ArticleNature communications2022
Glycolytic flux control by drugging phosphoglycolate phosphatase.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 11 citations in OpenAlex.
- Integrated Multi-Omic Analyses Reveal Gender-Specific Molecular Mechanisms Regulating Growth and Muscle Development in Zhongshan Partridge Ducks.Biomolecules · 2026Article
- Metabolic rewiring driven by phosphoglycolate phosphatase deletion inhibits ferroptosis.Science advances · 2026Article
- Suppressing Glycerol-3-phosphate Phosphatase and Enhancing Glycerol-3-Phosphate Shuttle Flux Crucial for High-Efficiency Fatty Acid Production in the Fast-Growing Oleaginous Schizochytrium.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Tumor microenvironment responsive Mn-based nanoplatform activate cGAS-STING pathway combined with metabolic interference for enhanced anti-tumor therapy.Journal of nanobiotechnology · 2025Article
- NMR-based metabolomics identification of potential serum biomarkers of disease progression in patients with multiple sclerosis.Scientific reports · 2024Article
- Article
- Glycolytic flux control by drugging phosphoglycolate phosphatase.Nature communications · 2022Article
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Targeting the intrinsic metabolism of immune or tumor cells is a therapeutic strategy in autoimmunity, chronic inflammation or cancer. Metabolite repair enzymes may represent an alternative target class for selective metabolic inhibition, but pharmacological tools to test this concept are needed. Here, we demonstrate that phosphoglycolate phosphatase (PGP), a prototypical metabolite repair enzyme in glycolysis, is a pharmacologically actionable target. Using a combination of small molecule screening, protein crystallography, molecular dynamics simulations and NMR metabolomics, we discover and analyze a compound (CP1) that inhibits PGP with high selectivity and submicromolar potency. CP1 locks the phosphatase in a catalytically inactive conformation, dampens glycolytic flux, and phenocopies effects of cellular PGP-deficiency. This study provides key insights into effective and precise PGP targeting, at the same time validating an allosteric approach to control glycolysis that could advance discoveries of innovative therapeutic candidates.
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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.