ArticleCerebral cortex (New York, N.Y. : 1991)2017
The Dyslexia-susceptibility Protein KIAA0319 Inhibits Axon Growth Through Smad2 Signaling.
Article in Cerebral cortex (New York, N.Y. : 1991), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 2 syntheses or guidelines pooled it, 40 citations in OpenAlex.
- Hypothesis-driven genome-wide association studies provide novel insights into genetics of reading disabilities.Translational psychiatry · 2022Pooled it
- A systematic review and meta-analysis of imaging genetics studies of specific reading disorder.Cognitive neuropsychology · 2021Pooled it
- Epigenetic Signatures in an Italian Cohort of Parkinson's Disease Patients from Sicily.Brain sciences · 2025Article
- Article
- Targeted analysis of dyslexia-associated regions on chromosomes 6, 12 and 15 in large multigenerational cohorts.PloS one · 2025Article
- Investigation of Association Between Expression of DYX1C1, KIAA0319, and ROBO1 Genes and Specific Learning Disorder in Children and Adolescents.Journal of molecular neuroscience : MN · 2024Article
- Developmental dyslexia susceptibility genes DNAAF4, DCDC2, and NRSN1 are associated with brain function in fluently reading adolescents and young adults.Cerebral cortex (New York, N.Y. : 1991) · 2024Article
- Integrative analysis of gene expression profiles of substantia nigra identifies potential diagnosis biomarkers in Parkinson's disease.Scientific reports · 2024Article
- Screening of pathologically significant diagnostic biomarkers in tears of thyroid eye disease based on bioinformatic analysis and machine learning.Frontiers in cell and developmental biology · 2024Article
- Patterns of Neural Functional Connectivity in Infants at Familial Risk of Developmental Dyslexia.JAMA network open · 2022Article
- KIAA0319 influences cilia length, cell migration and mechanical cell-substrate interaction.Scientific reports · 2022Article
- Dyslexia associated geneFrontiers in cell and developmental biology · 2022Article
- Animal models of developmental dyslexia.Frontiers in neuroscience · 2022Review
- BET Bromodomain Inhibition Blocks an AR-Repressed, E2F1-Activated Treatment-Emergent Neuroendocrine Prostate Cancer Lineage Plasticity Program.Clinical cancer research : an official journal of the American Association for Cancer Research · 2021Article
- Article
- The Polygenic Nature and Complex Genetic Architecture of Specific Learning Disorder.Brain sciences · 2021Review
- Neuroimaging genetic associations betweenJournal of clinical and experimental neuropsychology · 2021Article
- Systematic detection of brain protein-coding genes under positive selection during primate evolution and their roles in cognition.Genome research · 2021Article
- Dyslexia Candidate Gene and Ciliary Gene Expression Dynamics During Human Neuronal Differentiation.Molecular neurobiology · 2020Article
- The dyslexia susceptibility KIAA0319 gene shows a specific expression pattern during zebrafish development supporting a role beyond neuronal migration.The Journal of comparative neurology · 2019Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
KIAA0319 is a transmembrane protein associated with dyslexia with a presumed role in neuronal migration. Here we show that KIAA0319 expression is not restricted to the brain but also occurs in sensory and spinal cord neurons, increasing from early postnatal stages to adulthood and being downregulated by injury. This suggested that KIAA0319 participates in functions unrelated to neuronal migration. Supporting this hypothesis, overexpression of KIAA0319 repressed axon growth in hippocampal and dorsal root ganglia neurons; the intracellular domain of KIAA0319 was sufficient to elicit this effect. A similar inhibitory effect was observed in vivo as axon regeneration was impaired after transduction of sensory neurons with KIAA0319. Conversely, the deletion of Kiaa0319 in neurons increased neurite outgrowth in vitro and improved axon regeneration in vivo. At the mechanistic level, KIAA0319 engaged the JAK2-SH2B1 pathway to activate Smad2, which played a central role in KIAA0319-mediated repression of axon growth. In summary, we establish KIAA0319 as a novel player in axon growth and regeneration with the ability to repress the intrinsic growth potential of axons. This study describes a novel regulatory mechanism operating during peripheral nervous system and central nervous system axon growth, and offers novel targets for the development of effective therapies to promote axon regeneration.
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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 Socratic graph.