ArticleJournal of cell science2013
Evidence of a triosephosphate isomerase non-catalytic function crucial to behavior and longevity.
Article in Journal of cell science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
28 citing papers in PubMed, 37 citations in OpenAlex.
- Biophysical and biochemical studies support PHD inhibitor development as a TPI deficiency therapy.Journal of cell science · 2026Article
- Temporal- and sex-specific changes in proteasome-dependent and independent polyubiquitination in the amygdala during fear memory formation.Learning & memory (Cold Spring Harbor, N.Y.) · 2026Article
- Metabolites beyond metabolism: Exploring their atypical roles in protein modification and signaling transduction.Chinese medical journal · 2026Review
- Maternal slow-release nitrogen diets during late gestation optimize the energy metabolism in calves' skeletal muscle.PloS one · 2026Article
- Dysregulation of cellular metabolism within the gut-brain axis is associated with behavioural changes in chronic intestinal inflammation.Journal of neuroinflammation · 2025Article
- Molecular Adjustment to a Social Niche: Brain Transcriptomes Reveal Divergent Influence of Social Environment on the Two Queen Morphs of the Ant Temnothorax rugatulus.Molecular ecology · 2025Article
- Therapeutic and vaccinomic potential of moonlighting proteins for the discovery and design of drugs and vaccines against schistosomiasis.American journal of translational research · 2024Review
- C-Terminal Lysine Residue of Pneumococcal Triosephosphate Isomerase Contributes to Its Binding to Host Plasminogen.Microorganisms · 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
- Triosephosphate isomerase of Streptococcus pneumoniae is released extracellularly by autolysis and binds to host plasminogen to promote its activation.FEBS open bio · 2022Article
- Itavastatin and resveratrol increase triosephosphate isomerase protein in a newly identified variant of TPI deficiency.Disease models & mechanisms · 2022Article
- Impact of Maternal Feed Restriction at Different Stages of Gestation on the Proteomic Profile of the Newborn Skeletal Muscle.Animals : an open access journal from MDPI · 2022Article
- Identification of protein quality control regulators using a Drosophila model of TPI deficiency.Neurobiology of disease · 2021Article
- COX5A over-expression protects cortical neurons from hypoxic ischemic injury in neonatal rats associated with TPI up-regulation.BMC neuroscience · 2020Article
- Native aggregation is a common feature among triosephosphate isomerases of different species.Scientific reports · 2020Article
- Comparative Transcriptome Analysis ofFrontiers in immunology · 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
- Adaptive substitutions underlying cardiac glycoside insensitivity in insects exhibit epistasis in vivo.eLife · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Triosephosphate isomerase (TPI) is a glycolytic enzyme that converts dihydroxyacetone phosphate (DHAP) into glyceraldehyde 3-phosphate (GAP). Glycolytic enzyme dysfunction leads to metabolic diseases collectively known as glycolytic enzymopathies. Of these enzymopathies, TPI deficiency is unique in the severity of neurological symptoms. The Drosophila sugarkill mutant closely models TPI deficiency and encodes a protein prematurely degraded by the proteasome. This led us to question whether enzyme catalytic activity was crucial to the pathogenesis of TPI sugarkill neurological phenotypes. To study TPI deficiency in vivo we developed a genomic engineering system for the TPI locus that enables the efficient generation of novel TPI genetic variants. Using this system we demonstrate that TPI sugarkill can be genetically complemented by TPI encoding a catalytically inactive enzyme. Furthermore, our results demonstrate a non-metabolic function for TPI, the loss of which contributes significantly to the neurological dysfunction in this animal model.
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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.