Evidence map›Paper›PMID 28775312›Full record

ArticleScientific reports2017

Uracil Accumulation and Mutagenesis Dominated by Cytosine Deamination in CpG Dinucleotides in Mice Lacking UNG and SMUG1.

Lene Alsøe, Antonio Sarno, Sergio Carracedo, Diana Domanska, Felix Dingler, Lisa Lirussi, Tanima SenGupta, Nuriye Basdag Tekin, Laure Jobert, Ludmil B Alexandrov and 6 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

38 citing papers in PubMed, 58 citations in OpenAlex.

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  19. (5'International journal of molecular sciences · 2021
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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

16 authors at 5 institutions in 3 countries.

Lene AlsøeDepartment of Clinical Molecular Biology, Ahus Campus, University of Oslo, Oslo, Norway.
Antonio SarnoDepartment of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Sergio CarracedoDepartment of Clinical Molecular Biology, Ahus Campus, University of Oslo, Oslo, Norway.
Diana DomanskaDepartment of Informatics, University of Oslo, PO Box 1080 Blindern, NO-0316, Oslo, Norway.
Felix DinglerMRC Laboratory of Molecular Biology, Cambridge, UK.
Lisa LirussiDepartment of Clinical Molecular Biology, Ahus Campus, University of Oslo, Oslo, Norway.
Tanima SenGuptaDepartment of Clinical Molecular Biology, Ahus Campus, University of Oslo, Oslo, Norway.
Nuriye Basdag TekinDepartment of Clinical Molecular Biology, Ahus Campus, University of Oslo, Oslo, Norway.
Laure JobertDepartment of Clinical Molecular Biology, Ahus Campus, University of Oslo, Oslo, Norway.
Ludmil B AlexandrovTheoretical Biology and Biophysics (T-6), Los Alamos National Laboratory, Los Alamos, NM, 87545, USA.ORCID 0000-0003-3596-4515
Anastasia GalashevskayaDepartment of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Cristina RadaMRC Laboratory of Molecular Biology, Cambridge, UK.ORCID 0000-0003-4898-5550
Geir Kjetil SandveDepartment of Informatics, University of Oslo, PO Box 1080 Blindern, NO-0316, Oslo, Norway.
Torbjørn RognesDepartment of Informatics, University of Oslo, PO Box 1080 Blindern, NO-0316, Oslo, Norway.ORCID 0000-0002-9329-9974
Hans E KrokanDepartment of Cancer Research and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
Hilde NilsenDepartment of Clinical Molecular Biology, Ahus Campus, University of Oslo, Oslo, Norway. hilde.nilsen@medisin.uio.no.ORCID 0000-0003-2115-2663
University of Oslo · NONorwegian University of Science and Technology · NOMRC Laboratory of Molecular Biology · GBLos Alamos National Laboratory · USOslo University Hospital · NO

Funding

Medical Research Council MC_U105178806
6 · The paper itself

Abstract

Both a DNA lesion and an intermediate for antibody maturation, uracil is primarily processed by base excision repair (BER), either initiated by uracil-DNA glycosylase (UNG) or by single-strand selective monofunctional uracil DNA glycosylase (SMUG1). The relative in vivo contributions of each glycosylase remain elusive. To assess the impact of SMUG1 deficiency, we measured uracil and 5-hydroxymethyluracil, another SMUG1 substrate, in Smug1

Indexed as

AnimalsCpG IslandsCytosineDeaminationDinucleoside PhosphatesGenomeGenomicsMiceMice, KnockoutMutationUracilUracil-DNA GlycosidaseCpG dinucleotideCytosineDinucleoside PhosphatesUracilUracil-DNA Glycosidase

Identifiers

PMID28775312
PMCPMC5543110
OpenAlexW2740109815

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.