherInstitute for Genome Stability in Aging and Disease, Medical Faculty, University of Cologne; Cologne, Germany ; Cologne Excellence Cluster for Cellular Stress Responses in Aging-Associated Diseases (CECAD); Institute for Genetics; University of Cologne; Cologne, Germany.
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases · DEUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA damage causally contributes to cancer development and tissue degeneration with aging.(1) Cellular DNA damage responses (DDR) mediate cell cycle arrest to allow time for DNA repair, or induce cellular senescence and apoptosis to eliminate damaged cells.(2) In contrast to cell-autonomous DNA damage responses, it remains less clear how organisms respond to genome instability in certain cell types and how distinct tissues interact when responding to tissue-specific DNA damage. C. elegans comprises an intriguing system to study the interaction between distinct tissues as germ cells evoke conserved DDR mechanisms, while somatic tissues are highly radio resistant.(3) (,) (4) The recent discovery of the "germline DNA damage-induced systemic stress response" (GDISR) sheds new light on non-cell autonomous responses to genome instability.(5) GDISR is mediated by ERK MAP kinase MPK-1 induced putative secreted peptides that are associated with innate immunity. The innate immune response leads to activation of the ubiquitin-proteasome-system (UPS) in somatic tissues, which confers systemic stress resistance. We discuss the role of the innate immunity in mediating systemic DNA damage responses and how UPS activity promotes endurance of somatic tissues.

Indexed as

agingC. elegansDNA damage responseInnate immunitystress resistance

Identifiers

PMID25210580
PMCPMC3922787
OpenAlexW1986530960

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.