ArticleHuman molecular genetics2011
The COPI vesicle complex binds and moves with survival motor neuron within axons.
Article in Human molecular genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed, 79 citations in OpenAlex.
- The Role of the Golgi Apparatus in Neurodegeneration.Sub-cellular biochemistry · 2026Review
- SMN deficiency inhibits endochondral ossification via promoting TRAF6-induced ubiquitination degradation of YBX1 in spinal muscular atrophy.Bone research · 2025Article
- Conditional knockout mouse model demonstrates that Copa expression is required for viability in development and adulthood.Biochemical and biophysical research communications · 2025Article
- Whole-transcriptome sequencing in neural and non-neural tissues of a mouse model identifies miR-34a as a key regulator in SMA pathogenesis.Molecular therapy. Nucleic acids · 2025Article
- The SMN-ribosome interplay: a new opportunity for Spinal Muscular Atrophy therapies.Biochemical Society transactions · 2024Review
- COPI coatomer subunit α-COP interacts with the RNA binding protein Nucleolin via a C-terminal dilysine motif.Human molecular genetics · 2023Article
- COPI-regulated mitochondria-ER contact site formation maintains axonal integrity.Cell reports · 2023Article
- Nucleolin: a cell portal for viruses, bacteria, and toxins.Cellular and molecular life sciences : CMLS · 2022Review
- Spinal Muscular Atrophy Patient iPSC-Derived Motor Neurons Display Altered Proteomes at Early Stages of Differentiation.ACS omega · 2021Article
- CaMKK2 facilitates Golgi-associated vesicle trafficking to sustain cancer cell proliferation.Cell death & disease · 2021Article
- Identification of GOLPH3 Partners inCells · 2021Article
- What Genetics Has Told Us and How It Can Inform Future Experiments for Spinal Muscular Atrophy, a Perspective.International journal of molecular sciences · 2021Article
- Mutations in the COPI coatomer subunit α-COP induce release of Aβ-42 and amyloid precursor protein intracellular domain and increase tau oligomerization and release.Neurobiology of aging · 2021Article
- Biallelic variants in COPB1 cause a novel, severe intellectual disability syndrome with cataracts and variable microcephaly.Genome medicine · 2021Article
- Conditional deletion of SMN in cell culture identifies functional SMN alleles.Human molecular genetics · 2020Article
- Quantitative proteomics identifies proteins that resist translational repression and become dysregulated in ALS-FUS.Human molecular genetics · 2019Article
- Interaction between alpha-COP and SMN ameliorates disease phenotype in a mouse model of spinal muscular atrophy.Biochemical and biophysical research communications · 2019Article
- Abnormal Golgi morphology and decreased COPI function in cells with low levels of SMN.Brain research · 2019Article
- Local Translation in Axons: When Membraneless RNP Granules Meet Membrane-Bound Organelles.Frontiers in molecular biosciences · 2019Review
- Multi-Study Proteomic and Bioinformatic Identification of Molecular Overlap between Amyotrophic Lateral Sclerosis (ALS) and Spinal Muscular Atrophy (SMA).Brain sciences · 2018Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Spinal muscular atrophy (SMA), an inherited disease of motor neuron dysfunction, results from insufficient levels of the survival motor neuron (SMN) protein. Movement of the SMN protein as granules within cultured axons suggests that the pathogenesis of SMA may involve defects in neuronal transport, yet the nature of axon transport vesicles remains enigmatic. Here we show that SMN directly binds to the α-subunit of the coat protein I (COPI) vesicle coat protein. The α-COP protein co-immunoprecipitates with SMN, small nuclear ribonucleoprotein-associated assembly factors and β-actin mRNA. Although typically Golgi associated, in neuronal cells α-COP localizes to lamellipodia and growth cones and moves within the axon, with a subset of these granules traveling together with SMN. Depletion of α-COP resulted in mislocalization of SMN and actin at the leading edge at the lamellipodia. We propose that neurons utilize the Golgi-associated COPI vesicle to deliver cargoes necessary for motor neuron integrity and function.
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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.