Evidence map›Paper›PMID 33379193›Full record

ArticleBiomolecules2020

Non-Homologous End Joining Factors XLF, PAXX and DNA-PKcs Maintain the Neural Stem and Progenitor Cell Population.

Raquel Gago-Fuentes, Valentyn Oksenych

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

Article in Biomolecules, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. DNA damage and repair: underlying mechanisms leading to microcephaly.Frontiers in cell and developmental biology · 2023
    Review
  4. Article
  5. 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

2 authors at 2 institutions in 1 country.

Raquel Gago-FuentesDepartment for Cancer Research and Molecular Medicine (IKOM), Norwegian University of Science and Technology, 7491 Trondheim, Norway.
Valentyn OksenychDepartment for Cancer Research and Molecular Medicine (IKOM), Norwegian University of Science and Technology, 7491 Trondheim, Norway.ORCID 0000-0002-5088-3791
Norwegian University of Science and Technology · NOUniversity of Oslo · NO

Funding

Helse Midt-Norge 13477Helse Midt-Norge 38811Karolinska Institutet 2020-02155Kreftforeningen 182355Norges Forskningsråd 249774Norges Forskningsråd 270491Norges Forskningsråd 291217
6 · The paper itself

Abstract

Non-homologous end-joining (NHEJ) is a major DNA repair pathway in mammalian cells that recognizes, processes and fixes DNA damage throughout the cell cycle and is specifically important for homeostasis of post-mitotic neurons and developing lymphocytes. Neuronal apoptosis increases in the mice lacking NHEJ factors Ku70 and Ku80. Inactivation of other NHEJ genes, either

Indexed as

AnimalsApoptosisDNA-Activated Protein KinaseDNA-Binding ProteinsDNA DamageDNA End-Joining RepairDNA Ligase ATPDNA RepairGene Expression Regulation, DevelopmentalHumansKu AutoantigenMiceNeural Stem CellsNeuronsStem CellsDNA-Activated Protein KinaseDNA-Binding ProteinsDNA Ligase ATPKu AutoantigenLig4 protein, mousePaxx protein, mouseXLF protein, mouseXRCC4 protein, mouseXrcc5 protein, mouseXrcc6 protein, mouseDNA repairgenetic interactionNHEJsynthetic lethality

Identifiers

PMID33379193
PMCPMC7823790
OpenAlexW3111383854

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.