ArticleMolecular neurobiology2016
Inhibition of Protein Phosphatase 2A: Focus on the Glutamatergic System.
Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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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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
5 citing papers in PubMed.
- Blockade of Type 2A Protein Phosphatase Signaling Attenuates Complement C1q-Mediated Microglial Phagocytosis of Glutamatergic Synapses Induced by Amyloid Fibrils.Molecular neurobiology · 2023Article
- Prolyl oligopeptidase inhibition reduces alpha-synuclein aggregation in a cellular model of multiple system atrophy.Journal of cellular and molecular medicine · 2021Article
- HGF Mediates Clinical-Grade Human Umbilical Cord-Derived Mesenchymal Stem Cells Improved Functional Recovery in a Senescence-Accelerated Mouse Model of Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- Cornel Iridoid Glycoside Inhibits Tau Hyperphosphorylation via Regulating Cross-Talk Between GSK-3β and PP2A Signaling.Frontiers in pharmacology · 2018Article
- Fuzheng Quxie Decoction Ameliorates Learning and Memory Impairment in SAMP8 Mice by Decreasing Tau Hyperphosphorylation.Evidence-based complementary and alternative medicine : eCAM · 2017Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In a recent review published in Molecular Neurobiology, Kamat and colleagues (Mol Neurobiol. 2014 Dec;50(3):852-65) highlighted the cellular and molecular mechanisms involved in Okadaic acid (OKA)-induced neurotoxicity. In this review, the authors underline a wide range of pathological signaling pathways involved in OKA-induced neurotoxicity; however, the role of glutamate was only briefly described. We believe that the hyperactivation of the glutamatergic system is a key pathophysiological player in OKA-induced neurotoxicity and deserves serious attention. In this commentary, we propose an integrative model linking glutamate and PP2A and put forward some unanswered questions.
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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.