ArticleBiochimica et biophysica acta2015
Triosephosphate isomerase I170V alters catalytic site, enhances stability and induces pathology in a Drosophila model of TPI deficiency.
Article in Biochimica et biophysica acta, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 36 citations in OpenAlex.
- Emergence of specific binding and catalysis from a designed generalist binding protein.Nature chemistry · 2026Article
- Biophysical and biochemical studies support PHD inhibitor development as a TPI deficiency therapy.Journal of cell science · 2026Article
- The Remarkable Role of Triosephosphate Isomerase in Diabetes Pathophysiology.International journal of molecular sciences · 2025Review
- LKB1-Dependent Regulation of TPI1 Creates a Divergent Metabolic Liability between Human and Mouse Lung Adenocarcinoma.Cancer discovery · 2023Article
- Newly discovered roles of triosephosphate isomerase including functions within the nucleus.Molecular medicine (Cambridge, Mass.) · 2023Review
- Triose-phosphate isomerase deficiency is associated with a dysregulation of synaptic vesicle recycling inFrontiers in synaptic neuroscience · 2023Article
- Itavastatin and resveratrol increase triosephosphate isomerase protein in a newly identified variant of TPI deficiency.Disease models & mechanisms · 2022Article
- A High-Content Screening Assay for Small Molecules That Stabilize Mutant Triose Phosphate Isomerase (TPI) as Treatments for TPI Deficiency.SLAS discovery : advancing life sciences R & D · 2021Article
- Novel and selective inactivators of Triosephosphate isomerase with anti-trematode activity.Scientific reports · 2020Article
- Low catalytic activity is insufficient to induce disease pathology in triosephosphate isomerase deficiency.Journal of inherited metabolic disease · 2019Article
- Missense variant in TPI1 (Arg189Gln) causes neurologic deficits through structural changes in the triosephosphate isomerase catalytic site and reduced enzyme levels in vivo.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
- Active-Site Glu165 Activation in Triosephosphate Isomerase and Its Deprotonation Kinetics.The journal of physical chemistry. B · 2019Article
- Protein coding mitochondrial-targeted RNAs rescue mitochondrial disease in vivo.Neurobiology of disease · 2018Article
- Enzyme Architecture: Modeling the Operation of a Hydrophobic Clamp in Catalysis by Triosephosphate Isomerase.Journal of the American Chemical Society · 2017Article
- Natural Products as New Treatment Options for Trichomoniasis: A Molecular Docking Investigation.Scientia pharmaceutica · 2017Article
- Structural and Genetic Studies Demonstrate Neurologic Dysfunction in Triosephosphate Isomerase Deficiency Is Associated with Impaired Synaptic Vesicle Dynamics.PLoS genetics · 2016Article
- New strategy for drug discovery by large-scale association analysis of molecular networks of different species.Scientific reports · 2016Article
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11 authors at 2 institutions in 1 country.
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Abstract
Triosephosphate isomerase (TPI) is a glycolytic enzyme which homodimerizes for full catalytic activity. Mutations of the TPI gene elicit a disease known as TPI Deficiency, a glycolytic enzymopathy noted for its unique severity of neurological symptoms. Evidence suggests that TPI Deficiency pathogenesis may be due to conformational changes of the protein, likely affecting dimerization and protein stability. In this report, we genetically and physically characterize a human disease-associated TPI mutation caused by an I170V substitution. Human TPI(I170V) elicits behavioral abnormalities in Drosophila. An examination of hTPI(I170V) enzyme kinetics revealed this substitution reduced catalytic turnover, while assessments of thermal stability demonstrated an increase in enzyme stability. The crystal structure of the homodimeric I170V mutant reveals changes in the geometry of critical residues within the catalytic pocket. Collectively these data reveal new observations of the structural and kinetic determinants of TPI Deficiency pathology, providing new insights into disease pathogenesis.
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