ArticleBiochimica et biophysica acta2011
VDAC3 has differing mitochondrial functions in two types of striated muscles.
Article in Biochimica et biophysica acta, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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.
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.
Who cites it
19 citing papers in PubMed, 43 citations in OpenAlex.
- Conformational plasticity of mitochondrial VDAC2 controls the kinetics of its interaction with cytosolic proteins.Science advances · 2025Article
- Chloride ions in health and disease.Bioscience reports · 2024Review
- Mitochondrial ion channels in cardiac function.American journal of physiology. Cell physiology · 2021Review
- VDAC regulation of mitochondrial calcium flux: From channel biophysics to disease.Cell calcium · 2021Review
- Deletion of Voltage-Dependent Anion Channel 1 knocks mitochondria down triggering metabolic rewiring in yeast.Cellular and molecular life sciences : CMLS · 2020Article
- A lower affinity to cytosolic proteins reveals VDAC3 isoform-specific role in mitochondrial biology.The Journal of general physiology · 2020Article
- Integrated approach for data acquisition, visualization and processing of analog polarographic systems for bioenergetics studies.Analytical biochemistry · 2020Article
- Article
- Vdac1 Downregulation Causes Mitochondrial Disintegration Leading to Hippocampal Neurodegeneration in Scopolamine-Induced Amnesic Mice.Molecular neurobiology · 2019Article
- Knockout of mitochondrial voltage-dependent anion channel type 3 increases reactive oxygen species (ROS) levels and alters renal sodium transport.The Journal of biological chemistry · 2018Article
- Voltage-Dependent Anion Channel 1 As an Emerging Drug Target for Novel Anti-Cancer Therapeutics.Frontiers in oncology · 2017Review
- Mitochondrial VDAC1: A Key Gatekeeper as Potential Therapeutic Target.Frontiers in physiology · 2017Review
- Modular organization of cardiac energy metabolism: energy conversion, transfer and feedback regulation.Acta physiologica (Oxford, England) · 2015Review
- High fat diet-induced modifications in membrane lipid and mitochondrial-membrane protein signatures precede the development of hepatic insulin resistance in mice.Molecular metabolism · 2015Article
- Voltage-dependant anion channels: novel insights into isoform function through genetic models.Biochimica et biophysica acta · 2012Review
- VDAC structure, selectivity, and dynamics.Biochimica et biophysica acta · 2012Review
- The role of VDAC in cell death: friend or foe?Biochimica et biophysica acta · 2012Review
- VDAC1: from structure to cancer therapy.Frontiers in oncology · 2012Article
- Mitochondrial carnitine palmitoyltransferase 1a (CPT1a) is part of an outer membrane fatty acid transfer complex.The Journal of biological chemistry · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Voltage-dependent anion channel (VDAC) is an abundant mitochondrial outer membrane protein. In mammals, three VDAC isoforms have been characterized. We have previously reported alterations in the function of mitochondria when assessed in situ in different muscle types in VDAC1 deficient mice (Anflous et al., 2001). In the present report we extend the study to VDAC3 deficient muscles and measure the respiratory enzyme activity in both VDAC1 and VDAC3 deficient muscles. While in the heart the absence of VDAC3 causes a decrease in the apparent affinity of in situ mitochondria for ADP, in the gastrocnemius, a mixed glycolytic/oxidative muscle, the affinity of in situ mitochondria for ADP remains unchanged. The absence of VDAC1 causes multiple defects in respiratory complex activities in both types of muscle. However, in VDAC3 deficient mice the defect is restricted to the heart and only to complex IV. These functional alterations correlate with structural aberrations of mitochondria. These results demonstrate that, unlike VDAC1, there is muscle-type specificity for VDAC3 function and therefore in vivo these two isoforms may fulfill different physiologic functions.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.