ArticleBiological psychiatry2011
Loss of function studies in mice and genetic association link receptor protein tyrosine phosphatase α to schizophrenia.
Article in Biological psychiatry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- Phosphatase Signaling as a Therapeutic Strategy in Schizophrenia.International journal of molecular sciences · 2026Review
- Protein Tyrosine Phosphatases in Schizophrenia: A Review of Pathophysiology and Emerging Evidence.Cureus · 2026Review
- PTPα promotes fibroproliferative responses after acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- A Comprehensive Review of Receptor-Type Tyrosine-Protein Phosphatase Gamma (PTPRG) Role in Health and Non-Neoplastic Disease.Biomolecules · 2022Review
- Hereditable variants of classical protein tyrosine phosphatase genes: Will they prove innocent or guilty?Frontiers in cell and developmental biology · 2022Review
- Rare variants in Protein tyrosine phosphatase, receptor type A (PTPRA) in schizophrenia: Evidence from a family based study.Schizophrenia research · 2019Article
- Loss-of-function of PTPR γ and ζ, observed in sporadic schizophrenia, causes brain region-specific deregulation of monoamine levels and altered behavior in mice.Psychopharmacology · 2017Article
- Src kinase as a mediator of convergent molecular abnormalities leading to NMDAR hypoactivity in schizophrenia.Molecular psychiatry · 2015Article
- Striatal-enriched protein tyrosine phosphatase regulates the PTPα/Fyn signaling pathway.Journal of neurochemistry · 2015Article
- Novel implications of Lingo-1 and its signaling partners in schizophrenia.Translational psychiatry · 2014Article
- Resequencing and association analysis of PTPRA, a possible susceptibility gene for schizophrenia and autism spectrum disorders.PloS one · 2014Article
- Postmortem brain: an underutilized substrate for studying severe mental illness.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014Review
- Protein tyrosine phosphatase α in the dorsomedial striatum promotes excessive ethanol-drinking behaviors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Potential translational targets revealed by linking mouse grooming behavioral phenotypes to gene expression using public databases.Progress in neuro-psychopharmacology & biological psychiatry · 2013Article
- Maternal stress induces epigenetic signatures of psychiatric and neurological diseases in the offspring.PloS one · 2013Article
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Authors and funding
15 authors at 6 institutions in 4 countries.
Funding
Abstract
backgroundSolid evidence links schizophrenia (SZ) susceptibility to neurodevelopmental processes involving tyrosine phosphorylation-mediated signaling. Mouse studies implicate the Ptpra gene, encoding protein tyrosine phosphatase RPTPα, in the control of radial neuronal migration, cortical cytoarchitecture, and oligodendrocyte differentiation. The human gene encoding RPTPα, PTPRA, maps to a chromosomal region (20p13) associated with susceptibility to psychotic illness.
methodsWe characterized neurobehavioral parameters, as well as gene expression in the central nervous system, of mice with a null mutation in the Ptpra gene. We searched for genetic association between polymorphisms in PTPRA and schizophrenia risk (two independent cohorts, 1420 cases and 1377 controls), and we monitored PTPRA expression in prefrontal dorsolateral cortex of SZ patients (35 cases, 2 control groups of 35 cases).
resultsWe found that Ptpra⁻/⁻ mice reproduce neurobehavioral endophenotypes of human SZ: sensitization to methamphetamine-induced hyperactivity, defective sensorimotor gating, and defective habituation to a startle response. Ptpra loss of function also leads to reduced expression of multiple myelination genes, mimicking the hypomyelination-associated changes in gene expression observed in postmortem patient brains. We further report that a polymorphism at the PTPRA locus is genetically associated with SZ, and that PTPRA mRNA levels are reduced in postmortem dorsolateral prefrontal cortex of subjects with SZ.
conclusionsThe implication of this well-studied signaling protein in SZ risk and endophenotype manifestation provides novel entry points into the etiopathology of this disease.
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