ArticleThe Journal of biological chemistry2009
Live cell analysis of aquaporin-4 m1/m23 interactions and regulated orthogonal array assembly in glial cells.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06857136 (The Role of the Glymphatic System Avaluated Thourgh mr Imaging in the Diagnosis and Management of NPH), which is not on this map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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.
The Role of the Glymphatic System Avaluated Thourgh mr Imaging in the Diagnosis and Management of NPH
Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.
- Mechanisms Underlying Aquaporin-4 Subcellular Mislocalization in Epilepsy.Frontiers in cellular neuroscience · 2022Pooled it
- Aquaporin-4 Dysfunction in Depression: From Pathogenic Mechanisms to Novel Therapeutic Targeting.International journal of molecular sciences · 2026Review
- Article
- Non-coding RNAs and Aquaporin 4: Their Role in the Pathogenesis of Neurological Disorders.Neurochemical research · 2024Review
- AQP4 is an Emerging Regulator of Pathological Pain: A Narrative Review.Cellular and molecular neurobiology · 2023Review
- Pathogenic myelin-specific antibodies in multiple sclerosis target conformational proteolipid protein 1-anchored membrane domains.The Journal of clinical investigation · 2023Article
- T follicular helper cells contribute to pathophysiology in a model of neuromyelitis optica spectrum disorders.JCI insight · 2023Article
- Review
- Aquaporin-4 in Neuromyelitis Optica Spectrum Disorders: A Target of Autoimmunity in the Central Nervous System.Biomolecules · 2022Review
- Signaling Mechanisms and Pharmacological Modulators Governing Diverse Aquaporin Functions in Human Health and Disease.International journal of molecular sciences · 2022Review
- Cerebral microinfarct is emergency consequence of Alzheimer's disease: a new insight into development of neurodegenerative diseases.International journal of biological sciences · 2022Review
- Molecular Level Characterization of Circulating Aquaporin-4 Antibodies in Neuromyelitis Optica Spectrum Disorder.Neurology(R) neuroimmunology & neuroinflammation · 2021Article
- Review
- Instability of aquaglyceroporin (AQP) 2 contributes to drug resistance in Trypanosoma brucei.PLoS neglected tropical diseases · 2020Article
- Article
- Degradation of connexin 50 protein causes waterclefts in human lens.Open medicine (Warsaw, Poland) · 2020Article
- Membrane assembly of aquaporin-4 autoantibodies regulates classical complement activation in neuromyelitis optica.The Journal of clinical investigation · 2019Article
- AQP4ex is crucial for the anchoring of AQP4 at the astrocyte end-feet and for neuromyelitis optica antibody binding.Acta neuropathologica communications · 2019Article
- Review
- The aquaporin-4 water channel as a potential drug target in neurological disorders.Expert opinion on therapeutic targets · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Aquaporin-4 (AQP4) can assemble into supramolecular aggregates called orthogonal arrays of particles (OAPs). In cells expressing single AQP4 isoforms, we found previously that OAP formation by AQP4-M23 requires N terminus interactions just downstream of Met-23 and that the inability of AQP4-M1 to form OAPs involves blocking by residues upstream of Met-23. Here, we studied M1/M23 interactions and regulated OAP assembly by nanometer-resolution tracking of quantum dot-labeled AQP4 in live cells expressing differentially tagged AQP4 isoforms and in primary glial cell cultures in which native AQP4 was labeled with a monoclonal recombinant neuromyelitis optica autoantibody. OAP assembly was assessed independently by Blue Native gel electrophoresis. We found that OAPs in native glial cells could be reproduced in transfected cells expressing equal amounts of AQP4-M1 and -M23. Mutants of M23 that do not themselves form OAPs, including M23-F26Q and M23-G28P, were able to fully co-associate with native M23 to form large immobile OAPs. Analysis of a palmitoylation-null M1 mutant (C13A/C17A) indicated palmitoylation-dependent OAP assembly only in the presence of M23, with increased M1 palmitoylation causing progressive OAP disruption. Differential regulation of OAP assembly by palmitoylation, calcium elevation, and protein kinase C activation was found in primary glial cell cultures. We conclude that M1 and M23 co-assemble in AQP4 OAPs and that specific signaling events can regulate OAP assembly in glial cells.
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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.