ArticleJournal of neurochemistry2010
NR2B-NMDA receptor mediated modulation of the tyrosine phosphatase STEP regulates glutamate induced neuronal cell death.
Article in Journal of neurochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 68 citations in OpenAlex.
- The tyrosine phosphatase STEP is a developmental suppressor of synaptogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Effects of the STriatal Enriched Tyrosine Phosphatase (STEP) Inhibitor TC-2153 on Hippocampal Long-Term Depression and Synaptic Transmission: Paradoxical Effect on Phosphatase Activity and Role of Adenosine.CNS neuroscience & therapeutics · 2026Article
- Regulating the Impact of Hypertension on Stroke: Therapeutic Potential of a Peptide Mimetic of Tyrosine Phosphatase STEP.Journal of the American Heart Association · 2026Article
- Lack of striatal-enriched protein tyrosine phosphatase affected the serotonin system, behavior, and brain morphology in mice.Frontiers in psychiatry · 2025Article
- Impairment of neuronal tyrosine phosphatase STEP worsens post-ischemic inflammation and brain injury under hypertensive condition.Journal of neuroinflammation · 2024Article
- Uncovering the Significance of STEP61 in Alzheimer's Disease: Structure, Substrates, and Interactome.Cellular and molecular neurobiology · 2023Review
- Editorial: The Molecular Mechanisms of Synaptic Plasticity Impairments in Alzheimer's Disease.Frontiers in cell and developmental biology · 2022Article
- Regulation of post-ischemic inflammatory response: A novel function of the neuronal tyrosine phosphatase STEP.Brain, behavior, and immunity · 2021Article
- The Implication of STEP in Synaptic Plasticity and Cognitive Impairments in Alzheimer's Disease and Other Neurological Disorders.Frontiers in cell and developmental biology · 2021Review
- Insight into the Role of the STriatal-Enriched Protein Tyrosine Phosphatase (STEP) in AFrontiers in pharmacology · 2021Article
- N-Methyl-D-Aspartate Receptor Signaling-Protein Kinases Crosstalk in Cerebral Ischemia.Advances in experimental medicine and biology · 2021Article
- Emerging neuroprotective strategies for the treatment of ischemic stroke: An overview of clinical and preclinical studies.Experimental neurology · 2021Review
- Scutellarin Exerts Anti-Inflammatory Effects in Activated Microglia/Brain Macrophage in Cerebral Ischemia and in Activated BV-2 Microglia Through Regulation of MAPKs Signaling Pathway.Neuromolecular medicine · 2020Article
- Microglia Adopt Longitudinal Transcriptional Changes After Traumatic Brain Injury.The Journal of surgical research · 2020Article
- Functions of p38 MAP Kinases in the Central Nervous System.Frontiers in molecular neuroscience · 2020Review
- Ginsenoside Rg1 alleviates repeated alcohol exposure-induced psychomotor and cognitive deficits.Chinese medicine · 2020Article
- A peptide mimetic of tyrosine phosphatase STEP as a potential therapeutic agent for treatment of cerebral ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Article
- Excitotoxic inactivation of constitutive oxidative stress detoxification pathway in neurons can be rescued by PKD1.Nature communications · 2017Article
- BDNF Induces Striatal-Enriched Protein Tyrosine Phosphatase 61 Degradation Through the Proteasome.Molecular neurobiology · 2016Article
- Aging is associated with dimerization and inactivation of the brain-enriched tyrosine phosphatase STEP.Neurobiology of aging · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The present study examines the role of a neuron-specific tyrosine phosphatase (STEP, striatal-enriched tyrosine phosphatase) in excitotoxic cell death. Our findings demonstrate that p38 MAPK, a stress-activated kinase that is known to play a role in the etiology of excitotoxic cell death is a substrate of STEP. Glutamate-mediated NMDA receptor stimulation leads to rapid but transient activation of p38 MAPK, which is primarily dependent on NR2A-NMDA receptor activation. Conversely, activation of NR2B-NMDA receptors leads to dephosphorylation and subsequent activation of STEP, which in turn leads to inactivation of p38 MAPK. Thus, during transient NMDA receptor stimulation, increases in STEP activity appears to limit the duration of activation of p38 MAPK and improves neuronal survival. However, if NR2B-NMDA receptor stimulation is sustained, protective effects of STEP activation are lost, as these stimuli cause significant degradation of active STEP, leading to secondary activation of p38 MAPK. Consistent with this observation, a cell transducible TAT-STEP peptide that constitutively binds to p38 MAPK attenuated neuronal cell death caused by sustained NMDA receptor stimulation. The findings imply that the activation and levels of STEP are dependent on the duration and magnitude of NR2B-NMDA receptor stimulation and STEP serves as a modulator of NMDA receptor dependent neuronal injury, through its regulation of p38 MAPK.
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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.