ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Cytoskeletal requirements in axonal transport of slow component-b.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 53 citations in OpenAlex.
- Axonal Transport Deficits in Parkinson's Disease: Insights from Neurotoxin, Genetic, and Sporadic Models.Brain sciences · 2026Review
- Dynein Dysfunction Prevents Maintenance of High Concentrations of Slow Axonal Transport Cargos at the Axon Terminal: A Computational Study.Journal of biomechanical engineering · 2023Article
- Can the lack of fibrillar form of alpha-synuclein in Lewy bodies be explained by its catalytic activity?Mathematical biosciences · 2022Article
- Inhibition of LRRK2 kinase activity promotes anterograde axonal transport and presynaptic targeting of α-synuclein.Acta neuropathologica communications · 2021Article
- The Non-amyloidal Component Region of α-Synuclein Is Important for α-Synuclein Transport Within Axons.Frontiers in cellular neuroscience · 2019Article
- Axonal Transport, Phase-Separated Compartments, and Neuron Mechanics - A New Approach to Investigate Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2018Review
- Bidirectional actin transport is influenced by microtubule and actin stability.Cellular and molecular life sciences : CMLS · 2015Article
- Drag of the cytosol as a transport mechanism in neurons.Biophysical journal · 2014Article
- Synaptic vesicle recycling: steps and principles.The EMBO journal · 2014Review
- Seeing the unseen: the hidden world of slow axonal transport.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2014Review
- Amyloid-β signals through tau to drive ectopic neuronal cell cycle re-entry in Alzheimer's disease.Journal of cell science · 2013Article
- Selective vulnerability of synaptic signaling and metabolism to nitrosative stress.Antioxidants & redox signaling · 2012Review
- Neuron-to-neuron transmission of α-synuclein fibrils through axonal transport.Annals of neurology · 2012Article
- Interaction with a kinesin-2 tail propels choline acetyltransferase flow towards synapse.Traffic (Copenhagen, Denmark) · 2012Article
- The emerging role of forces in axonal elongation.Progress in neurobiology · 2011Review
- Article
- A synthetic peptide shows retro- and anterograde neuronal transport before disrupting the chemosensation of plant-pathogenic nematodes.PloS one · 2011Article
- Alpha-synuclein loss in spinal muscular atrophy.Journal of molecular neuroscience : MN · 2011Article
- A pathologic cascade leading to synaptic dysfunction in alpha-synuclein-induced neurodegeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Dynamic transport and localization of alpha-synuclein in primary hippocampal neurons.Molecular neurodegeneration · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
Slow component-b (SCb) translocates approximately 200 diverse proteins from the cell body to the axon and axon tip at average rates of approximately 2-8 mm/d. Several studies suggest that SCb proteins are cotransported as one or more macromolecular complexes, but the basis for this cotransport is unknown. The identification of actin and myosin in SCb led to the proposal that actin filaments function as a scaffold for the binding of other SCb proteins and that transport of these complexes is powered by myosin: the "microfilament-complex" model. Later, several SCb proteins were also found to bind F-actin, supporting the idea, but despite this, the model has never been directly tested. Here, we test this model by disrupting the cytoskeleton in a live-cell model system wherein we directly visualize transport of SCb cargoes. We focused on three SCb proteins that we previously showed were cotransported in our system: alpha-synuclein, synapsin-I, and glyceraldehyde-3-phosphate dehydrogenase. Disruption of actin filaments with latrunculin had no effect on the velocity or frequency of transport of these three proteins. Furthermore, cotransport of these three SCb proteins continued in actin-depleted axons. We conclude that actin filaments do not function as a scaffold to organize and transport these and possibly other SCb proteins. In contrast, depletion of microtubules led to a dramatic inhibition of vectorial transport of SCb cargoes. These findings do not support the microfilament-complex model, but instead indicate that the transport of protein complexes in SCb is powered by microtubule motors.
Indexed as
Identifiers
What OpenQuestion holds
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.