ArticleScientific reports2017
The KIF1A homolog Unc-104 is important for spontaneous release, postsynaptic density maturation and perisynaptic scaffold organization.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
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- Loss of SYD-2 leads to decreased short-term memory inmicroPublication biology · 2026Article
- Formation, Organization, and Maintenance of Synaptic Vesicle Pools: From Molecules to Structure and Dynamics.Advances in neurobiology · 2026Review
- Wings of Discovery: UsingCells · 2025Review
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- Mechanisms controlling the trafficking, localization, and abundance of presynaptic CaFrontiers in molecular neuroscience · 2022Review
- Autophagy inhibition rescues structural and functional defects caused by the loss of mitochondrial chaperoneAutophagy · 2021Article
- Drosophila Rab39 Attenuates Lysosomal Degradation.International journal of molecular sciences · 2021Article
- Enhancing WNT Signaling Restores Cortical Neuronal Spine Maturation and Synaptogenesis in Tbr1 Mutants.Cell reports · 2020Article
- Anterograde Axonal Transport in Neuronal Homeostasis and Disease.Frontiers in molecular neuroscience · 2020Review
- Regional Differences and Similarities in the Brain Transcriptome for Mice Selected for Ethanol Preference From HS-CC Founders.Frontiers in genetics · 2018Article
- Article
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7 authors.
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Abstract
The kinesin-3 family member KIF1A has been shown to be important for experience dependent neuroplasticity. In Drosophila, amorphic mutations in the KIF1A homolog unc-104 disrupt the formation of mature boutons. Disease associated KIF1A mutations have been associated with motor and sensory dysfunctions as well as non-syndromic intellectual disability in humans. A hypomorphic mutation in the forkhead-associated domain of Unc-104, unc-104
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