ArticleHuman molecular genetics2008
Atlastin GTPases are required for Golgi apparatus and ER morphogenesis.
Article in Human molecular genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers, 1 of them a synthesis that pooled it.
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Who cites it
125 citing papers in PubMed, 1 synthesis or guideline pooled it, 204 citations in OpenAlex.
- Peripheral Biomarkers in Schizophrenia: A Meta-Analysis of Microarray Gene Expression Datasets.The international journal of neuropsychopharmacology · 2019Pooled it
- Mammalian MemPrep establishes the lipid composition of ER membranes in HEK293T cells.EMBO reports · 2026Article
- Atlastin-2-mediated endoplasmic reticulum membrane tethering is critical for flavivirus replication.PLoS biology · 2026Article
- Rab10 Promotes Atlastin-Mediated Endoplasmic Reticulum Membrane Fusion.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- ATL2 Recruits TRAK1 to Promote Mitochondrial Transport at ER-Mitochondria Contact Sites.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Phosphatase PTP-4 downregulates ATLN-1-mediated host defense againstFrontiers in pharmacology · 2026Article
- Cellular Biology: Virus-Host Interactions and RNA Structure and Function.Current topics in microbiology and immunology · 2026Review
- LXR agonist rescues synaptic dysfunction and degeneration in SPG3A patient-specific iPSC-derived neurons.Acta neuropathologica communications · 2025Article
- Tubular ER dysfunction in neurodegenerative diseases.Neurobiology of disease · 2025Review
- The synaptic vesicle cluster as a controller of pre- and postsynaptic structure and function.The Journal of physiology · 2025Review
- Reticulophagy and viral infection.Autophagy · 2025Review
- Atlastin-1 regulates endosomal tubulation and lysosomal proteolysis in human cortical neurons.Neurobiology of disease · 2024Article
- Dissecting the mechanism of atlastin-mediated homotypic membrane fusion at the single-molecule level.Nature communications · 2024Article
- Differential Efficacy of Small Molecules Dynasore and Mdivi-1 for the Treatment of Dry Eye Epitheliopathy or as a Countermeasure for Nitrogen Mustard Exposure of the Ocular Surface.The Journal of pharmacology and experimental therapeutics · 2024Article
- Hereditary spastic paraplegia: Novel insights into the pathogenesis and management.SAGE open medicine · 2024Review
- Yeast lunapark regulates the formation ofiScience · 2023Article
- Drosophila Atlastin regulates synaptic vesicle mobilization independent of bone morphogenetic protein signaling.Biological research · 2023Article
- The atlastin ER morphogenic proteins promote formation of a membrane penetration site during non-enveloped virus entry.Journal of virology · 2023Article
- Article
- The atlastin paralogs: The complexity in the tails.The Journal of cell biology · 2023Article
65 more citing papers are in PubMed but not listed here.
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 3 institutions in 2 countries.
Funding
Abstract
The hereditary spastic paraplegias (SPG1-33) comprise a cluster of inherited neurological disorders characterized principally by lower extremity spasticity and weakness due to a length-dependent, retrograde axonopathy of corticospinal motor neurons. Mutations in the gene encoding the large oligomeric GTPase atlastin-1 are responsible for SPG3A, a common autosomal dominant hereditary spastic paraplegia. Here we describe a family of human GTPases, atlastin-2 and -3 that are closely related to atlastin-1. Interestingly, while atlastin-1 is predominantly localized to vesicular tubular complexes and cis-Golgi cisternae, mostly in brain, atlastin-2 and -3 are localized to the endoplasmic reticulum (ER) and are most enriched in other tissues. Knockdown of atlastin-2 and -3 levels in HeLa cells using siRNA (small interfering RNA) causes disruption of Golgi morphology, and these Golgi structures remain sensitive to brefeldin A treatment. Interestingly, expression of SPG3A mutant or dominant-negative atlastin proteins lacking GTPase activity causes prominent inhibition of ER reticularization, suggesting a role for atlastin GTPases in the formation of three-way junctions in the ER. However, secretory pathway trafficking as assessed using vesicular stomatitis virus G protein fused to green fluorescent protein (VSVG-GFP) as a reporter was essentially normal in both knockdown and dominant-negative overexpression conditions for all atlastins. Thus, the atlastin family of GTPases functions prominently in both ER and Golgi morphogenesis, but they do not appear to be required generally for anterograde ER-to-Golgi trafficking. Abnormal morphogenesis of the ER and Golgi resulting from mutations in atlastin-1 may ultimately underlie SPG3A by interfering with proper membrane distribution or polarity of the long corticospinal motor neurons.
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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.