Evidence map›Paper›PMID 28273955›Full record

ArticleScientific reports2017

Lack of XPC leads to a shift between respiratory complexes I and II but sensitizes cells to mitochondrial stress.

Mateus P Mori, Rute A P Costa, Daniela T Soltys, Thiago de S Freire, Franco A Rossato, Ignácio Amigo, Alicia J Kowaltowski, Aníbal E Vercesi, Nadja C de Souza-Pinto

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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  5. Mitochondrial DNA Instability in Mammalian Cells.Antioxidants & redox signaling · 2022
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  7. 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

9 authors at 2 institutions in 1 country.

Mateus P MoriDepartamento de Bioquímica, Instituto de Química, Universidade de São Paulo (USP), São Paulo, SP, Brazil.ORCID 0000-0003-1349-6378
Rute A P CostaDepartment of Clinical Pathology, School of Medical Sciences, Universidade Estadual de Campinas (UNICAMP), Campinas, SP, Brazil.ORCID 0000-0003-1795-9819
Daniela T SoltysDepartamento de Bioquímica, Instituto de Química, Universidade de São Paulo (USP), São Paulo, SP, Brazil.ORCID 0000-0002-1024-3108
Thiago de S FreireDepartamento de Bioquímica, Instituto de Química, Universidade de São Paulo (USP), São Paulo, SP, Brazil.
Franco A RossatoDepartment of Clinical Pathology, School of Medical Sciences, Universidade Estadual de Campinas (UNICAMP), Campinas, SP, Brazil.ORCID 0000-0002-4132-2271
Ignácio AmigoDepartamento de Bioquímica, Instituto de Química, Universidade de São Paulo (USP), São Paulo, SP, Brazil.
Alicia J KowaltowskiDepartamento de Bioquímica, Instituto de Química, Universidade de São Paulo (USP), São Paulo, SP, Brazil.
Aníbal E VercesiDepartment of Clinical Pathology, School of Medical Sciences, Universidade Estadual de Campinas (UNICAMP), Campinas, SP, Brazil.
Nadja C de Souza-PintoDepartamento de Bioquímica, Instituto de Química, Universidade de São Paulo (USP), São Paulo, SP, Brazil. nadja@iq.usp.br.
Universidade de São Paulo · BRUniversidade Estadual de Campinas (UNICAMP) · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Genomic instability drives tumorigenesis and DNA repair defects are associated with elevated cancer. Metabolic alterations are also observed during tumorigenesis, although a causal relationship between these has not been clearly established. Xeroderma pigmentosum (XP) is a DNA repair disease characterized by early cancer. Cells with reduced expression of the XPC protein display a metabolic shift from OXPHOS to glycolysis, which was linked to accumulation of nuclear DNA damage and oxidants generation via NOX-1. Using XP-C cells, we show that mitochondrial respiratory complex I (CI) is impaired in the absence of XPC, while complex II (CII) is upregulated in XP-C cells. The CI/CII metabolic shift was dependent on XPC, as XPC complementation reverted the phenotype. We demonstrate that mitochondria are the primary source of H

Indexed as

Cell LineDNA-Binding ProteinsDNA, MitochondrialElectron Transport Complex IElectron Transport Complex IIGene Expression RegulationGlutathione PeroxidaseHumansHydrogen PeroxideMitochondriaOxidative StressSequence DeletionXeroderma PigmentosumDNA-Binding ProteinsDNA, MitochondrialElectron Transport Complex IElectron Transport Complex IIGlutathione PeroxidaseHydrogen Peroxiderespiratory complex IIXPC protein, human

Identifiers

PMID28273955
PMCPMC5427820
OpenAlexW2592869119

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.