Evidence map›Paper›PMID 25941166›Full record

ArticleCell death and differentiation2015

XLS (c9orf142) is a new component of mammalian DNA double-stranded break repair.

A Craxton, J Somers, D Munnur, R Jukes-Jones, K Cain, M Malewicz

Open access · hybridAbstract read
In one paragraph

Article in Cell death and differentiation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

43 citing papers in PubMed, 69 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

A CraxtonMRC Toxicology Unit, Hodgkin Building, Lancaster Road, Leicester LE1 9HN, UK.
J SomersMRC Toxicology Unit, Hodgkin Building, Lancaster Road, Leicester LE1 9HN, UK.
D MunnurMRC Toxicology Unit, Hodgkin Building, Lancaster Road, Leicester LE1 9HN, UK.
R Jukes-JonesMRC Toxicology Unit, Hodgkin Building, Lancaster Road, Leicester LE1 9HN, UK.
K CainMRC Toxicology Unit, Hodgkin Building, Lancaster Road, Leicester LE1 9HN, UK.
M MalewiczMRC Toxicology Unit, Hodgkin Building, Lancaster Road, Leicester LE1 9HN, UK.
MRC Toxicology Unit · GB

Funding

Medical Research Council MC_UP_A600_1109
6 · The paper itself

Abstract

Repair of double-stranded DNA breaks (DSBs) in mammalian cells primarily occurs by the non-homologous end-joining (NHEJ) pathway, which requires seven core proteins (Ku70/Ku86, DNA-PKcs (DNA-dependent protein kinase catalytic subunit), Artemis, XRCC4-like factor (XLF), XRCC4 and DNA ligase IV). Here we show using combined affinity purification and mass spectrometry that DNA-PKcs co-purifies with all known core NHEJ factors. Furthermore, we have identified a novel evolutionary conserved protein associated with DNA-PKcs-c9orf142. Computer-based modelling of c9orf142 predicted a structure very similar to XRCC4, hence we have named c9orf142-XLS (XRCC4-like small protein). Depletion of c9orf142/XLS in cells impaired DSB repair consistent with a defect in NHEJ. Furthermore, c9orf142/XLS interacted with other core NHEJ factors. These results demonstrate the existence of a new component of the NHEJ DNA repair pathway in mammalian cells.

Indexed as

Computer SimulationDNA Breaks, Double-StrandedCell LineChromatography, AffinityDNA-Binding ProteinsDNA RepairHumansImmunoblottingRNA, Small InterferingTandem Mass SpectrometryDNA-Binding ProteinsPAXX protein, humanRNA, Small Interfering

Identifiers

PMID25941166
PMCPMC4423191
OpenAlexW2041529030

What OpenQuestion holds

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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.