ArticleGenetics2012
Three routes to suppression of the neurodegenerative phenotypes caused by kinesin heavy chain mutations.
Article in Genetics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 20 citations in OpenAlex.
- Wings of Discovery: UsingCells · 2025Review
- Pericentrin interacts with Kinesin-1 to drive centriole motility.The Journal of cell biology · 2022Article
- Dual control of Kinesin-1 recruitment to microtubules by Ensconsin inDevelopment (Cambridge, England) · 2019Article
- Structural consequences of hereditary spastic paraplegia disease-related mutations in kinesin.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Ethanol stimulates the in vivo axonal movement of neuropeptide dense-core vesicles in Drosophila motor neurons.Journal of neurochemistry · 2018Article
- Limited distal organelles and synaptic function in extensive monoaminergic innervation.Journal of cell science · 2017Article
- Common general anesthetic propofol impairs kinesin processivity.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Hippocampal to basal forebrain transport of MnNeuroImage · 2017Article
- Characterization of kinesin switch I mutations that cause hereditary spastic paraplegia.PloS one · 2017Article
- Dynamic microtubule organization and mitochondrial transport are regulated by distinct Kinesin-1 pathways.Biology open · 2015Article
- Pavarotti/MKLP1 regulates microtubule sliding and neurite outgrowth in Drosophila neurons.Current biology : CB · 2015Article
- Kinesin-5 allosteric inhibitors uncouple the dynamics of nucleotide, microtubule, and neck-linker binding sites.Biophysical journal · 2014Article
- Ensconsin/Map7 promotes microtubule growth and centrosome separation in Drosophila neural stem cells.The Journal of cell biology · 2014Article
- Article
- Spastic paraplegia mutation N256S in the neuronal microtubule motor KIF5A disrupts axonal transport in a Drosophila HSP model.PLoS genetics · 2012Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Kinesin-1 is a motor protein that moves stepwise along microtubules by employing dimerized kinesin heavy chain (Khc) subunits that alternate cycles of microtubule binding, conformational change, and ATP hydrolysis. Mutations in the Drosophila Khc gene are known to cause distal paralysis and lethality preceded by the occurrence of dystrophic axon terminals, reduced axonal transport, organelle-filled axonal swellings, and impaired action potential propagation. Mutations in the equivalent human gene, Kif5A, result in similar problems that cause hereditary spastic paraplegia (HSP) and Charcot-Marie-Tooth type 2 (CMT2) distal neuropathies. By comparing the phenotypes and the complementation behaviors of a large set of Khc missense alleles, including one that is identical to a human Kif5A HSP allele, we identified three routes to suppression of Khc phenotypes: nutrient restriction, genetic background manipulation, and a remarkable intramolecular complementation between mutations known or likely to cause reciprocal changes in the rate of microtubule-stimulated ADP release by kinesin-1. Our results reveal the value of large-scale complementation analysis for gaining insight into protein structure-function relationships in vivo and point to possible paths for suppressing symptoms of HSP and related distal neuropathies.
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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 OpenQuestion graph.