ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Neuroprotective role of a brain-enriched tyrosine phosphatase, STEP, in focal cerebral ischemia.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 46 citations in OpenAlex.
- Regulating the Impact of Hypertension on Stroke: Therapeutic Potential of a Peptide Mimetic of Tyrosine Phosphatase STEP.Journal of the American Heart Association · 2026Article
- Protein Tyrosine Phosphatases in Schizophrenia: A Review of Pathophysiology and Emerging Evidence.Cureus · 2026Review
- 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
- Regulation of post-ischemic inflammatory response: A novel function of the neuronal tyrosine phosphatase STEP.Brain, behavior, and immunity · 2021Article
- Emerging neuroprotective strategies for the treatment of ischemic stroke: An overview of clinical and preclinical studies.Experimental neurology · 2021Review
- Insight into the Role of the STriatal-Enriched Protein Tyrosine Phosphatase (STEP) in AFrontiers in pharmacology · 2021Article
- Functions of p38 MAP Kinases in the Central Nervous System.Frontiers in molecular neuroscience · 2020Review
- Hyperhomocysteinemia leads to exacerbation of ischemic brain damage: Role of GluN2A NMDA receptors.Neurobiology of disease · 2019Article
- 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
- Targeting NMDA receptors in stroke: new hope in neuroprotection.Molecular brain · 2018Review
- Excitotoxic inactivation of constitutive oxidative stress detoxification pathway in neurons can be rescued by PKD1.Nature communications · 2017Article
- Aging is associated with dimerization and inactivation of the brain-enriched tyrosine phosphatase STEP.Neurobiology of aging · 2016Article
- Zn2+-dependent Activation of the Trk Signaling Pathway Induces Phosphorylation of the Brain-enriched Tyrosine Phosphatase STEP: MOLECULAR BASIS FOR ZN2+-INDUCED ERK MAPK ACTIVATION.The Journal of biological chemistry · 2016Article
- Role of Striatal-Enriched Tyrosine Phosphatase in Neuronal Function.Neural plasticity · 2016Review
- Molecular underpinnings of neurodegenerative disorders: striatal-enriched protein tyrosine phosphatase signaling and synaptic plasticity.F1000Research · 2016Review
- Electroacupuncture at different frequencies (5Hz and 25Hz) ameliorates cerebral ischemia-reperfusion injury in rats: possible involvement of p38 MAPK-mediated anti-apoptotic signaling pathways.BMC complementary and alternative medicine · 2015Article
- Striatal-enriched protein tyrosine phosphatase controls responses to aversive stimuli: implication for ethanol drinking.PloS one · 2015Article
- Disruption of striatal-enriched protein tyrosine phosphatase (STEP) function in neuropsychiatric disorders.Neuroscience research · 2014Review
- Inhibitor of the tyrosine phosphatase STEP reverses cognitive deficits in a mouse model of Alzheimer's disease.PLoS biology · 2014Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
The striatal-enriched phosphatase (STEP) is a component of the NMDA-receptor-mediated excitotoxic signaling pathway, which plays a key role in ischemic brain injury. Using neuronal cultures and a rat model of ischemic stroke, we show that STEP plays an initial role in neuroprotection, during the insult, by disrupting the p38 MAPK pathway. Degradation of active STEP during reperfusion precedes ischemic brain damage and is associated with secondary activation of p38 MAPK. Application of a cell-permeable STEP-derived peptide that is resistant to degradation and binds to p38 MAPK protects cultured neurons from hypoxia-reoxygenation injury and reduces ischemic brain damage when injected up to 6 h after the insult. Conversely, genetic deletion of STEP in mice leads to sustained p38 MAPK activation and exacerbates brain injury and neurological deficits after ischemia. Administration of the STEP-derived peptide at the onset of reperfusion not only prevents the sustained p38 MAPK activation but also reduces ischemic brain damage in STEP KO mice. The findings indicate a neuroprotective role of STEP and suggest a potential role of the STEP-derived peptide in stroke therapy.
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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.