ArticleFrontiers in molecular neuroscience2024
Mutations in the postsynaptic density signaling hub TNIK disrupt PSD signaling in human models of neurodevelopmental disorders.
Article in Frontiers in molecular neuroscience, 2024. 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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6 citing papers in PubMed, 9 citations in OpenAlex.
- 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
- Profiling of 5-hydroxymethylcytosine in blood reveals preferential enrichment at exon-intron junctions and predictive value for Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Disruption of the SYNGAP1 PDZ ligand motif accelerates differentiation of human iPSC-derived GABAergic neurons.bioRxiv : the preprint server for biology · 2026Article
- Structural variations in evolutionary novel genomic regions: new insights into neurodevelopmental disorders by long-read DNA Sequencing.Molecular medicine (Cambridge, Mass.) · 2026Article
- A system-wide investigation into the phosphoregulatory network of TNIK and its cellular implications.Frontiers in bioinformatics · 2026Article
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11 authors at 3 institutions in 3 countries.
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Abstract
A large number of synaptic proteins have been recurrently associated with complex brain disorders. One of these proteins, the Traf and Nck interacting kinase (TNIK), is a postsynaptic density (PSD) signaling hub, with many variants reported in neurodevelopmental disorder (NDD) and psychiatric disease. While rodent models of TNIK dysfunction have abnormal spontaneous synaptic activity and cognitive impairment, the role of mutations found in patients with TNIK protein deficiency and TNIK protein kinase activity during early stages of neuronal and synapse development has not been characterized. Here, using hiPSC-derived excitatory neurons, we show that TNIK mutations dysregulate neuronal activity in human immature synapses. Moreover, the lack of TNIK protein kinase activity impairs MAPK signaling and protein phosphorylation in structural components of the PSD. We show that the TNIK interactome is enriched in NDD risk factors and TNIK lack of function disrupts signaling networks and protein interactors associated with NDD that only partially overlap to mature mouse synapses, suggesting a differential role of TNIK in immature synapsis in NDD.
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