ArticleMolecular psychiatry2021
Defects in syntabulin-mediated synaptic cargo transport associate with autism-like synaptic dysfunction and social behavioral traits.
Article in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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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.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Traffic Jams in the Brain: How Kinesin Dysfunction Shapes Neurodevelopmental Disorders.Current issues in molecular biology · 2026Review
- Neuroplasticity mechanisms of NDBIs in autism: a review from brain connectivity to behavioral improvement.European journal of medical research · 2026Review
- Presynaptic perspective: Axonal transport defects in neurodevelopmental disorders.The Journal of cell biology · 2024Review
- Syntabulin regulates neuronal excitation/inhibition balance and epileptic seizures by transporting syntaxin 1B.Cell death discovery · 2023Article
- Highly Specialized Mechanisms for Mitochondrial Transport in Neurons: From Intracellular Mobility to Intercellular Transfer of Mitochondria.Biomolecules · 2023Review
- Effects of arginine vasopressin on the transcriptome of prefrontal cortex in autistic rat model.Journal of cellular and molecular medicine · 2022Article
- Advances in autism research, 2021: continuing to decipher the secrets of autism.Molecular psychiatry · 2021Article
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Authors and funding
8 authors at 1 institution in 1 country.
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Abstract
The formation and maintenance of synapses require long-distance delivery of newly synthesized synaptic proteins from the soma to distal synapses, raising the fundamental question of whether impaired transport is associated with neurodevelopmental disorders such as autism. We previously revealed that syntabulin acts as a motor adapter linking kinesin-1 motor and presynaptic cargos. Here, we report that defects in syntabulin-mediated transport and thus reduced formation and maturation of synapses are one of core synaptic mechanisms underlying autism-like synaptic dysfunction and social behavioral abnormalities. Syntabulin expression in the mouse brain peaks during the first 2 weeks of postnatal development and progressively declines during brain maturation. Neurons from conditional syntabulin
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Registered trials
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