ArticleThe EMBO journal2022
A neuropathy-associated kinesin KIF1A mutation hyper-stabilizes the motor-neck interaction during the ATPase cycle.
Article in The EMBO journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 28 citations in OpenAlex.
- KIF1A-associated neurological disorders: therapeutic opportunities and challenges.European journal of human genetics : EJHG · 2026Review
- FTO promotes weight gain via altering Kif1a splicing and axonal vesicle trafficking in AgRP neurons.The EMBO journal · 2025Article
- Sculpting excitable membranes: voltage-gated ion channel delivery and distribution.Nature reviews. Neuroscience · 2025Review
- Genotype-phenotype correlations in 18 European patients with heterozygousFrontiers in medicine · 2025Article
- Cryo-EM unveils kinesin KIF1A's processivity mechanism and the impact of its pathogenic variant P305L.Nature communications · 2024Article
- Presynaptic perspective: Axonal transport defects in neurodevelopmental disorders.The Journal of cell biology · 2024Review
- A Model for Chemomechanical Coupling of Kinesin-3 Motor.Cellular and molecular bioengineering · 2024Article
- Cargo specificity, regulation, and therapeutic potential of cytoplasmic dynein.Experimental & molecular medicine · 2024Review
- Modeling the motion of disease-associated KIF1A heterodimers.Biophysical journal · 2023Article
- Peripheral mechanisms of peripheral neuropathic pain.Frontiers in molecular neuroscience · 2023Review
- De novo mutations in KIF1A-associated neuronal disorder (KAND) dominant-negatively inhibit motor activity and axonal transport of synaptic vesicle precursors.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- A neuropathy-associated kinesin KIF1A mutation hyper-stabilizes the motor-neck interaction during the ATPase cycle.The EMBO journal · 2022Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
The mechanochemical coupling of ATPase hydrolysis and conformational dynamics in kinesin motors facilitates intramolecular interaction cycles between the kinesin motor and neck domains, which are essential for microtubule-based motility. Here, we characterized a charge-inverting KIF1A-E239K mutant that we identified in a family with axonal-type Charcot-Marie-Tooth disease and also in 24 cases in human neuropathies including spastic paraplegia and hereditary sensory and autonomic neuropathy. We show that Glu239 in the β7 strand is a key residue of the motor domain that regulates the motor-neck interaction. Expression of the KIF1A-E239K mutation has decreased ability to complement Kif1a
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Registered trials
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