ArticleMolecular psychiatry2011
The psychiatric disease risk factors DISC1 and TNIK interact to regulate synapse composition and function.
Article in Molecular psychiatry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 2 of them syntheses that pooled it.
What it found
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Who cites it
95 citing papers in PubMed, 2 syntheses or guidelines pooled it, 146 citations in OpenAlex.
- A systematic review of genome-wide association studies of antipsychotic response.Pharmacogenomics · 2019Pooled it
- The impact of Disrupted-in-Schizophrenia 1 (DISC1) on the dopaminergic system: a systematic review.Translational psychiatry · 2017Pooled it
- Identification of a Ste20-like kinase-dependent signaling network orchestrating cytoskeletal and synaptic development of cortical neurons.Cell communication and signaling : CCS · 2026Article
- Interactome Analysis of the CC2D1A Scaffold Reveals Novel Neuronal Interactions and a Postsynaptic Role.Molecular & cellular proteomics : MCP · 2026Article
- Single-cell analysis reveals neuroprotective histone deacetylase inhibitor pathways.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Genetic interaction ofFrontiers in neuroscience · 2026Article
- TNIK-driven regulation of ERK5 transcriptional activity in endothelial cells.Frontiers in cardiovascular medicine · 2025Article
- FMR1 genetically interacts with DISC1 to regulate glutamatergic synaptogenesis.Schizophrenia (Heidelberg, Germany) · 2024Article
- The Traf2 and NcK interacting kinase inhibitor NCB-0846 suppresses seizure activity involving the decrease of GRIA1.Genes & diseases · 2024Article
- Transcriptome analysis to explore the mechanism of downregulated TNIK influencing the effect of risperidone.Frontiers in pharmacology · 2024Article
- Mutations in the postsynaptic density signaling hub TNIK disrupt PSD signaling in human models of neurodevelopmental disorders.Frontiers in molecular neuroscience · 2024Article
- Effects of MAP4K inhibition on neurite outgrowth.Molecular brain · 2023Article
- Rare coding variants as risk modifiers of the 22q11.2 deletion implicate postnatal cortical development in syndromic schizophrenia.Molecular psychiatry · 2023Article
- TNIK regulation of interferon signaling and endothelial cell response to virus infection.Frontiers in cardiovascular medicine · 2023Article
- Article
- Mutations in DISC1 alter IPNeuronal signaling · 2021Review
- TNIK influence the effects of antipsychotics on Wnt/β-catenin signaling pathway.Psychopharmacology · 2021Article
- Phosphorylation-dependent control of Activity-regulated cytoskeleton-associated protein (Arc) protein by TNIK.Journal of neurochemistry · 2021Article
- Dissecting Molecular Genetic Mechanisms of 1q21.1 CNV in Neuropsychiatric Disorders.International journal of molecular sciences · 2021Review
- Structural interaction between DISC1 and ATF4 underlying transcriptional and synaptic dysregulation in an iPSC model of mental disorders.Molecular psychiatry · 2021Article
35 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
24 authors at 8 institutions in 3 countries.
Funding
Abstract
Disrupted in schizophrenia 1 (DISC1), a genetic risk factor for multiple serious psychiatric diseases including schizophrenia, bipolar disorder and autism, is a key regulator of multiple neuronal functions linked to both normal development and disease processes. As these diseases are thought to share a common deficit in synaptic function and architecture, we have analyzed the role of DISC1 using an approach that focuses on understanding the protein-protein interactions of DISC1 specifically at synapses. We identify the Traf2 and Nck-interacting kinase (TNIK), an emerging risk factor itself for disease, as a key synaptic partner for DISC1, and provide evidence that the DISC1-TNIK interaction regulates synaptic composition and activity by stabilizing the levels of key postsynaptic density proteins. Understanding the novel DISC1-TNIK interaction is likely to provide insights into the etiology and underlying synaptic deficits found in major psychiatric diseases.
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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.