ArticleNeurochemical research2017
Down-regulation of Pin1 in Temporal Lobe Epilepsy Patients and Mouse Model.
Article in Neurochemical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Temperature-sensitive sodium beta-glycerophosphate/chitosan hydrogel loaded with all-trans retinoic acid regulates Pin1 to inhibit the formation of spinal cord injury-induced rat glial scar.Bioengineering & translational medicine · 2025Article
- Upregulation of Pin1 contributes to alleviation of cognitive dysfunction in diabetic mice.Brain and behavior · 2023Article
- The role of molecular chaperones in the mechanisms of epileptogenesis.Cell stress & chaperones · 2023Review
- The regulatory role of Pin1 in neuronal death.Neural regeneration research · 2023Review
- The role of peptidyl-prolyl isomerase Pin1 in neuronal signaling in epilepsy.Frontiers in molecular neuroscience · 2022Review
- The Pin1-CaMKII-AMPA Receptor Axis Regulates Epileptic Susceptibility.Cerebral cortex (New York, N.Y. : 1991) · 2021Article
- The Peptidyl-prolyl Isomerase Pin1 in Neuronal Signaling: from Neurodevelopment to Neurodegeneration.Molecular neurobiology · 2021Review
- Liraglutide Treatment Ameliorates Neurotoxicity Induced by Stable Silencing of Pin1.International journal of molecular sciences · 2019Article
- Pin1 Modulation in Physiological Status and Neurodegeneration. Any Contribution to the Pathogenesis of Type 3 Diabetes?International journal of molecular sciences · 2018Review
- Pin1 Promotes Regulated Necrosis Induced by Glutamate in Rat Retinal Neurons via CAST/Calpain2 Pathway.Frontiers in cellular neuroscience · 2017Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1 (Pin1) is a unique PPIase belonging to the parvulin family, and it isomerizes peptide bond between phospho-(Ser/Thr) and Pro. Pin1 has been linked to the pathogenesis of various human diseases; however, its exact biological functions remain unclear. The aim of the present study is to explore the expression pattern of Pin1 in patients with refractory epilepsy and in a chronic pilocarpine-induced epileptic mouse model. Using Western blot, immunofluorescence and immunoprecipitation analysis, we found that Pin1 protein was mainly distributed in neurons, demonstrated by colocalization with the dendritic marker, MAP2. However, the expression of Pin1 decreased remarkably in epileptic patients and experimental mice. Furthermore, the reciprocal coimmunoprecipitation analysis showed that Pin1 interacted with NR2A and NR2B-containing NMDA receptors not AMPA receptors in epileptic mouse models. Our results are the first to indicate that the expression of Pin1 in epileptic brain tissue could play important roles in epilepsy.
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