ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2007
Rapid and intermittent cotransport of slow component-b proteins.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 103 citations in OpenAlex.
- Axonal Transport Deficits in Parkinson's Disease: Insights from Neurotoxin, Genetic, and Sporadic Models.Brain sciences · 2026Review
- Lipids and α-Synuclein: adding further variables to the equation.Frontiers in molecular biosciences · 2024Review
- The alpha-synuclein oligomers activate nuclear factor of activated T-cell (NFAT) modulating synaptic homeostasis and apoptosis.Molecular medicine (Cambridge, Mass.) · 2023Article
- Dynein Dysfunction Prevents Maintenance of High Concentrations of Slow Axonal Transport Cargos at the Axon Terminal: A Computational Study.Journal of biomechanical engineering · 2023Article
- Inhibition of LRRK2 kinase activity promotes anterograde axonal transport and presynaptic targeting of α-synuclein.Acta neuropathologica communications · 2021Article
- Neuronal Soma-Derived Degradative Lysosomes Are Continuously Delivered to Distal Axons to Maintain Local Degradation Capacity.Cell reports · 2019Article
- The Non-amyloidal Component Region of α-Synuclein Is Important for α-Synuclein Transport Within Axons.Frontiers in cellular neuroscience · 2019Article
- Cholinergic activity is essential for maintaining the anterograde transport of Choline Acetyltransferase in Drosophila.Scientific reports · 2018Article
- Internalization, axonal transport and release of fibrillar forms of alpha-synuclein.Neurobiology of disease · 2018Review
- Mitochondrial dynamics in Parkinson's disease: a role for α-synuclein?Disease models & mechanisms · 2017Review
- Differential effects of immunotherapy with antibodies targeting α-synuclein oligomers and fibrils in a transgenic model of synucleinopathy.Neurobiology of disease · 2017Article
- Selective lowering of synapsins induced by oligomeric α-synuclein exacerbates memory deficits.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Anti-α-synuclein immunotherapy reduces α-synuclein propagation in the axon and degeneration in a combined viral vector and transgenic model of synucleinopathy.Acta neuropathologica communications · 2017Article
- Axonal transport and secretion of fibrillar forms of α-synuclein, Aβ42 peptide and HTTExon 1.Acta neuropathologica · 2016Article
- Bidirectional actin transport is influenced by microtubule and actin stability.Cellular and molecular life sciences : CMLS · 2015Article
- Formation of α-synuclein Lewy neurite-like aggregates in axons impedes the transport of distinct endosomes.Molecular biology of the cell · 2014Article
- A refined reaction-diffusion model of tau-microtubule dynamics and its application in FDAP analysis.Biophysical journal · 2014Article
- Reducing C-terminal-truncated alpha-synuclein by immunotherapy attenuates neurodegeneration and propagation in Parkinson's disease-like models.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Drag of the cytosol as a transport mechanism in neurons.Biophysical journal · 2014Article
- CNS axons globally increase axonal transport after peripheral conditioning.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
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5 authors at 3 institutions in 1 country.
Funding
Abstract
After synthesis in neuronal perikarya, proteins destined for synapses and other distant axonal sites are transported in three major groups that differ in average velocity and protein composition: fast component (FC), slow component-a (SCa), and slow component-b (SCb). The FC transports mainly vesicular cargoes at average rates of approximately 200-400 mm/d. SCa transports microtubules and neurofilaments at average rates of approximately 0.2-1 mm/d, whereas SCb translocates approximately 200 diverse proteins critical for axonal growth, regeneration, and synaptic function at average rates of approximately 2-8 mm/d. Several neurodegenerative diseases are characterized by abnormalities in one or more SCb proteins, but little is known about mechanisms underlying SCb compared with FC and SCa. Here, we use live-cell imaging to visualize and quantify the axonal transport of three SCb proteins, alpha-synuclein, synapsin-I, and glyceraldehyde-3-phosphate dehydrogenase in cultured hippocampal neurons, and directly compare their transport to synaptophysin, a prototypical FC protein. All three SCb proteins move rapidly but infrequently with pauses during transit, unlike synaptophysin, which moves much more frequently and persistently. By simultaneously visualizing the transport of proteins at high temporal and spatial resolution, we show that the dynamics of alpha-synuclein transport are distinct from those of synaptophysin but similar to other SCb proteins. Our observations of the cotransport of multiple SCb proteins in single axons suggest that they move as multiprotein complexes. These studies offer novel mechanistic insights into SCb and provide tools for further investigating its role in disease processes.
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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.