ReviewNeural plasticity2016
Role of Striatal-Enriched Tyrosine Phosphatase in Neuronal Function.
Review in Neural plasticity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 34 citations in OpenAlex.
- Resilience mechanisms underlying Alzheimer's disease.Metabolic brain disease · 2025Review
- Cells and Molecules Underpinning Cannabis-Related Variations in Cortical Thickness during Adolescence.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Reelin Signaling in Neurodevelopmental Disorders and Neurodegenerative Diseases.Brain sciences · 2023Review
- Fbxo45-mediated NP-STEPMolecular oncology · 2022Article
- Dl-3-n-butylphthalide alleviates cognitive impairment in amyloid precursor protein/presenilin 1 transgenic mice by regulating the striatal-enriched protein tyrosine phosphatase/ERK/cAMP-response element-binding protein signaling pathway.Experimental and therapeutic medicine · 2022Article
- Hereditable variants of classical protein tyrosine phosphatase genes: Will they prove innocent or guilty?Frontiers in cell and developmental biology · 2022Review
- Regulation of glutamate receptors by striatal-enriched tyrosine phosphatase 61 (STEPThe Journal of physiology · 2021Review
- Insight into the Role of the STriatal-Enriched Protein Tyrosine Phosphatase (STEP) in AFrontiers in pharmacology · 2021Article
- Inhibition of striatal-enriched protein tyrosine phosphatase (STEP) activity reverses behavioral deficits in a rodent model of autism.Behavioural brain research · 2020Article
- Alterations of STEP46 and STEP61 Expression in the Rat Retina with Age and AMD-Like Retinopathy Development.International journal of molecular sciences · 2020Article
- How Do Post-Translational Modifications Influence the Pathomechanistic Landscape of Huntington's Disease? A Comprehensive Review.International journal of molecular sciences · 2020Review
- Profiling changes in cortical astroglial cells following chronic stress.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Article
- Linkage analysis of multiplex Caribbean Hispanic families loaded for unexplained early-onset cases identifies novel Alzheimer's disease loci.Alzheimer's & dementia (Amsterdam, Netherlands) · 2018Article
- Activation of Phosphotyrosine-Mediated Signaling Pathways in the Cortex and Spinal Cord of SOD1Neural plasticity · 2018Article
- Targeting Tyrosine Phosphatases: Time to End the Stigma.Trends in pharmacological sciences · 2017Review
- Molecular underpinnings of neurodegenerative disorders: striatal-enriched protein tyrosine phosphatase signaling and synaptic plasticity.F1000Research · 2016Review
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Striatal-enriched protein tyrosine phosphatase (STEP) is a CNS-enriched protein implicated in multiple neurologic and neuropsychiatric disorders. STEP regulates key signaling proteins required for synaptic strengthening as well as NMDA and AMPA receptor trafficking. Both high and low levels of STEP disrupt synaptic function and contribute to learning and behavioral deficits. High levels of STEP are present in human postmortem samples and animal models of Alzheimer's disease, Parkinson's disease, and schizophrenia and in animal models of fragile X syndrome. Low levels of STEP activity are present in additional disorders that include ischemia, Huntington's chorea, alcohol abuse, and stress disorders. Thus the current model of STEP is that optimal levels are required for optimal synaptic function. Here we focus on the role of STEP in Alzheimer's disease and the mechanisms by which STEP activity is increased in this illness. Both genetic lowering of STEP levels and pharmacological inhibition of STEP activity in mouse models of Alzheimer's disease reverse the biochemical and cognitive abnormalities that are present. These findings suggest that STEP is an important point for modulation of proteins required for synaptic plasticity.
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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.