ArticleBiochimica et biophysica acta. Gene regulatory mechanisms2019
TDP-43 and NOVA-1 RNA-binding proteins as competitive splicing regulators of the schizophrenia-associated TNIK gene.
Article in Biochimica et biophysica acta. Gene regulatory mechanisms, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 19 citations in OpenAlex.
- CRISPR/Cas9 a genomic engineering technology for treatment in ALS mouse models.Regenerative therapy · 2025Review
- ELAV/Hu RNA-binding protein family: key regulators in neurological disorders, cancer, and other diseases.RNA biology · 2025Review
- Role of RNA-binding proteins in exercise-induced mRNA regulation: Unveiling biomarkers and therapeutic targets for schizophrenia.World journal of psychiatry · 2025Review
- Modulation of DAPK1 expression by its alternative splice variant DAPK1-215 in cancer.Journal of translational medicine · 2025Article
- Decoding TDP-43: the molecular chameleon of neurodegenerative diseases.Acta neuropathologica communications · 2024Review
- NTRK fusion promotes tumor migration and invasion through epithelial-mesenchymal transition and closely interacts with ECM1 and NOVA1.BMC cancer · 2024Article
- PTBP1 mediates Sertoli cell actin cytoskeleton organization by regulating alternative splicing of actin regulators.Nucleic acids research · 2024Article
- TNIK in disease: from molecular insights to therapeutic prospects.Apoptosis : an international journal on programmed cell death · 2024Review
- PTBP1 mediates Sertoli cell actin cytoskeleton organization by regulating alternative splicing of actin regulators.bioRxiv : the preprint server for biology · 2024Article
- Implications of TDP-43 in non-neuronal systems.Cell communication and signaling : CCS · 2023Review
- Human motor neurons derived from induced pluripotent stem cells are susceptible to SARS-CoV-2 infection.Frontiers in cellular neuroscience · 2023Article
- Altered TDP-43 Structure and Function: Key Insights into Aberrant RNA, Mitochondrial, and Cellular and Systemic Metabolism in Amyotrophic Lateral Sclerosis.Metabolites · 2022Review
- Review
- Targeting the RNA-Binding Protein HuR as Potential Thera-Peutic Approach for Neurological Disorders: Focus on Amyo-Trophic Lateral Sclerosis (ALS), Spinal Muscle Atrophy (SMA) and Multiple Sclerosis.International journal of molecular sciences · 2021Review
- Roles of the microRNA‑338‑3p/NOVA1 axis in retinoblastoma.Molecular medicine reports · 2021Article
- Review
- Alternative Splicing by NOVA Factors: From Gene Expression to Cell Physiology and Pathology.International journal of molecular sciences · 2020Review
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Authors and funding
8 authors at 4 institutions in 2 countries.
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Abstract
The RNA-binding protein TDP-43, associated to amyotrophic lateral sclerosis and frontotemporal dementia, regulates the alternative splicing of several genes, including the skipping of TNIK exon 15. TNIK, a genetic risk factor for schizophrenia and causative for intellectual disability, encodes for a Ser/Thr kinase regulating negatively F-actin dynamics. Here we show that in the human adult nervous system TNIK exon 15 is mostly included compared to the other tissues and that, during neuronal differentiation of human induced pluripotent stem cells and of human neuroblastoma cells, TNIK exon 15 inclusion increases independently of TDP-43 protein content. By studying the possible molecular interplay of TDP-43 with brain-specific splicing factors, we found that the neuronal NOVA-1 protein competitively inhibits both TDP-43 and hnRNPA2/B1 skipping activity on TNIK by means of a RNA-dependent interaction and that this competitive mechanism is common to other TDP-43 RNA targets. We also show that the TNIK protein isoforms including/excluding exon 15 differently regulate cell spreading in non-neuronal cells and neuritogenesis in primary cortical neurons. Our data suggest a complex regulation between the ubiquitous TDP-43 and the neuron-specific NOVA-1 splicing factors in the brain that may help better understand the pathobiology of both neurodegenerative diseases and schizophrenia.
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