ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
The kinesin-2 family member KIF3C regulates microtubule dynamics and is required for axon growth and regeneration.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 83 citations in OpenAlex.
- A systems-level proteomic analysis identifies kinesin targets of KIFBP during neuronal development.bioRxiv : the preprint server for biology · 2026Article
- Neuronal overexpression of Nrf2 reduces dystrophic neurites in 5XFAD Alzheimer's disease model mice.Alzheimer's research & therapy · 2026Article
- Motor Protein Disruption Critically Alters Organelle Trafficking and Excitation-Contraction Coupling.eNeuro · 2026Article
- Neuronal overexpression of Nrf2 reduces dystrophic neurites in 5XFAD Alzheimer's disease model mice.bioRxiv : the preprint server for biology · 2026Article
- Unraveling the core: hub genes bridging familial and sporadic Parkinson's disease.Journal of neurology · 2026Article
- Time‑resolved multi-omic analysis of paclitaxel exposure in human iPSC‑derived sensory neurons unveils mechanisms of chemotherapy‑induced peripheral neuropathy.Cell death & disease · 2026Article
- KIF3C inhibits the progression and proliferation of colorectal cancer.BMC gastroenterology · 2025Article
- Targeting Kinesins for Therapeutic Exploitation of Chromosomal Instability in Lung Cancer.Cancers · 2025Review
- Involvement of kinesins in skeletal dysplasia: a review.American journal of physiology. Cell physiology · 2024Review
- Efficient axonal transport of endolysosomes relies on the balanced ratio of microtubule tyrosination and detyrosination.Journal of cell science · 2024Article
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- EGFR-mediated hyperacetylation of tubulin induced docetaxel resistance by downregulation of HDAC6 and upregulation of MCAK and PLK1 in prostate cancer cells.The Kaohsiung journal of medical sciences · 2024Article
- Deciphering the Tubulin Language: Molecular Determinants and Readout Mechanisms of the Tubulin Code in Neurons.International journal of molecular sciences · 2023Review
- KAP is the neuronal organelle adaptor for Kinesin-2 KIF3AB and KIF3AC.Molecular biology of the cell · 2022Article
- Selective motor activation in organelle transport along axons.Nature reviews. Molecular cell biology · 2022Review
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- Genetics Responses to Hypoxia and Reoxygenation Stress inAnimals : an open access journal from MDPI · 2021Article
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- Comparative transcriptomics between Drosophila mojavensis and D. arizonae reveals transgressive gene expression and underexpression of spermatogenesis-related genes in hybrid testes.Scientific reports · 2021Article
- Tubulin post-translational modifications control neuronal development and functions.Developmental neurobiology · 2021Review
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Axon regeneration after injury requires the extensive reconstruction, reorganization, and stabilization of the microtubule cytoskeleton in the growth cones. Here, we identify KIF3C as a key regulator of axonal growth and regeneration by controlling microtubule dynamics and organization in the growth cone. KIF3C is developmentally regulated. Rat embryonic sensory axons and growth cones contain undetectable levels of KIF3C protein that is locally translated immediately after injury. In adult neurons, KIF3C is axonally transported from the cell body and is enriched at the growth cone where it preferentially binds to tyrosinated microtubules. Functionally, the interaction of KIF3C with EB3 is necessary for its localization at the microtubule plus-ends in the growth cone. Depletion of KIF3C in adult neurons leads to an increase in stable, overgrown and looped microtubules because of a strong decrease in the microtubule frequency of catastrophes, suggesting that KIF3C functions as a microtubule-destabilizing factor. Adult axons lacking KIF3C, by RNA interference or KIF3C gene knock-out, display an impaired axonal outgrowth in vitro and a delayed regeneration after injury both in vitro and in vivo. Murine KIF3C knock-out embryonic axons grow normally but do not regenerate after injury because they are unable to locally translate KIF3C. These data show that KIF3C is an injury-specific kinesin that contributes to axon growth and regeneration by regulating and organizing the microtubule cytoskeleton in the growth cone.
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Registered trials
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