ArticleBiochimica et biophysica acta2009
Adenine nucleotide translocator 1 deficiency increases resistance of mouse brain and neurons to excitotoxic insults.
Article in Biochimica et biophysica acta, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- A Function-Centric Framework for Mitochondrial Quality Control.Biomolecules · 2026Review
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- Impacts of mitochondrial dysfunction on axonal microtubule bundles as a potential mechanism of neurodegeneration.Frontiers in neuroscience · 2025Review
- Mitochondrial Chronic Progressive External Ophthalmoplegia.Brain sciences · 2024Review
- Mitochondrial Permeability Transition: A Pore Intertwines Brain Aging and Alzheimer's Disease.Cells · 2021Review
- Ant1 mutant mice bridge the mitochondrial and serotonergic dysfunctions in bipolar disorder.Molecular psychiatry · 2020Article
- Reply to "Correspondence to Ant1 mutant mice bridge the mitochondrial and serotonergic dysfunctions in bipolar disorder".Molecular psychiatry · 2020Article
- Regulation of the mitochondrial permeability transition pore and its effects on aging.Microbial cell (Graz, Austria) · 2020Article
- Hippocampal tau oligomerization early in tau pathology coincides with a transient alteration of mitochondrial homeostasis and DNA repair in a mouse model of tauopathy.Acta neuropathologica communications · 2020Article
- Ant1 mutant mice bridge the mitochondrial and serotonergic dysfunctions in bipolar disorder.Molecular psychiatry · 2018Article
- HDNetDB: A Molecular Interaction Database for Network-Oriented Investigations into Huntington's Disease.Scientific reports · 2017Article
- Transcription factor NF-kappa B represses ANT1 transcription and leads to mitochondrial dysfunctions.Scientific reports · 2017Article
- Alterations in voltage-sensing of the mitochondrial permeability transition pore in ANT1-deficient cells.Scientific reports · 2016Article
- Differential Mitochondrial Requirements for Radially and Non-radially Migrating Cortical Neurons: Implications for Mitochondrial Disorders.Cell reports · 2016Article
- Mitochondrial Diseases Part II: Mouse models of OXPHOS deficiencies caused by defects in regulatory factors and other components required for mitochondrial function.Mitochondrion · 2015Review
- Electron Transport Disturbances and Neurodegeneration: From Albert Szent-Györgyi's Concept (Szeged) till Novel Approaches to Boost Mitochondrial Bioenergetics.Oxidative medicine and cellular longevity · 2015Review
- Phenotypic rescue of a Drosophila model of mitochondrial ANT1 disease.Disease models & mechanisms · 2014Article
- Anticancer activity of the cholesterol exporter ABCA1 gene.Cell reports · 2012Article
- A mitochondrial etiology of Alzheimer and Parkinson disease.Biochimica et biophysica acta · 2012Review
- The therapeutic potential of mitochondrial channels in cancer, ischemia-reperfusion injury, and neurodegeneration.Mitochondrion · 2012Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
The mitochondrial adenine nucleotide translocators (Ant) are bi-functional proteins that transport ADP and ATP across the mitochondrial inner membrane, and regulate the mitochondrial permeability transition pore (mtPTP) which initiates apoptosis. The mouse has three Ant isoforms: Ant1 expressed in heart, muscle, and brain; Ant2 expressed in all tissues but muscle; and Ant4 expressed primarily in testis. Ant1-deficient mice manifest muscle and heart but not brain pathology. Brain Ant1 is induced by stress, while Ant2 is not. Ant1-deficient mice are resistant to death induced by systemic exposure to the brain excitotoxin, kainic acid (KA), and their hippocampal and cortical neurons are significantly more resistant to neuronal death induced by glutamate, KA, and etoposide. The mitochondrial membrane potential of Ant1-deficient brain mitochondria is increased and the mtPTP is more resistance to Ca(++) induced permeability transition. Hence, Ant1-deficiency may protect the brain from excitotoxicity by desensitizing the mtPTP and by blocking the pro-apoptotic induction of Ant1 by stress.
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