ArticleJournal of cell science2009
Determinants of aquaporin-4 assembly in orthogonal arrays revealed by live-cell single-molecule fluorescence imaging.
Article in Journal of cell science, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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.
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Who cites it
60 citing papers in PubMed, 89 citations in OpenAlex.
- Dynamic characterization of pathological and functional deterioration in a mouse model of optic neuritis related to neuromyelitis optica spectrum disorder.Neural regeneration research · 2026Article
- Aquaporin-4 Dysfunction in Depression: From Pathogenic Mechanisms to Novel Therapeutic Targeting.International journal of molecular sciences · 2026Review
- Structural basis of aquaporin-4 autoantibody binding in neuromyelitis optica.Science advances · 2025Article
- Development of perivascular astrocyte processes.Frontiers in neuroscience · 2025Review
- Structural Basis of Aquaporin-4 Autoantibody Binding in Neuromyelitis Optica.bioRxiv : the preprint server for biology · 2024Article
- Thermodynamics andThe journal of physical chemistry. B · 2024Article
- Aquaporins and Ion Channels as Dual Targets in the Design of Novel Glioblastoma Therapeutics to Limit Invasiveness.Cancers · 2023Review
- Evaluation of gliovascular functions of AQP4 readthrough isoforms.Frontiers in cellular neuroscience · 2023Article
- AQP4-A25Q Point Mutation in Mice Depolymerizes Orthogonal Arrays of Particles and Decreases Polarized Expression of AQP4 Protein in Astrocytic Endfeet at the Blood-Brain Barrier.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Review
- Strategies to Screen Anti-AQP4 Antibodies from Yeast Surface Display Libraries.Antibodies (Basel, Switzerland) · 2022Article
- Aquaporin-4 in Neuromyelitis Optica Spectrum Disorders: A Target of Autoimmunity in the Central Nervous System.Biomolecules · 2022Review
- Review
- Membrane assembly of aquaporin-4 autoantibodies regulates classical complement activation in neuromyelitis optica.The Journal of clinical investigation · 2019Article
- Article
- Blood-Brain Barrier Damage as the Starting Point of Leukoaraiosis Caused by Cerebral Chronic Hypoperfusion and Its Involved Mechanisms: Effect of Agrin and Aquaporin-4.BioMed research international · 2018Article
- The aquaporin-4 water channel as a potential drug target in neurological disorders.Expert opinion on therapeutic targets · 2017Review
- AQP4e-Based Orthogonal Arrays Regulate Rapid Cell Volume Changes in Astrocytes.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Aquaporin Protein-Protein Interactions.International journal of molecular sciences · 2017Review
- Aquaporin 4 Forms a Macromolecular Complex with Glutamate Transporter 1 and Mu Opioid Receptor in Astrocytes and Participates in Morphine Dependence.Journal of molecular neuroscience : MN · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
We investigated the molecular determinants of aquaporin-4 (AQP4) assembly in orthogonal arrays of particles (OAPs) by visualizing fluorescently labeled AQP4 mutants in cell membranes using quantum-dot single-particle tracking and total internal reflection fluorescence microscopy. The full-length ;long' (M1) form of AQP4 diffused freely in membranes and did not form OAPs, whereas the ;short' (M23) form of AQP4 formed OAPs and was nearly immobile. Analysis of AQP4 deletion mutants revealed progressive disruption of OAPs by the addition of three to seven residues at the AQP4-M23 N-terminus, with polyalanines as effective as native AQP4 fragments. OAPs disappeared upon downstream deletions of AQP4-M23, which, from analysis of point mutants, involves N-terminus interactions of residues Val24, Ala25 and Phe26. OAP formation was also prevented by introducing proline residues at sites just downstream from the hydrophobic N-terminus of AQP4-M23. AQP1, an AQP4 homolog that does not form OAPs, was induced to form OAPs upon replacement of its N-terminal domain with that of AQP4-M23. Our results indicate that OAP formation by AQP4-M23 is stabilized by hydrophobic intermolecular interactions involving N-terminus residues, and that absence of OAPs in AQP4-M1 results from non-selective blocking of this interaction by seven residues just upstream from Met23.
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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.