ArticleThe Journal of biological chemistry2010
Nucleoside diphosphate kinase B knock-out mice have impaired activation of the K+ channel KCa3.1, resulting in defective T cell activation.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.
- Mechanisms of non-metastatic 2 (NME2)-mediated control of metastasis across tumor types.Naunyn-Schmiedeberg's archives of pharmacology · 2011Pooled it
- Kcnn4 Knockout Induces Salivary Gland Fibrosis, Immune Cell Infiltration, and B-Cell Dysfunction in Mice.Chemical biology & drug design · 2026Article
- Early Cardiomyopathy in Prediabetic NDPK-B-Deficient Mice Is Associated with Remodeling of the Mitochondrial O-GlcNAc Proteome.International journal of molecular sciences · 2026Article
- Disrupting VE-cadherin Y685 phosphorylation inhibits development of experimental diabetic and prediabetic retinopathy.The Journal of clinical investigation · 2026Article
- Deficiency in nucleoside diphosphate kinase B leads to endothelial activation of the hexosamine biosynthesis pathway and cardiac dysfunction.Cardiovascular diabetology · 2025Article
- Kinase-catalyzed biotinylation for discovery and validation of substrates to multispecificity kinases NME1 and NME2.The Journal of biological chemistry · 2024Article
- Histidine Phosphorylation: Protein Kinases and Phosphatases.International journal of molecular sciences · 2024Review
- Histidine dephosphorylation of the Gβ protein GPB-1 promotes axon regeneration in C. elegans.EMBO reports · 2022Article
- Biomarkers of connective tissue disease-associated interstitial lung disease in bronchoalveolar lavage fluid: A label-free mass spectrometry-based relative quantification study.Journal of clinical laboratory analysis · 2022Article
- Loss of the Metastasis Suppressor NME1, But Not of Its Highly Related Isoform NME2, Induces a Hybrid Epithelial-Mesenchymal State in Cancer Cells.International journal of molecular sciences · 2021Article
- Emerging Molecular Connections between NM23 Proteins, Telomeres and Telomere-Associated Factors: Implications in Cancer Metastasis and Ageing.International journal of molecular sciences · 2021Review
- Article
- NME/NM23/NDPK and Histidine Phosphorylation.International journal of molecular sciences · 2020Review
- Role of the Ang2-Tie2 Axis in Vascular Damage Driven by High Glucose or Nucleoside Diphosphate Kinase B Deficiency.International journal of molecular sciences · 2020Article
- A Compartmentalized Reduction in Membrane-Proximal Calmodulin Reduces the Immune Surveillance Capabilities of CD8Frontiers in pharmacology · 2020Article
- The Function of NM23-H1/NME1 and Its Homologs in Major Processes Linked to Metastasis.Pathology oncology research : POR · 2020Review
- Green Tea Polyphenol-Sensitive Calcium Signaling in Immune T Cell Function.Frontiers in nutrition · 2020Review
- KJournal of the American Heart Association · 2019Article
- NME proteins regulate class switch recombination.FEBS letters · 2019Article
- Histone Deacetylases Enhance CaInternational journal of molecular sciences · 2018Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Nucleoside diphosphate kinases (NDPKs) are encoded by the Nme (non-metastatic cell) gene family. Although they comprise a family of 10 genes, NDPK-A and -B are ubiquitously expressed and account for most of the NDPK activity. We previously showed that NDPK-B activates the K(+) channel KCa3.1 via histidine phosphorylation of the C terminus of KCa3.1, which is required for T cell receptor-stimulated Ca(2+) flux and proliferation of activated naive human CD4 T cells. We now report the phenotype of NDPK-B(-/-) mice. NDPK-B(-/-) mice are phenotypically normal at birth with a normal life span. Although T and B cell development is normal in NDPK-B(-/-) mice, KCa3.1 channel activity and cytokine production are markedly defective in T helper 1 (Th1) and Th2 cells, whereas Th17 function is normal. These findings phenocopy studies in the same cells isolated from KCa3.1(-/-) mice and thereby support genetically that NDPK-B functions upstream of KCa3.1. NDPK-A and -B have been linked to an astonishing array of disparate cellular and biochemical functions, few of which have been confirmed in vivo in physiological relevant systems. NDPK-B(-/-) mice will be an essential tool with which to definitively address the biological functions of NDPK-B. Our finding that NDPK-B is required for activation of Th1 and Th2 CD4 T cells, together with the normal overall phenotype of NDPK-B(-/-) mice, suggests that specific pharmacological inhibitors of NDPK-B may provide new opportunities to treat Th1- and Th2-mediated autoimmune diseases.
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