ArticleNeuron2012
Dynactin is required for transport initiation from the distal axon.
Article in Neuron, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.
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Who cites it
125 citing papers in PubMed, 200 citations in OpenAlex.
- Retrograde mitochondrial transport is required for mitochondrial biogenesis in zebrafish neurons.Nature communications · 2026Article
- The Long Haul: Microtubule Motors as the Essential Supply Line for Neuronal Longevity.Journal of neurochemistry · 2026Review
- Adaptor-mediated recruitment of three dyneins to dynactin enhances force generation.Nature cell biology · 2026Article
- CDKL5 regulates the initiation of retrograde axonal transport through CLIP170-dynactin complex formation.The FEBS journal · 2026Article
- Regulation of nuclear transport of the transcriptional factor REST improves axon regeneration in peripheral nerves.Molecular medicine reports · 2025Article
- Article
- Retrograde mitochondrial transport regulates mitochondrial biogenesis in zebrafish neurons.bioRxiv : the preprint server for biology · 2025Article
- Neuroaxonal Degeneration as a Converging Mechanism in Motor Neuron Diseases (MNDs): Molecular Insights into RNA Dysregulation and Emerging Therapeutic Targets.International journal of molecular sciences · 2025Review
- Role of LRRK2 in axonal transport and Parkinson's disease.The Biochemical journal · 2025Review
- Interfacial Interactions between Neural Tracing Lectin-Gold Nanoparticle Conjugate and Cell Membrane Glycoproteins.Langmuir : the ACS journal of surfaces and colloids · 2025Article
- Dynein-driven regulation of postsynaptic membrane architecture and synaptic function.Journal of cell science · 2025Article
- Engine breakdown of lysosomes and related organelles and the resulting physiology.Frontiers in cell and developmental biology · 2025Review
- The role of autophagy in the pathogenesis and treatment of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).Autophagy reports · 2025Review
- VezA/vezatin facilitates proper assembly of the dynactin complex in vivo.Cell reports · 2024Article
- Herpes simplex virus type-1 cVAC formation in neuronal cells is mediated by dynein motor function and glycoprotein retrieval from the plasma membrane.Journal of virology · 2024Article
- VezA/vezatin facilitates proper assembly of the dynactin complex in vivo.bioRxiv : the preprint server for biology · 2024Article
- Dysregulation of stress granule dynamics by DCTN1 deficiency exacerbates TDP-43 pathology in Drosophila models of ALS/FTD.Acta neuropathologica communications · 2024Article
- Perry Disease: Bench to Bedside Circulation and a Team Approach.Biomedicines · 2024Article
- Axonal transport of autophagosomes is regulated by dynein activators JIP3/JIP4 and ARF/RAB GTPases.The Journal of cell biology · 2023Article
- Control of motor landing and processivity by the CAP-Gly domain in the KIF13B tail.Nature communications · 2023Article
65 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Dynactin is a required cofactor for the minus-end-directed microtubule motor cytoplasmic dynein. Mutations within the highly conserved CAP-Gly domain of dynactin cause neurodegenerative disease. Here, we show that the CAP-Gly domain is necessary to enrich dynactin at the distal end of primary neurons. While the CAP-Gly domain is not required for sustained transport along the axon, we find that the distal accumulation facilitates the efficient initiation of retrograde vesicular transport from the neurite tip. Neurodegenerative disease mutations in the CAP-Gly domain prevent the distal enrichment of dynactin thereby inhibiting the initiation of retrograde transport. Thus, we propose a model in which distal dynactin is a key mediator in promoting the interaction among the microtubule, dynein motor, and cargo for the efficient initiation of transport. Mutations in the CAP-Gly domain disrupt the formation of the motor-cargo complex, highlighting the specific defects in axonal transport that may lead to neurodegeneration.
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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.