ArticlePsychopharmacology2021
TNIK influence the effects of antipsychotics on Wnt/β-catenin signaling pathway.
Article in Psychopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- Whole transcriptome sequencing to uncover CircRNA expression patterns linked to schizophrenia pathogenesis.European journal of medical research · 2025Article
- TNIK in disease: from molecular insights to therapeutic prospects.Apoptosis : an international journal on programmed cell death · 2024Review
- Therapeutic targeting of TNIK in papillary thyroid carcinoma: a novel approach for tumor growth suppression.Medical oncology (Northwood, London, England) · 2024Article
- Transcriptome analysis to explore the mechanism of downregulated TNIK influencing the effect of risperidone.Frontiers in pharmacology · 2024Article
- Regulation of the hippocampal translatome by Apoer2-ICD release.Molecular neurodegeneration · 2023Article
- Apoer2-ICD-dependent regulation of hippocampal ribosome mRNA loading.Research square · 2023Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
RationaleTraf2- and Nck-interacting kinase (TNIK), a member of germinal center kinase (GCK) family, has been implicated as a risk factor in schizophrenia and bipolar disorder as well as the action of antipsychotics. TNIK is an essential activator of Wnt/β-catenin signaling pathway which has been identified involved in the mechanism underlying the effects of antipsychotics. Thus, the effects of TNIK on antipsychotics may be achieved by influencing Wnt/β-catenin signaling pathway proteins.Objectives and methodsIn the current study, the effects of up- or downregulated TNIK on β-catenin, T-cell factor 4 (TCF-4), glycogen synthase kinase-3β (GSK3β), and phosphorylated GSK3β (p-GSK3β) were examined in the human glioma U251 cells. Then, we observed the effects of antipsychotics (clozapine and risperidone) on the above proteins and evaluated the role of differentially expressed TNIK on antipsychotic-treated cell groups.ResultsThe result showed that clozapine treatment decreased β-catenin and TCF-4 levels in U251 cells, and risperidone had the similar effects on β-catenin and p-GSK3β. The downregulated TNIK using siRNA impeded the regulation of antipsychotics on Wnt pathway proteins via increasing the expression levels of TCF-4, β-catenin, or p-GSK3β, whereas the upregulated TNIK made no significant change.ConclusionsThe influence of TNIK on the effects of antipsychotics may be partly through Wnt/β-catenin signaling pathway.
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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 Socratic graph.