ArticleNeurochemical research2005
Mitochondrial aconitase is a transglutaminase 2 substrate: transglutamination is a probable mechanism contributing to high-molecular-weight aggregates of aconitase and loss of aconitase activity in Huntington disease brain.
Article in Neurochemical research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 45 citations in OpenAlex.
- Mitochondrial Aconitase and Its Contribution to the Pathogenesis of Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Genome-Wide Identification and Expression Profiling of Aconitase Gene Family Members Reveals Their Roles in Plant Development and Adaptation to Diverse Stress inPlants (Basel, Switzerland) · 2022Article
- The protective role of exercise against age-related neurodegeneration.Ageing research reviews · 2022Review
- Brain Energy and Oxygen Metabolism: Emerging Role in Normal Function and Disease.Frontiers in molecular neuroscience · 2018Review
- Altered Aconitase 2 Activity in Huntington's Disease Peripheral Blood Cells and Mouse Model Striatum.International journal of molecular sciences · 2017Article
- Towards an Understanding of Energy Impairment in Huntington's Disease Brain.Journal of Huntington's disease · 2017Review
- Polyglutamine toxicity in yeast induces metabolic alterations and mitochondrial defects.BMC genomics · 2015Article
- Enhanced neuronal glucose transporter expression reveals metabolic choice in a HD Drosophila model.PloS one · 2015Article
- Transglutaminase regulation of cell function.Physiological reviews · 2014Review
- A possible role of transglutaminase 2 in the nucleus of INS-1E and of cells of human pancreatic islets.Journal of proteomics · 2014Article
- Aconitase post-translational modification as a key in linkage between Krebs cycle, iron homeostasis, redox signaling, and metabolism of reactive oxygen species.Redox report : communications in free radical research · 2014Review
- Tissue transglutaminase overexpression does not modify the disease phenotype of the R6/2 mouse model of Huntington's disease.Experimental neurology · 2012Article
- Cellular functions of tissue transglutaminase.International review of cell and molecular biology · 2012Review
- Anti-inflammatory effects of the R2 peptide, an inhibitor of transglutaminase 2, in a mouse model of allergic asthma, induced by ovalbumin.British journal of pharmacology · 2011Article
- Diurnal changes in mitochondrial function reveal daily optimization of light and dark respiratory metabolism in Arabidopsis.Molecular & cellular proteomics : MCP · 2010Article
- Cause and consequence: mitochondrial dysfunction initiates and propagates neuronal dysfunction, neuronal death and behavioral abnormalities in age-associated neurodegenerative diseases.Biochimica et biophysica acta · 2010Review
- Dissecting the mechanisms of tissue transglutaminase-induced cross-linking of alpha-synuclein: implications for the pathogenesis of Parkinson disease.The Journal of biological chemistry · 2009Article
- Aconitate hydratase of mammals under oxidative stress.Biochemistry. Biokhimiia · 2008Review
- Transglutaminase activity is present in highly purified nonsynaptosomal mouse brain and liver mitochondria.Biochemistry · 2005Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Transglutaminase activity was found to be present in highly purified non-synaptosomal rat brain mitochondria. A 78-kDa protein in these organelles was shown to be a transglutaminase 2 substrate, and incubation of a non-synaptosomal mitochondrial lysate with transglutaminase 2 yielded high-Mr proteins. The 78-kDa protein was identified as mitochondrial aconitase by MALDI-TOF analysis. Aconitase activity was decreased in a dose-dependent manner when non-synaptosomal rat brain mitochondria were incubated with transglutaminase 2. Transglutaminase activity is increased about 2-fold in the mitochondrial fraction of HD caudate. Moreover, Western blotting of the mitochondrial fraction revealed that most of the mitochondrial aconitase in HD caudate is present as high-Mr aggregates. Aconitase activity was previously shown to be decreased in Huntington disease (HD) caudate (a region severely damaged by the disease). The present findings suggest that an increase of transglutaminase activity in HD caudate may contribute to mitochondrial dysfunction by incorporating aconitase into inactive polymers.
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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.