ArticleCell research2015
FXYD2, a γ subunit of Na⁺, K⁺-ATPase, maintains persistent mechanical allodynia induced by inflammation.
Article in Cell research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 45 citations in OpenAlex.
- Direct cellular contact byScience advances · 2026Article
- The functions of FXYD family members in human health and disease.Genes & diseases · 2026Review
- Systemic delivery of drug-free polymeric nanoparticles reprograms innate immunity in a sex-dependent manner after spinal cord injury.bioRxiv : the preprint server for biology · 2026Article
- Knockdown of FXYD2 inhibits mepivacaine-induced cardiomyocyte injury by activating the PI3K/AKT signaling pathway.European journal of medical research · 2025Article
- FXYD2 marks and regulates maturity of β cells via ion channel-mediated signal transduction.Nature communications · 2025Article
- NaResearch (Washington, D.C.) · 2025Article
- Evaluation of the neuroprotective potential of benzylidene digoxin 15 against oxidative stress in a neuroinflammation models induced by lipopolysaccharide and on neuronal differentiation of hippocampal neural precursor cells.Frontiers in pharmacology · 2025Article
- Inflammatory Alterations to Renal Lymphatic Endothelial Cell Gene Expression in Mouse Models of Hypertension.Kidney & blood pressure research · 2024Article
- Identification of FXYD6 as the novel biomarker for glioma based on differential expression and DNA methylation.Cancer medicine · 2023Article
- Low Dopamine D2 Receptor Expression Drives Gene Networks Related to GABA, cAMP, Growth and Neuroinflammation in Striatal Indirect Pathway Neurons.Biological psychiatry global open science · 2023Article
- Single cell multiomic analysis reveals diabetes-associated β-cell heterogeneity driven by HNF1A.Nature communications · 2023Article
- FXYD2 antisense oligonucleotide provides an efficient approach for long-lasting relief of chronic peripheral pain.JCI insight · 2023Article
- A human coronavirus OC43-derived polypeptide causes neuropathic pain.EMBO reports · 2022Article
- The Development of Mechanical Allodynia in Diabetic Rats Revealed by Single-Cell RNA-Seq.Frontiers in molecular neuroscience · 2022Article
- FXYD2 mRNA expression represents a new independent factor that affects survival of glioma patients and predicts chemosensitivity of patients to temozolomide.BMC neurology · 2021Article
- Effect of a purine derivative containing selenium to improve memory decline and anxiety through modulation of the cholinergic system and NaMetabolic brain disease · 2021Article
- A NaFrontiers in cell and developmental biology · 2021Article
- Application of Proteomics and Metabonomics to Reveal the Molecular Basis of Atractylodis Macrocephalae Rhizome for Ameliorating Hypothyroidism Instead of Hyperthyroidism.Frontiers in pharmacology · 2021Article
- Deletion of the Gene Encoding the NMDA Receptor GluN1 Subunit in Schwann Cells Causes Ultrastructural Changes in Remak Bundles and Hypersensitivity in Pain Processing.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Beta Cell Imaging-From Pre-Clinical Validation to First in Man Testing.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Na⁺, K⁺-ATPase (NKA) is required to generate the resting membrane potential in neurons. Nociceptive afferent neurons express not only the α and β subunits of NKA but also the γ subunit FXYD2. However, the neural function of FXYD2 is unknown. The present study shows that FXYD2 in nociceptive neurons is necessary for maintaining the mechanical allodynia induced by peripheral inflammation. FXYD2 interacted with α1NKA and negatively regulated the NKA activity, depolarizing the membrane potential of nociceptive neurons. Mechanical allodynia initiated in FXYD2-deficient mice was abolished 4 days after inflammation, whereas it persisted for at least 3 weeks in wild-type mice. Importantly, the FXYD2/α1NKA interaction gradually increased after inflammation and peaked on day 4 post inflammation, resulting in reduction of NKA activity, depolarization of neuron membrane and facilitation of excitatory afferent neurotransmission. Thus, the increased FXYD2 activity may be a fundamental mechanism underlying the persistent hypersensitivity to pain induced by inflammation.
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