ArticleThe Biochemical journal2020
Biochemical and transcript level differences between the three human phosphofructokinases show optimisation of each isoform for specific metabolic niches.
Article in The Biochemical journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 55 citations in OpenAlex.
- A Tarui Disease Phenotype with Compensated Hemolysis and a HomozygousJournal of clinical medicine · 2026Article
- A covalent PFKL activator suppresses tumor growth.Nature chemical biology · 2026Article
- Proteomic Profiling of Primary Hippocampal Neurons Reveals Noncanonical GFAP Expression and Metabolic Adaptations in Glia-Free Culture.Proteomics · 2026Article
- Article
- First-in-Class Covalent Inhibitors of PFKFB3: Discovery and Characterization in PDAC Models.Journal of medicinal chemistry · 2026Article
- High-Speed AFM Reveals Ligand-Dependent Supramolecular Switching of Human Phosphofructokinase-1.Research square · 2026Article
- Unveiling lactylation: A novel frontier in the pathogenesis of diabetic nephropathy (Review).International journal of molecular medicine · 2026Review
- USP7 facilitates brain tumor survival upon glucose deprivation by regulating phosphofructokinase muscle-type nuclear translocation in mice.PLoS biology · 2026Article
- Bidirectional allosteric ligand regulation in a central glycolytic enzyme.bioRxiv : the preprint server for biology · 2026Article
- PFKM governs metabolic shifts throughout skeletal muscle differentiation.Nature metabolism · 2026Article
- PFKP in malignant tumors: bridging metabolic reprogramming, post-translational modifications, and the immunosuppressive microenvironment.Frontiers in cell and developmental biology · 2026Review
- Functional requirements of the liver isoform of phosphofructokinase-1 in breast cancer cell migration.Journal of cell science · 2025Article
- Spatial Partitioning of Core Glycolysis Enables Tissue-Specific Metabolic Programs In Vivo.bioRxiv : the preprint server for biology · 2025Article
- Activity-dependent citrate dynamics in neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The noncanonical function of liver-type phosphofructokinase potentiates the efficacy of HDAC inhibitors in cancer.Signal transduction and targeted therapy · 2025Article
- A Covalent PFKL Activator Suppresses Tumor Growth.bioRxiv : the preprint server for biology · 2025Article
- Phosphofructokinase-1 redefined: a metabolic hub orchestrating cancer hallmarks through multi-dimensional control networks.Journal of translational medicine · 2025Review
- PFKM phosphorylates histone H3 and promotes mitotic progression by sensing the levels of citrate.Nature communications · 2025Article
- The role of gene duplication and paralog specialisation in the evolution of the mammalian PRPS complex.Nature communications · 2025Article
- Glycolytic control proteins in urinary extracellular vesicles are elevated during kidney transplant T cell-mediated rejection.BMC nephrology · 2025Observational
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5 authors at 1 institution in 1 country.
Funding
Abstract
6-Phosphofructokinase-1-kinase (PFK) tetramers catalyse the phosphorylation of fructose 6-phosphate (F6P) to fructose 1,6-bisphosphate (F16BP). Vertebrates have three PFK isoforms (PFK-M, PFK-L, and PFK-P). This study is the first to compare the kinetics, structures, and transcript levels of recombinant human PFK isoforms. Under the conditions tested PFK-M has the highest affinities for F6P and ATP (K0.5ATP 152 µM; K0.5F6P 147 µM), PFK-P the lowest affinities (K0.5ATP 276 µM; K0.5F6P 1333 µM), and PFK-L demonstrates a mixed picture of high ATP affinity and low F6P affinity (K0.5ATP 160 µM; K0.5F6P 1360 µM). PFK-M is more resistant to ATP inhibition compared with PFK-L and PFK-P (respectively, 23%, 31%, 50% decreases in specificity constants). GTP is an alternate phospho donor. Interface 2, which regulates the inactive dimer to active tetramer equilibrium, differs between isoforms, resulting in varying tetrameric stability. Under the conditions tested PFK-M is less sensitive to fructose 2,6-bisphosphate (F26BP) allosteric modulation than PFK-L or PFK-P (allosteric constants [K0.5ATP+F26BP/K0.5ATP] 1.10, 0.92, 0.54, respectively). Structural analysis of two allosteric sites reveals one may be specialised for AMP/ADP and the other for smaller/flexible regulators (citrate or phosphoenolpyruvate). Correlations between PFK-L and PFK-P transcript levels indicate that simultaneous expression may expand metabolic capacity for F16BP production whilst preserving regulatory capabilities. Analysis of cancer samples reveals intriguing parallels between PFK-P and PKM2 (pyruvate kinase M2), and simultaneous increases in PFK-P and PFKFB3 (responsible for F26BP production) transcript levels, suggesting prioritisation of metabolic flexibility in cancers. Our results describe the kinetic and transcript level differences between the three PFK isoforms, explaining how each isoform may be optimised for distinct roles.
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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.