ArticleTraffic (Copenhagen, Denmark)2009
Selective targeting of ER exit sites supports axon development.
Article in Traffic (Copenhagen, Denmark), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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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.
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Who cites it
34 citing papers in PubMed, 58 citations in OpenAlex.
- In situ cryo-ET defines the ultrastructure of ER exit sites in human cells.Nature cell biology · 2026Article
- Reticulon-1 synthesis controls outgrowth and microtubule dynamics in injured cortical axons.Life science alliance · 2026Article
- The Neuronal Golgi Network and Its Acolytes.Sub-cellular biochemistry · 2026Review
- Beyond Vesicular Traffic: The ERES as the Gateway for Biosynthetic Secretion.Sub-cellular biochemistry · 2026Review
- Mechanisms of COPII coat assembly and cargo recognition in the secretory pathway.Nature reviews. Molecular cell biology · 2025Review
- The role of ER exit sites in maintaining P-body organization and integrity during Drosophila melanogaster oogenesis.EMBO reports · 2025Article
- The role of ER exit sites in maintaining P-body organization and transmitting ER stress response duringbioRxiv : the preprint server for biology · 2024Article
- The neuronal Golgi in neural circuit formation and reorganization.Frontiers in neural circuits · 2024Review
- Retinal ganglion cell-specific genetic regulation in primary open-angle glaucoma.Cell genomics · 2022Article
- Ribosome-associated vesicles: A dynamic subcompartment of the endoplasmic reticulum in secretory cells.Science advances · 2020Article
- Review
- Architecture and Dynamics of the Neuronal Secretory Network.Annual review of cell and developmental biology · 2019Review
- Extended Synaptotagmin Localizes to Presynaptic ER and Promotes Neurotransmission and Synaptic Growth inGenetics · 2017Article
- Mutations in Membrin/GOSR2 Reveal Stringent Secretory Pathway Demands of Dendritic Growth and Synaptic Integrity.Cell reports · 2017Article
- Review
- Axonal Degeneration in Retinal Ganglion Cells Is Associated with a Membrane Polarity-Sensitive Redox Process.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Axons provide the secretory machinery for trafficking of voltage-gated sodium channels in peripheral nerve.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Extended Synaptotagmin (ESyt) Triple Knock-Out Mice Are Viable and Fertile without Obvious Endoplasmic Reticulum Dysfunction.PloS one · 2016Article
- Identification of dietary alanine toxicity and trafficking dysfunction in a Drosophila model of hereditary sensory and autonomic neuropathy type 1.Human molecular genetics · 2015Article
- Insights from human congenital disorders of intestinal lipid metabolism.Journal of lipid research · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
During neuron development, the biosynthetic needs of the axon initially outweigh those of dendrites. However, although a localized role for the early secretory pathway in dendrite development has been observed, such a role in axon growth remains undefined. We therefore studied the localization of Sar1, a small GTPase that controls ER export, during early stages of neuronal development that are characterized by selective and robust axon growth. At these early stages, Sar1 was selectively targeted to the axon where it gradually concentrated within varicosities in which additional proteins that function in the early secretory pathway were detected. Sar1 targeting to the axon followed axon specification and was dependent on localized actin instability. Changes in Sar1 expression levels at these early development stages modulated axon growth. Specifically, reduced expression of Sar1, which was initially only detectable in the axon, correlated with reduced axon growth, where as overexpression of Sar1 supported the growth of longer axons. In support of the former finding, expression of dominant negative Sar1 inhibited axon growth. Thus, as observed in lower organisms, mammalian cells use temporal and spatial regulation of endoplasmic reticulum exit site (ERES) to address developmental biosynthetic demands. Furthermore, axons, such as dendrites, rely on ERES targeting and assembly for growth.
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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.