ArticlePsychopharmacology2017
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.
Article in Psychopharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 26 citations in OpenAlex.
- Tail-rattling in rodents: more than a threat display.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2026Review
- Article
- Phosphatase Signaling as a Therapeutic Strategy in Schizophrenia.International journal of molecular sciences · 2026Review
- The autism-linked gut microbial metabolite p-cresol inhibits host catecholamine biosynthesizing enzymes to elicit social deficits.Communications biology · 2025Article
- Knocking down tumor suppressor gene PTPRG enhances axonal regeneration of dorsal root ganglion neurons.Frontiers in cell and developmental biology · 2025Article
- Pleiotrophin Overexpression Reduces Adolescent Ethanol Consumption and Modulates Ethanol-Induced Glial Responses and Changes in the Perineuronal Nets in the Mouse Hippocampus.CNS neuroscience & therapeutics · 2024Article
- Analysis of single-cell transcriptome data from a mouse model implicates protein synthesis dysfunction in schizophrenia.Genes & genomics · 2024Article
- Comparative transcriptomics reveals human-specific cortical features.Science (New York, N.Y.) · 2023Article
- Implication of the PTN/RPTPβ/ζ Signaling Pathway in Acute Ethanol Neuroinflammation in Both Sexes: A Comparative Study with LPS.Biomedicines · 2023Article
- Inhibition of RPTPβ/ζ reduces chronic ethanol intake in adolescent mice and modulates ethanol effects on hippocampal neurogenesis and glial responses in a sex-dependent manner.Neuropharmacology · 2023Article
- Article
- A Comprehensive Review of Receptor-Type Tyrosine-Protein Phosphatase Gamma (PTPRG) Role in Health and Non-Neoplastic Disease.Biomolecules · 2022Review
- Protein tyrosine phosphatase receptor-ζ1 deletion triggers defective heart morphogenesis in mice and zebrafish.American journal of physiology. Heart and circulatory physiology · 2022Article
- Hereditable variants of classical protein tyrosine phosphatase genes: Will they prove innocent or guilty?Frontiers in cell and developmental biology · 2022Review
- Behavioral Tasks Evaluating Schizophrenia-like Symptoms in Animal Models: A Recent Update.Current neuropharmacology · 2021Review
- The Expression, Functions, Interactions and Prognostic Values of PTPRZ1: A Review and Bioinformatic Analysis.Journal of Cancer · 2019Review
- Mapping the Proteome of the Synaptic Cleft through Proximity Labeling Reveals New Cleft Proteins.Proteomes · 2018Article
- A New 3p14.2 Microdeletion in a Patient with Intellectual Disability and Language Impairment: Case Report and Review of the Literature.Molecular syndromology · 2018Article
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleThe receptor protein tyrosine phosphatase PTPRG has been genetically associated with psychiatric disorders and is a ligand for members of the contactin family, which are themselves linked to autism spectrum disorders.
objectiveBased on our finding of a phosphatase-null de novo mutation in PTPRG associated with a case of sporadic schizophrenia, we used PTPRG knockout (KO) mice to model the effect of a loss-of-function mutation. We compared the results with loss-of-function in its close paralogue PTPRZ, previously associated with schizophrenia. We tested PTPRG
resultsThe most notable behavioral consequences of PTPRG gene inactivation were reduced immobilization in the forced swim test, suggestive of some negative symptoms of schizophrenia. By contrast, PTPRZ
conclusionPTPRG and PTPRZ gene loss therefore induces distinct patterns of behavioral change and region-specific alterations in neurotransmitters, highlighting their usefulness as models for neuropsychiatric disorder mechanisms and making these receptors attractive targets for 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.