Evidence map›Paper›PMID 25124032›Full record

ArticleThe Journal of biological chemistry2014

Ca2+-mediated mitochondrial reactive oxygen species metabolism augments Wnt/β-catenin pathway activation to facilitate cell differentiation.

Tareck Rharass, Heiko Lemcke, Margareta Lantow, Sergei A Kuznetsov, Dieter G Weiss, Daniela Panáková

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 2 pooled it
5.8field-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

60 citing papers in PubMed, 2 syntheses or guidelines pooled it, 107 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Tareck RharassFrom Electrochemical Signaling in Development and Disease, Max-Delbrück-Center for Molecular Medicine, Robert-Rössle-Strasse 10, D-13125 Berlin-Buch and Cell Biology and Biosystems Technology, Institute of Biological Sciences, and Live Cell Imaging Center, University of Rostock, Albert-Einstein-Strasse 3, D-18059 Rostock, Germany.
Heiko LemckeCell Biology and Biosystems Technology, Institute of Biological Sciences, and Live Cell Imaging Center, University of Rostock, Albert-Einstein-Strasse 3, D-18059 Rostock, Germany.
Margareta LantowCell Biology and Biosystems Technology, Institute of Biological Sciences, and.
Sergei A KuznetsovLive Cell Imaging Center, University of Rostock, Albert-Einstein-Strasse 3, D-18059 Rostock, Germany.
Dieter G WeissCell Biology and Biosystems Technology, Institute of Biological Sciences, and Live Cell Imaging Center, University of Rostock, Albert-Einstein-Strasse 3, D-18059 Rostock, Germany.
Daniela PanákováFrom Electrochemical Signaling in Development and Disease, Max-Delbrück-Center for Molecular Medicine, Robert-Rössle-Strasse 10, D-13125 Berlin-Buch and daniela.panakova@mdc-berlin.de.
University of Rostock · DEMax Delbrück Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Emerging evidence suggests that reactive oxygen species (ROS) can stimulate the Wnt/β-catenin pathway in a number of cellular processes. However, potential sources of endogenous ROS have not been thoroughly explored. Here, we show that growth factor depletion in human neural progenitor cells induces ROS production in mitochondria. Elevated ROS levels augment activation of Wnt/β-catenin signaling that regulates neural differentiation. We find that growth factor depletion stimulates the release of Ca(2+) from the endoplasmic reticulum stores. Ca(2+) subsequently accumulates in the mitochondria and triggers ROS production. The inhibition of mitochondrial Ca(2+) uptake with simultaneous growth factor depletion prevents the rise in ROS metabolism. Moreover, low ROS levels block the dissociation of the Wnt effector Dishevelled from nucleoredoxin. Attenuation of the response amplitudes of pathway effectors delays the onset of the Wnt/β-catenin pathway activation and results in markedly impaired neuronal differentiation. Our findings reveal Ca(2+)-mediated ROS metabolic cues that fine-tune the efficiency of cell differentiation by modulating the extent of the Wnt/β-catenin signaling output.

Indexed as

Cell DifferentiationWnt Signaling Pathwaybeta CateninCalciumHumansMitochondriaNeural Stem CellsReactive Oxygen SpeciesWnt Proteinsbeta CateninCalciumReactive Oxygen SpeciesWnt ProteinsCalcium SignalingDishevelledHuman Neural Progenitor CellsMitochondrial MetabolismNucleoredoxinReactive Oxygen Species (ROS)Redox SignalingWnt Pathway

Identifiers

PMID25124032
PMCPMC4183826
OpenAlexW1521072705

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.