Evidence map›Paper›PMID 29293500›Full record

ArticlePloS one2018

PARP10 (ARTD10) modulates mitochondrial function.

Judit Márton, Tamás Fodor, Lilla Nagy, András Vida, Gréta Kis, Attila Brunyánszki, Miklós Antal, Bernhard Lüscher, Péter Bai

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.3field-weighted citation impact, top 9% 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

34 citing papers in PubMed, 48 citations in OpenAlex.

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  17. Functional roles of ADP-ribosylation writers, readers and erasers.Frontiers in cell and developmental biology · 2022
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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 2 countries.

Judit MártonDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Tamás FodorDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Lilla NagyDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
András VidaDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Gréta KisDepartment of Anatomy, Histology and Embryology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Attila BrunyánszkiDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Miklós AntalDepartment of Anatomy, Histology and Embryology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Bernhard LüscherInstitute of Biochemistry and Molecular Biology, Medical School, RWTH Aachen University, Aachen, Germany.
Péter BaiDepartment of Medical Chemistry, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
University of Debrecen · HURWTH Aachen University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Poly(ADP-ribose) polymerase (PARP)10 is a PARP family member that performs mono-ADP-ribosylation of target proteins. Recent studies have linked PARP10 to metabolic processes and metabolic regulators that prompted us to assess whether PARP10 influences mitochondrial oxidative metabolism. The depletion of PARP10 by specific shRNAs increased mitochondrial oxidative capacity in cellular models of breast, cervical, colorectal and exocrine pancreas cancer. Upon silencing of PARP10, mitochondrial superoxide production decreased in line with increased expression of antioxidant genes pointing out lower oxidative stress upon PARP10 silencing. Improved mitochondrial oxidative capacity coincided with increased AMPK activation. The silencing of PARP10 in MCF7 and CaCo2 cells decreased the proliferation rate that correlated with increased expression of anti-Warburg enzymes (Foxo1, PGC-1α, IDH2 and fumarase). By analyzing an online database we showed that lower PARP10 expression increases survival in gastric cancer. Furthermore, PARP10 expression decreased upon fasting, a condition that is characterized by increases in mitochondrial biogenesis. Finally, lower PARP10 expression is associated with increased fatty acid oxidation.

Indexed as

Adenylate KinaseAnimalsBlotting, WesternCell LineCell ProliferationElectrophoresis, Polyacrylamide GelGene SilencingHumansMaleMice, Inbred C57BLMitochondriaOxidation-ReductionOxidative StressOxygen ConsumptionPoly(ADP-ribose) PolymerasesProto-Oncogene ProteinsAdenylate KinasePARP10 protein, humanPoly(ADP-ribose) PolymerasesProto-Oncogene Proteins

Identifiers

PMID29293500
PMCPMC5749700
OpenAlexW2781783863

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.