ArticleThe Journal of cell biology2003
Abnormal neurofilament transport caused by targeted disruption of neuronal kinesin heavy chain KIF5A.
Article in The Journal of cell biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 papers.
What it found
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Who cites it
157 citing papers in PubMed, 348 citations in OpenAlex.
- Bisphenol-A impairs hippocampal neurogenesis by disrupting kinesin-1-dependent mitochondrial trafficking.The Journal of biological chemistry · 2026Article
- Traffic Jams in the Brain: How Kinesin Dysfunction Shapes Neurodevelopmental Disorders.Current issues in molecular biology · 2026Review
- A systems-level proteomic analysis identifies kinesin targets of KIFBP during neuronal development.bioRxiv : the preprint server for biology · 2026Article
- Visualization of peripheral nerves in developing and regenerating limbs using a novel peripherin reporter line of Xenopus laevis.Biology open · 2026Article
- The Long Haul: Microtubule Motors as the Essential Supply Line for Neuronal Longevity.Journal of neurochemistry · 2026Review
- From Axonal Growth to Neurodegeneration: The Dual Role of Neurofilament Dynamics in Health and Disease.NeuroSci · 2026Review
- Mitochondrial dynamics in neurodevelopment and neurodevelopmental disorders.Nature reviews. Neuroscience · 2026Review
- Consequences of the Novel ALS-AssociatedNeurology. Genetics · 2026Article
- Kinesin-1 is highly flexible and adopts an open conformation in the absence of cargo.iScience · 2026Article
- Kinesins inOpen biology · 2025Review
- MiR-140-3p regulates axonal motor protein KIF5A and contributes to axonal transport degeneration in SMA.Cell death discovery · 2025Article
- ALS Mutations Shift the Isoelectric Point of the KIF5A C Terminal Inducing Protein Aggregation and TDP-43 Mislocalization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- One gene, many phenotypes: the role of KIF5A in neurodegenerative and neurodevelopmental diseases.Cell communication and signaling : CCS · 2025Review
- Deciphering distinct genetic risk factors for FTLD-TDP pathological subtypes via whole-genome sequencing.Nature communications · 2025Article
- Altered molecular and cellular mechanisms in KIF5A-associated neurodegenerative or neurodevelopmental disorders.Cell death & disease · 2024Article
- KIF5A regulates axonal repair and time-dependent axonal transport of SFPQ granules and mitochondria in human motor neurons.bioRxiv : the preprint server for biology · 2024Article
- Involvement of kinesins in skeletal dysplasia: a review.American journal of physiology. Cell physiology · 2024Review
- Loss-of-function mutation in DDX53 associated with hereditary spastic paraplegia-like disorder.Journal of molecular medicine (Berlin, Germany) · 2024Article
- Neurofilament Biophysics: From Structure to Biomechanics.Molecular biology of the cell · 2024Review
- A novel in-frame deletion in KIF5C gene causes infantile onset epilepsy and psychomotor retardation.MedComm · 2024Article
97 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
To test the hypothesis that fast anterograde molecular motor proteins power the slow axonal transport of neurofilaments (NFs), we used homologous recombination to generate mice lacking the neuronal-specific conventional kinesin heavy chain, KIF5A. Because null KIF5A mutants die immediately after birth, a synapsin-promoted Cre-recombinase transgene was used to direct inactivation of KIF5A in neurons postnatally. Three fourths of such mutant mice exhibited seizures and death at around 3 wk of age; the remaining animals survived to 3 mo or longer. In young mutant animals, fast axonal transport appeared to be intact, but NF-H, as well as NF-M and NF-L, accumulated in the cell bodies of peripheral sensory neurons accompanied by a reduction in sensory axon caliber. Older animals also developed age-dependent sensory neuron degeneration, an accumulation of NF subunits in cell bodies and a reduction in axons, loss of large caliber axons, and hind limb paralysis. These data support the hypothesis that a conventional kinesin plays a role in the microtubule-dependent slow axonal transport of at least one cargo, the NF proteins.
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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.