ArticleGenetics2008
Degradation of functional triose phosphate isomerase protein underlies sugarkill pathology.
Article in Genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Article
- Discovery and validation of small molecule stabilizers of mutant triose phosphate isomerase (TPI) as potential lead candidates for TPI deficiency.SLAS discovery : advancing life sciences R & D · 2025Article
- Triose-phosphate isomerase deficiency is associated with a dysregulation of synaptic vesicle recycling inFrontiers in synaptic neuroscience · 2023Article
- TPI1 activates the PI3K/AKT/mTOR signaling pathway to induce breast cancer progression by stabilizing CDCA5.Journal of translational medicine · 2022Article
- Itavastatin and resveratrol increase triosephosphate isomerase protein in a newly identified variant of TPI deficiency.Disease models & mechanisms · 2022Article
- Murine model of triosephosphate isomerase deficiency with anemia and severe neuromuscular dysfunction.Current research in neurobiology · 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
- Identification of protein quality control regulators using a Drosophila model of TPI deficiency.Neurobiology of disease · 2021Article
- Pilot Evaluation of TwoMolecules (Basel, Switzerland) · 2020Article
- 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
- Flux Control in Glycolysis Varies Across the Tree of Life.Journal of molecular evolution · 2016Article
- Structural and Genetic Studies Demonstrate Neurologic Dysfunction in Triosephosphate Isomerase Deficiency Is Associated with Impaired Synaptic Vesicle Dynamics.PLoS genetics · 2016Article
- Molecular identification, immunolocalization, and characterization of Clonorchis sinensis triosephosphate isomerase.Parasitology research · 2015Article
- Proteomic Analysis Reveals PGAM1 Altering cis-9, trans-11 Conjugated Linoleic Acid Synthesis in Bovine Mammary Gland.Lipids · 2015Article
- Triosephosphate isomerase I170V alters catalytic site, enhances stability and induces pathology in a Drosophila model of TPI deficiency.Biochimica et biophysica acta · 2015Article
- Article
- Evidence of a triosephosphate isomerase non-catalytic function crucial to behavior and longevity.Journal of cell science · 2013Article
- Early mitochondrial dysfunction leads to altered redox chemistry underlying pathogenesis of TPI deficiency.Neurobiology of disease · 2013Article
- A novel Drosophila SOD2 mutant demonstrates a role for mitochondrial ROS in neurodevelopment and disease.Brain and behavior · 2012Article
- Modes of metabolic compensation during mitochondrial disease using the Drosophila model of ATP6 dysfunction.PloS one · 2011Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Triose phosphate isomerase (TPI) deficiency glycolytic enzymopathy is a progressive neurodegenerative condition that remains poorly understood. The disease is caused exclusively by specific missense mutations affecting the TPI protein and clinically features hemolytic anemia, adult-onset neurological impairment, degeneration, and reduced longevity. TPI has a well-characterized role in glycolysis, catalyzing the isomerization of dihydroxyacetone phosphate (DHAP) to glyceraldehyde-3-phosphate (G3P); however, little is known mechanistically about the pathogenesis associated with specific recessive mutations that cause progressive neurodegeneration. Here, we describe key aspects of TPI pathogenesis identified using the TPI(sugarkill) mutation, a Drosophila model of human TPI deficiency. Specifically, we demonstrate that the mutant protein is expressed, capable of forming a homodimer, and is functional. However, the mutant protein is degraded by the 20S proteasome core leading to loss-of-function pathogenesis.
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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.