ArticleProceedings of the National Academy of Sciences of the United States of America2020
β-Arrestin2 oligomers impair the clearance of pathological tau and increase tau aggregates.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
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.
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Who cites it
32 citing papers in PubMed, 44 citations in OpenAlex.
- CHCHD2 mitigates age-associated proteostatic collapse by maintaining homeostasis of the mitochondria-lysosome axis.Acta neuropathologica · 2026Article
- The clinical implication of β-arrestins-mediated signaling in memory and cognition.Molecular and cellular biochemistry · 2025Review
- Cystic Fibrosis-related neurodegenerative disease associated with tauopathy and cognitive decline in aged CF mice.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2025Article
- The PKCι-β-arrestin2 axis disrupts SORLA retrograde trafficking, driving its degradation and amyloid pathology in Alzheimer's disease.Molecular neurodegeneration · 2025Article
- A Focus on the Link Between Metal Dyshomeostasis, Norepinephrine, and Protein Aggregation.Antioxidants (Basel, Switzerland) · 2025Review
- Label-free, real-time monitoring of membrane binding events at zeptomolar concentrations using frequency-locked optical microresonators.Nature communications · 2024Article
- Proximity labeling reveals dynamic changes in the SQSTM1 protein network.bioRxiv : the preprint server for biology · 2024Article
- Development of an anti-tauopathy mucosal vaccine specifically targeting pathologic conformers.NPJ vaccines · 2024Article
- Arrestins: A Small Family of Multi-Functional Proteins.International journal of molecular sciences · 2024Review
- The multifaceted functions of β-arrestins and their therapeutic potential in neurodegenerative diseases.Experimental & molecular medicine · 2024Review
- Exploring orphan GPCRs in neurodegenerative diseases.Frontiers in pharmacology · 2024Review
- Label-free, real-time monitoring of membrane binding events at zeptomolar concentrations using frequency-locked optical microresonators.bioRxiv : the preprint server for biology · 2023Article
- Slingshot homolog-1-mediated Nrf2 sequestration tips the balance from neuroprotection to neurodegeneration in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- A Par3/LIM Kinase/Cofilin Pathway Mediates Human Airway Smooth Muscle Relaxation by TAS2R14.American journal of respiratory cell and molecular biology · 2023Article
- Interactions between β-arrestin proteins and the cytoskeletal system, and their relevance to neurodegenerative disorders.Frontiers in endocrinology · 2023Review
- Pathological characterization of a novel mouse model expressing the PD-linked CHCHD2-T61I mutation.Human molecular genetics · 2022Article
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- β-arrestin1 promotes tauopathy by transducing GPCR signaling, disrupting microtubules and autophagy.Life science alliance · 2022Article
- Biased β-Agonists Favoring Gs over β-Arrestin for Individualized Treatment of Obstructive Lung Disease.Journal of personalized medicine · 2022Review
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Multiple G protein-coupled receptors (GPCRs) are targets in the treatment of dementia, and the arrestins are common to their signaling. β-Arrestin2 was significantly increased in brains of patients with frontotemporal lobar degeneration (FTLD-tau), a disease second to Alzheimer's as a cause of dementia. Genetic loss and overexpression experiments using genetically encoded reporters and defined mutant constructs in vitro, and in cell lines, primary neurons, and tau P301S mice crossed with β-arrestin2
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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.