ArticleThe Journal of cell biology2014
Aggregation state determines the localization and function of M1- and M23-aquaporin-4 in astrocytes.
Article in The Journal of cell biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
80 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mechanisms Underlying Aquaporin-4 Subcellular Mislocalization in Epilepsy.Frontiers in cellular neuroscience · 2022Pooled it
- Central nervous system lymphatic network: from the maintenance of brain homeostasis to emerging therapeutic perspectives in neurodegenerative diseases.Translational neurodegeneration · 2026Review
- Agomelatine Targets Aquaporin-4 Polarization to Rescue Glymphatic Dysfunction in Parkinson's Disease.Neuroscience bulletin · 2026Article
- Supramolecular aggregation of aquaporin-4 shapes astrocyte collective migration and mechanics.Scientific reports · 2026Article
- Aquaporin-4 deficiency induced white matter injury via upregulated complement component 3 in cerebral small vessel disease.Journal of neuroinflammation · 2026Article
- Orchestrating brain fluid dynamics: circadian regulation of CSF, glymphatic exchange, and waste clearance.Frontiers in cell and developmental biology · 2026Review
- Analysis of AQP4 SNPs and Their Association With REM Sleep Behavior Disorder and Hallucinations in Parkinson's Disease.Molecular neurobiology · 2025Article
- Targeting TRPV4 to restore glymphatic system function and alleviate cerebral edema in ischemic stroke.Brain pathology (Zurich, Switzerland) · 2025Article
- Promoting glymphatic flow: A non-invasive strategy using 40 Hz light flickering.Purinergic signalling · 2025Review
- Association Between Single Nucleotide Polymorphisms in the Aquaporin-4 Gene and Longitudinal Changes in White Matter Free Water and Cognitive Function in Non-Demented Older Adults.Human brain mapping · 2025Article
- Aquaporin-4 in glioblastoma: a nexus of glymphatic dysfunction, edema, immune evasion, and treatment resistance.Frontiers in cellular neuroscience · 2025Review
- Glymphatic system function in patients with ischemic stroke evaluated by the DTI-ALPS method: a comprehensive review.Frontiers in neurology · 2025Review
- NOTCH3 Mutation Causes Glymphatic Impairment and Promotes Brain Senescence in CADASIL.CNS neuroscience & therapeutics · 2025Article
- Update on the intriguing roles of AQP4 expression and redistribution in the progression and treatment of glioma.Annals of medicine · 2024Review
- 40 Hz light flickering facilitates the glymphatic flow via adenosine signaling in mice.Cell discovery · 2024Article
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- Functional aspects of the brain lymphatic drainage system in aging and neurodegenerative diseases.Journal of biomedical research · 2024Article
- Aquaporin-4 and Parkinson's Disease.International journal of molecular sciences · 2024Review
- Thermodynamics andThe journal of physical chemistry. B · 2024Article
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
The astrocyte water channel aquaporin-4 (AQP4) is expressed as heterotetramers of M1 and M23 isoforms in which the presence of M23-AQP4 promotes formation of large macromolecular aggregates termed orthogonal arrays. Here, we demonstrate that the AQP4 aggregation state determines its subcellular localization and cellular functions. Individually expressed M1-AQP4 was freely mobile in the plasma membrane and could diffuse into rapidly extending lamellipodial regions to support cell migration. In contrast, M23-AQP4 formed large arrays that did not diffuse rapidly enough to enter lamellipodia and instead stably bound adhesion complexes and polarized to astrocyte end-feet in vivo. Co-expressed M1- and M23-AQP4 formed aggregates of variable size that segregated due to diffusional sieving of small, mobile M1-AQP4-enriched arrays into lamellipodia and preferential interaction of large, M23-AQP4-enriched arrays with the extracellular matrix. Our results therefore demonstrate an aggregation state-dependent mechanism for segregation of plasma membrane protein complexes that confers specific functional roles to M1- and M23-AQP4.
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What OpenQuestion holds
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.