Evidence map›Paper›PMID 27137888›Full record

ArticleNucleic acids research2016

Xpg limits the expansion of haematopoietic stem and progenitor cells after ionising radiation.

Alush I Avila, Anett Illing, Friedrich Becker, Lars D Maerz, Yohei Morita, Melanie Philipp, Martin D Burkhalter

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2016. 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
0.9field-weighted citation impact, top 24% 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. DNA repair fidelity in stem cell maintenance, health, and disease.Biochimica et biophysica acta. Molecular basis of disease · 2020
    Review
  3. Article
  4. 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 2 institutions in 1 country.

Alush I AvilaLeibniz Institute on Aging, Fritz Lipmann Institute, 07745 Jena, Germany.
Anett IllingDepartment of Internal Medicine I, Ulm University, 89081 Ulm, Germany.
Friedrich BeckerLeibniz Institute on Aging, Fritz Lipmann Institute, 07745 Jena, Germany.
Lars D MaerzInstitute for Biochemistry and Molecular Biology, Ulm University, 89081 Ulm, Germany.
Yohei MoritaLeibniz Institute on Aging, Fritz Lipmann Institute, 07745 Jena, Germany.
Melanie PhilippInstitute for Biochemistry and Molecular Biology, Ulm University, 89081 Ulm, Germany.ORCID 0000-0003-2714-965X
Martin D BurkhalterLeibniz Institute on Aging, Fritz Lipmann Institute, 07745 Jena, Germany Institute for Biochemistry and Molecular Biology, Ulm University, 89081 Ulm, Germany martin.burkhalter@uni-ulm.de.
Universität Ulm · DELeibniz Institute on Aging - Fritz Lipmann Institute (FLI) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reduced capacity of genome maintenance represents a problem for any organism, potentially causing premature death, carcinogenesis, or accelerated ageing. Strikingly though, loss of certain genome stability factors can be beneficial, especially for the maintenance of tissue stem cells of the intestine and the haematopoietic system. We therefore screened for genome stability factors negatively impacting maintenance of haematopoietic stem cells (HSC) in the context of ionising radiation (IR). We found that in vivo knock down of Xeroderma pigmentosum, complementation group G (Xpg) causes elevation of HSC numbers after IR treatment, while numbers of haematopoietic progenitors are elevated to a lesser extent. IR rapidly induces Xpg both on mRNA and on protein level. Prevention of this induction does not influence activation of the checkpoint cascade, yet attenuates late checkpoint steps such as induction of p21 and Noxa. This causes a leaky cell cycle arrest and lower levels of apoptosis, both contributing to increased colony formation and transformation rates. Xpg thus helps to adequately induce DNA damage responses after IR, thereby keeping the expansion of damaged cells under control. This represents a new function of Xpg in the response to IR, in addition to its well-characterized role in nucleotide excision repair.

Indexed as

ApoptosisCarcinogenesisCell Cycle CheckpointsDNA-Binding ProteinsDNA DamageDNA Excision Repair Protein ERCC-5DNA RepairEndonucleasesGene Expression RegulationGene Knockdown TechniquesGenomic InstabilityHematopoietic Stem CellsHumansNuclear ProteinsRadiation, IonizingRNA, MessengerDNA-Binding ProteinsDNA Excision Repair Protein ERCC-5EndonucleasesNuclear ProteinsRNA, MessengerTranscription Factors

Identifiers

PMID27137888
PMCPMC5291257
OpenAlexW2346512117

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.