Evidence map›Paper›PMID 31655859›Full record

ArticleCellular and molecular life sciences : CMLS2020

Deletion of Voltage-Dependent Anion Channel 1 knocks mitochondria down triggering metabolic rewiring in yeast.

Andrea Magrì, Maria Carmela Di Rosa, Ivan Orlandi, Francesca Guarino, Simona Reina, Maria Guarnaccia, Giovanna Morello, Antonio Spampinato, Sebastiano Cavallaro, Angela Messina and 2 more

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

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  5. Developing a Novel and Optimized Yeast Model for Human VDAC Research.International journal of molecular sciences · 2024
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  19. Article
  20. High-Resolution Respirometry Reveals MPPInternational journal of molecular sciences · 2020
    Article
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

12 authors at 3 institutions in 1 country.

Andrea MagrìDepartment of Biomedical and Biotechnological Sciences, University of Catania, Via S. Sofia, 64, Catania, Italy.
Maria Carmela Di RosaDepartment of Biomedical and Biotechnological Sciences, University of Catania, Via S. Sofia, 64, Catania, Italy.
Ivan OrlandiDepartment of Biotechnologies and Biosciences, University of Milano-Bicocca, Piazza della Scienza, 2, Milan, Italy.
Francesca GuarinoDepartment of Biomedical and Biotechnological Sciences, University of Catania, Via S. Sofia, 64, Catania, Italy.
Simona ReinaDepartment of Biomedical and Biotechnological Sciences, University of Catania, Via S. Sofia, 64, Catania, Italy.
Maria GuarnacciaInstitute for Biomedical Research and Innovation (IRIB), National Research Council (CNR), Via P. Gaifami, 18, Catania, Italy.
Giovanna MorelloInstitute for Biomedical Research and Innovation (IRIB), National Research Council (CNR), Via P. Gaifami, 18, Catania, Italy.
Antonio SpampinatoInstitute for Biomedical Research and Innovation (IRIB), National Research Council (CNR), Via P. Gaifami, 18, Catania, Italy.
Sebastiano CavallaroInstitute for Biomedical Research and Innovation (IRIB), National Research Council (CNR), Via P. Gaifami, 18, Catania, Italy.
Angela MessinaDepartment of Biological, Geological and Environmental Sciences, University of Catania, Via A. Longo, 19, Catania, Italy.
Marina VaiDepartment of Biotechnologies and Biosciences, University of Milano-Bicocca, Piazza della Scienza, 2, Milan, Italy. marina.vai@unimib.it.
Vito De PintoDepartment of Biomedical and Biotechnological Sciences, University of Catania, Via S. Sofia, 64, Catania, Italy. vdpbiofa@unict.it.ORCID http://orcid.org/0000-0001-5513-2906
University of Catania · ITInstitute for Biomedical Research and Innovation · ITUniversity of Milano-Bicocca · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Voltage-Dependent Anion-selective Channel (VDAC) is the pore-forming protein of mitochondrial outer membrane, allowing metabolites and ions exchanges. In Saccharomyces cerevisiae, inactivation of POR1, encoding VDAC1, produces defective growth in the presence of non-fermentable carbon source. Here, we characterized the whole-genome expression pattern of a VDAC1-null strain (Δpor1) by microarray analysis, discovering that the expression of mitochondrial genes was completely abolished, as consequence of the dramatic reduction of mtDNA. To overcome organelle dysfunction, Δpor1 cells do not activate the rescue signaling retrograde response, as ρ

Indexed as

Energy MetabolismGenes, MitochondrialMitochondriaMitochondrial MembranesOxidation-ReductionPorinsSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsVoltage-Dependent Anion Channel 1Por1 protein, S cerevisiaePorinsSaccharomyces cerevisiae ProteinsVoltage-Dependent Anion Channel 1Fatty acidsInositolMitochondrial DNAPDH bypassPorinRetrograde signalingWarburg effect

Identifiers

PMID31655859
PMCPMC11104908
OpenAlexW2982142319

What OpenQuestion holds

Textmetadata
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.