Evidence map›Paper›PMID 21984833›Full record

ArticleThe Journal of biological chemistry2011

Properties of Ca(2+) transport in mitochondria of Drosophila melanogaster.

Sophia von Stockum, Emy Basso, Valeria Petronilli, Patrizia Sabatelli, Michael A Forte, Paolo Bernardi

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 58 citations in OpenAlex.

  1. Phenotypic CRISPR screens identify NLRX1 as an essential activator of the human mitochondrial permeability transition.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  2. bioRxiv : the preprint server for biology · 2026
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  15. Mitochondrial calcium uniporter regulator 1 (MCUR1) regulates the calcium threshold for the mitochondrial permeability transition.Proceedings of the National Academy of Sciences of the United States of America · 2016
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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 4 institutions in 2 countries.

Sophia von StockumConsiglio Nazionale delle Ricerche Institute of Neuroscience and Department of Biomedical Sciences, University of I-35121 Padova, Italy.
Emy BassoConsiglio Nazionale delle Ricerche Institute of Neuroscience and Department of Biomedical Sciences, University of I-35121 Padova, Italy.
Valeria PetronilliConsiglio Nazionale delle Ricerche Institute of Neuroscience and Department of Biomedical Sciences, University of I-35121 Padova, Italy.
Patrizia SabatelliInstitute of Molecular Genetics at the Istituto Ortopedico Rizzoli, I-40126 Bologna, Italy.
Michael A ForteVollum Institute, Oregon Health & Sciences University, Portland, Oregon 97239.
Paolo BernardiConsiglio Nazionale delle Ricerche Institute of Neuroscience and Department of Biomedical Sciences, University of I-35121 Padova, Italy. Electronic address: bernardi@bio.unipd.it.
Neuroscience Institute · ITIstituto Ortopedico Rizzoli · ITNational Research Council · ITVollum Institute · US

Funding

Molecular Structure and Regulation of the Permeability Transition PoreR01GM069883 · NIGMS · OREGON HEALTH & SCIENCE UNIVERSITY · PI FORTE, MICHAEL A · 2004 to 2016
$3.3M
NIGMS NIH HHS GM069883NIGMS NIH HHS R01 GM069883
6 · The paper itself

Abstract

We have studied the pathways for Ca(2+) transport in mitochondria of the fruit fly Drosophila melanogaster. We demonstrate the presence of ruthenium red (RR)-sensitive Ca(2+) uptake, of RR-insensitive Ca(2+) release, and of Na(+)-stimulated Ca(2+) release in energized mitochondria, which match well characterized Ca(2+) transport pathways of mammalian mitochondria. Following larger matrix Ca(2+) loading Drosophila mitochondria underwent spontaneous RR-insensitive Ca(2+) release, an event that in mammals is due to opening of the permeability transition pore (PTP). Like the PTP of mammals, Drosophila Ca(2+)-induced Ca(2+) release could be triggered by uncoupler, diamide, and N-ethylmaleimide, indicating the existence of regulatory voltage- and redox-sensitive sites and was inhibited by tetracaine. Unlike PTP-mediated Ca(2+) release in mammals, however, it was (i) insensitive to cyclosporin A, ubiquinone 0, and ADP; (ii) inhibited by P(i), as is the PTP of yeast mitochondria; and (iii) not accompanied by matrix swelling and cytochrome c release even in KCl-based medium. We conclude that Drosophila mitochondria possess a selective Ca(2+) release channel with features intermediate between the PTP of yeast and mammals.

Indexed as

Adenosine DiphosphateAnimalsAntifungal AgentsBenzoquinonesCalciumCyclosporineDrosophila melanogasterDrosophila ProteinsDrug ResistanceIndicators and ReagentsIon TransportMammalsMitochondriaMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreRuthenium RedAdenosine DiphosphateAntifungal AgentsBenzoquinonesCalciumCyclosporineDrosophila ProteinsIndicators and ReagentsMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreRuthenium Redubiquinone-O

Identifiers

PMID21984833
PMCPMC3308830
OpenAlexW1992417877

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.