ArticleProceedings of the National Academy of Sciences of the United States of America1997
Transglutaminase-catalyzed inactivation of glyceraldehyde 3-phosphate dehydrogenase and alpha-ketoglutarate dehydrogenase complex by polyglutamine domains of pathological length.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. 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, 92 citations in OpenAlex.
- Transglutaminase 2 in diabetes mellitus: Unraveling its multifaceted role and therapeutic implications for vascular complications.Theranostics · 2024Review
- Article
- The vicious cycle between transglutaminase 2 and reactive oxygen species in hyperglycemic memory-induced endothelial dysfunction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Brain Energy and Oxygen Metabolism: Emerging Role in Normal Function and Disease.Frontiers in molecular neuroscience · 2018Review
- Novel Metabolic Abnormalities in the Tricarboxylic Acid Cycle in Peripheral Cells From Huntington's Disease Patients.PloS one · 2016Article
- BMP2 cross-linked by transglutaminase 2 to collagen-plla scaffold promotes osteogenic differentiation in mesenchymal stem cells.Biotechnology letters · 2014Article
- Biological functionalities of transglutaminase 2 and the possibility of its compensation by other members of the transglutaminase family.TheScientificWorldJournal · 2014Review
- Induction of chondrogenic differentiation in mesenchymal stem cells by TGF-beta cross-linked to collagen-PLLA [poly(L-lactic acid)] scaffold by transglutaminase 2.Biotechnology letters · 2013Article
- Factors Affecting Aggregate Formation in Cell Models of Huntington's Disease and Amyotrophic Lateral Sclerosis.Acta naturae · 2013Article
- γ-Glutamylamines and neurodegenerative diseases.Amino acids · 2013Review
- Déjà vu with a twist: transglutaminases in bioenergetics and transcriptional dysfunction in Huntington's disease.EMBO molecular medicine · 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
- Transglutaminase activation in neurodegenerative diseases.Future neurology · 2009Article
- Transglutaminases and neurodegeneration.Journal of neurochemistry · 2009Review
- Article
- Mutant huntingtin: nuclear translocation and cytotoxicity mediated by GAPDH.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Transglutaminase activity is present in highly purified nonsynaptosomal mouse brain and liver mitochondria.Biochemistry · 2005Article
- The alpha-ketoglutarate-dehydrogenase complex: a mediator between mitochondria and oxidative stress in neurodegeneration.Molecular neurobiology · 2005Review
- The energetics of Huntington's disease.Neurochemical research · 2004Review
- Structural characterization of transglutaminase-catalyzed cross-linking between glyceraldehyde 3-phosphate dehydrogenase and polyglutamine repeats.Protein science : a publication of the Protein Society · 2003Article
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
Abstract
Several adult-onset neurodegenerative diseases are caused by genes with expanded CAG triplet repeats within their coding regions and extended polyglutamine (Qn) domains within the expressed proteins. Generally, in clinically affected individuals n >/= 40. Glyceraldehyde 3-phosphate dehydrogenase binds tightly to four Qn disease proteins, but the significance of this interaction is unknown. We now report that purified glyceraldehyde 3-phosphate dehydrogenase is inactivated by tissue transglutaminase in the presence of glutathione S-transferase constructs containing a Qn domain of pathological length (n = 62 or 81). The dehydrogenase is less strongly inhibited by tissue transglutaminase in the presence of constructs containing shorter Qn domains (n = 0 or 10). Purified alpha-ketoglutarate dehydrogenase complex also is inactivated by tissue transglutaminase plus glutathione S-transferase constructs containing pathological-length Qn domains (n = 62 or 81). The results suggest that tissue transglutaminase-catalyzed covalent linkages involving the larger poly-Q domains may disrupt cerebral energy metabolism in CAG/Qn expansion diseases.
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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.