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STEP plays an important role at nerve terminals in the regulation of Ca(2+) homeostasis and neurotransmitter release.
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STEP61 degradation is an important event in BDNF-mediated effects.
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STEP has a key role in the regulation of psychomotor action and physical dependency to morphine. These data suggest that STEP inhibition may be a critical target for the treatment of withdrawal symptoms associated with morphine.
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This study demonistrated that behavioral, molecular, and electrophysiological data indicate that spinal STEP61 plays a regulatory role in nociception.
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STEP61 regulates BDNF expression, with implications for cognitive functioning in CNS disorders.
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The study provides further insight into the mechanisms of regulation of STEP61 and also offers a molecular basis for the Zn(2+)-induced sustained activation of ERK2.
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STEP contributes, at least in part, to the protection against the ingestion of aversive agents.
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These results indicate that STEP61 is a novel substrate of parkin, although further studies are necessary to determine whether elevated STEP61 levels directly contribute to the pathophysiology of PD.
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Abeta regulating STEP61 activity is mediated by Abeta binding to alpha7 nAChRs
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Increased STEP and calpain activation contribute to altered NMDAR localization in an Huntington's disease mouse model.
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genetically reducing STEP significantly diminishes seizures and restores select social and nonsocial anxiety-related behaviors in Fmr1(KO) mice
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the first study to identify Pyk2 as a substrate for STEP.
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Increased STEP61 plays a role in amyloid Abeta-mediated internalization of the (AMPAR) subunits GluA1/GluA2 (formerly GluR1/GluR2).
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The absence of STEP improves cognitive performance, and may do so by the regulation of downstream effectors necessary for synaptic transmission.
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STEP pathway is severely downregulated in the presence of mutant huntingtin and may participate in compensatory mechanisms activated by striatal neurons that lead to resistance to excitotoxicity.
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STEP may be required for ethanol's amnesic effects.
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Electrical stimulation of the hippocampal-entorhinal cortex pathway in STEP knockout mice resulted in less activation of the dentate gyrus granule cell layer (GCL), but greater activation of the hilus in STEP knockouts, compared with heterozygous slices.
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genetic manipulations to reduce STEP activity in a triple transgenic AD mouse model and show that a decrease in STEP levels reverses cognitive and cellular deficits observed in these mice.
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These results suggest that STEP is an important mediator in the dopamine D2R-mediated activation of ERK signaling and in the regulation of dopaminergic neuronal development.
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results reveal a novel mechanism by which Abeta-mediated accumulation of STEP61 results in increased internalization of NR1/NR2B receptor that may contribute to the cognitive deficits in Alzheimer's disease