ReviewCell communication and signaling : CCS2025
One gene, many phenotypes: the role of KIF5A in neurodegenerative and neurodevelopmental diseases.
Review in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
7 citing papers in PubMed.
- Selective Dopamine Transporter Inhibition with CE-123 Promotes Fear Extinction and Alters the Basolateral Amygdala Proteome Following Fear Extinction in Adolescent Male Rats.International journal of molecular sciences · 2026Article
- Targeted plasma proteomics uncover proteins associated with KIF5A-linked SPG10 and ALS spectrum disorders.HGG advances · 2026Article
- Non-transport functions of motor proteins in corticogenesis.Frontiers in cell and developmental biology · 2026Review
- Functional validation of the novel KIF5A p.R17Q VUS reveals defective axonal transport in iPSC-motoneurons from a SPG10 patient.Frontiers in genetics · 2026Article
- Effect of ALA on preventing diabetic peripheral neuropathy in rats through mitochondrial axonal transport.PloS one · 2026Article
- A guide to selecting high-performing renewable antibodies for KIF5A (Q12840) across western blot, immunoprecipitation, and immunofluorescence.F1000Research · 2026Article
- Spatial transcriptomics on an expanded dataset at the brain-electrode interface: exploration of variability and identification of novel biomarkers.Frontiers in neuroscience · 2026Article
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
Kinesin family member 5 A (KIF5A) is a neuron-specific molecular motor involved in anterograde transport. KIF5A mediates a wide range of trafficking processes that are only partially shared with the other members of the KIF5 family. Since 2002, several disease-causing mutations have been found in the KIF5A gene and a link between the specific domain in the encoded protein affected by mutations and the associated phenotype has become evident. Point mutations targeting KIF5A motor and stalk domains, that are expected to impair KIF5A motility, mainly associate with spastic paraplegia type 10 (SPG10) and axonal Charcot-Marie-Tooth (CMT) disease. Oppositely, translational frameshifts causing the elongation of KIF5A tail enhance KIF5A migration towards cell periphery, induce kinesin aggregation, and are linked to amyotrophic lateral sclerosis (ALS) or neonatal intractable myoclonus (NEIMY). This review correlates KIF5A structure and roles in neuronal trafficking with its involvement in the above-mentioned neurodegenerative and neurodevelopmental conditions.
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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.