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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Protein tyrosine phosphatase, non-receptor type 5

a putative protein-tyrosine-phosphatase that is found enriched within the striatum [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: ACID, ERK, HAD, CAN, alpha-Synuclein
Papers on STEP
Genetics of long-term treatment outcome in bipolar disorder.
Serretti et al., Bologna, Italy. In Prog Neuropsychopharmacol Biol Psychiatry, Mar 2016
The present study investigated genetic predictors of long-term treatment-outcome in 723 patients with BD type I from the STEP-BD (Systematic Treatment Enhancement Program for Bipolar Disorder) genome-wide dataset.
Glutamatergic and HPA-axis pathway genes in bipolar disorder comorbid with alcohol- and substance use disorders.
Stein et al., Cape Town, South Africa. In Metab Brain Dis, Feb 2016
The research cohort consisted of 498 individuals with BD type I from the Systematic Treatment Enhancement Program for Bipolar Disorder (STEP-BD).
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.
Paul et al., Albuquerque, United States. In J Biol Chem, Feb 2016
Here we show that exposure to high concentrations of Zn(2+) led to a progressive increase in phosphorylation of the striatal-enriched phosphatase (STEP), a component of the excitotoxic-signaling pathway that plays a role in neuroprotection.
Cocaine self-administration causes signaling deficits in corticostriatal circuitry that are reversed by BDNF in early withdrawal.
Sun et al., Charleston, United States. In Brain Res, Jan 2016
These changes are accompanied by a marked increase in STEP tyrosine phosphatase activation.
Fragile X Syndrome FMRP Co-localizes with Regulatory Targets PSD-95, GABA Receptors, CaMKIIα, and mGluR5 at Fiber Cell Membranes in the Eye Lens.
Kasinathan et al., Newark, United States. In Neurochem Res, Nov 2015
Lenses express FMRP along with γ-aminobutyric acid (GABA) receptors (GABARs), post-synaptic density protein 95 (PSD-95), Tyr-phosphatase STEP, CaMKIIα and Alzheimer's disease Aβ precursor protein, which are verified targets of FMRP regulation in neurons and outline major topics in FXS/ASD research.
Inhibition of the tyrosine phosphatase STEP61 restores BDNF expression and reverses motor and cognitive deficits in phencyclidine-treated mice.
Lombroso et al., New Haven, United States. In Cell Mol Life Sci, Nov 2015
The reduction in BDNF expression was prevented by STEP61 knockdown or use of the STEP inhibitor, TC-2153.
The STEP model: Characterizing simultaneous time effects on practice for flight simulator performance among middle-aged and older pilots.
Lazzeroni et al., Stanford, United States. In Psychol Aging, Sep 2015
We developed a new Simultaneous Time Effects on Practice (STEP) model: (a) to model the simultaneous effects of practice and interval on performance of the 5 flights, and (b) to examine the effects of selected covariates (i.e., age, flight expertise, and 3 composite measures of cognitive ability).
Down-regulation of BDNF in cell and animal models increases striatal-enriched protein tyrosine phosphatase 61 (STEP61 ) levels.
Lombroso et al., New Haven, United States. In J Neurochem, Sep 2015
STriatal-Enriched protein tyrosine Phosphatase (STEP) is also implicated in many of the same disorders as BDNF but, in contrast to BDNF, STEP opposes the development of synaptic strengthening.
STEP modulates nociception: evidences from genetic deletion and pharmacological inhibition.
Pérez-Navarro et al., Barcelona, Spain. In Pain, Sep 2015
STriatal-Enriched protein tyrosine Phosphatase (STEP) dephosphorylates GluN2B and ERK1/2, promoting internalization of GluN2B and inactivation of ERK1/2.
Tissue-specific tagging of endogenous loci in Drosophila melanogaster.
Rodal et al., Waltham, United States. In Biol Open, 2014
To address these limitations, we have developed a method called T-STEP (tissue-specific tagging of endogenous proteins) that allows endogenous loci to be tagged in a tissue specific manner.
Disruption of striatal-enriched protein tyrosine phosphatase (STEP) function in neuropsychiatric disorders.
Lombroso et al., Kasugai, Japan. In Neurosci Res, 2014
Striatal-enriched protein tyrosine phosphatase (STEP) is a brain-specific tyrosine phosphatase that plays a major role in the development of synaptic plasticity.
Protein tyrosine phosphatases as potential therapeutic targets.
Zhang et al., Indianapolis, United States. In Acta Pharmacol Sin, 2014
This review summarizes recent findings on several highly recognized PTP family drug targets, including PTP1B, Src homology phosphotyrosyl phosphatase 2(SHP2), lymphoid-specific tyrosine phosphatase (LYP), CD45, Fas associated phosphatase-1 (FAP-1), striatal enriched tyrosine phosphatases (STEP), mitogen-activated protein kinase/dual-specificity phosphatase 1 (MKP-1), phosphatases of regenerating liver-1 (PRL), low molecular weight PTPs (LMWPTP), and CDC25.
Excitotoxicity and stroke: identifying novel targets for neuroprotection.
Wang et al., Wuxue, China. In Prog Neurobiol, 2014
During a brief episode of ischemia, the extracellular glutamate concentration rises abruptly, and stimulation of the GluN2B-containing NMDAR in the extrasynaptic sites triggers excitotoxic neuronal death via PTEN, cdk5, and DAPK1, which are directly bound to the NMDAR, nNOS, which is indirectly coupled to the NMDAR via PSD95, and calpain, p25, STEP, p38, JNK, and SREBP1, which are further downstream.
The influence of delivery vectors on HIV vaccine efficacy.
Ondondo, Oxford, United Kingdom. In Front Microbiol, 2013
Conversely, in the STEP study (HVTN 502) where human adenovirus serotype 5 (Ad5) was used, strong immune responses were induced but vaccination was more associated with increased risk of HIV acquisition than protection in vaccinees with pre-existing Ad5 immunity.
Involvement of PTPN5, the gene encoding the striatal-enriched protein tyrosine phosphatase, in schizophrenia and cognition.
Kohn et al., Jerusalem, Israel. In Psychiatr Genet, 2012
The results imply a model in which PTPN5 may play a role in normal cognitive functioning and contribute to aspects of the neuropathology of schizophrenia.
Genetic manipulation of STEP reverses behavioral abnormalities in a fragile X syndrome mouse model.
Lombroso et al., New Haven, United States. In Genes Brain Behav, 2012
genetically reducing STEP significantly diminishes seizures and restores select social and nonsocial anxiety-related behaviors in Fmr1(KO) mice
Striatal-enriched protein-tyrosine phosphatase (STEP) regulates Pyk2 kinase activity.
Lombroso et al., New Haven, United States. In J Biol Chem, 2012
the first study to identify Pyk2 as a substrate for STEP.
A critical role for protein tyrosine phosphatase nonreceptor type 5 in determining individual susceptibility to develop stress-related cognitive and morphological changes.
Hsu et al., Tainan City, Taiwan. In J Neurosci, 2012
This study identified a novel role for PTPN5 in mediating the development of stress-related cognitive and morphological changes.
Therapeutic implications for striatal-enriched protein tyrosine phosphatase (STEP) in neuropsychiatric disorders.
Lombroso et al., New Haven, United States. In Pharmacol Rev, 2012
Striatal-enriched protein tyrosine phosphatase (STEP) is a brain-specific phosphatase that modulates key signaling molecules involved in synaptic plasticity and neuronal function.
Reduced levels of the tyrosine phosphatase STEP block β amyloid-mediated GluA1/GluA2 receptor internalization.
Lombroso et al., New Haven, United States. In J Neurochem, 2011
Increased STEP61 plays a role in amyloid Abeta-mediated internalization of the (AMPAR) subunits GluA1/GluA2 (formerly GluR1/GluR2).
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