ArticleHuman molecular genetics2015
α-COP binding to the survival motor neuron protein SMN is required for neuronal process outgrowth.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Extracellular vesicles as biomarkers of disease progression and therapeutic response in patients with spinal muscular atrophy.Molecular therapy. Advances · 2026Article
- The survival motor neuron protein: structure, functions, stability, and therapeutic targeting.Frontiers in cellular neuroscience · 2026Review
- Coatomer protein complex I is required for efficient secretion of dengue virus non-structural protein 1.Journal of virology · 2025Article
- Conditional knockout mouse model demonstrates that Copa expression is required for viability in development and adulthood.Biochemical and biophysical research communications · 2025Article
- Sm-site containing mRNAs can accept Sm-rings and are downregulated in Spinal Muscular Atrophy.Nucleic acids research · 2025Article
- COPI coatomer subunit α-COP interacts with the RNA binding protein Nucleolin via a C-terminal dilysine motif.Human molecular genetics · 2023Article
- Spinal Muscular Atrophy Patient iPSC-Derived Motor Neurons Display Altered Proteomes at Early Stages of Differentiation.ACS omega · 2021Article
- Sumoylation regulates the assembly and activity of the SMN complex.Nature communications · 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
- Conditional deletion of SMN in cell culture identifies functional SMN alleles.Human molecular genetics · 2020Article
- A paralog-specific role of COPI vesicles in the neuronal differentiation of mouse pluripotent cells.Life science alliance · 2020Article
- Local Secretory Trafficking Pathways in Neurons and the Role of Dendritic Golgi Outposts in Different Cell Models.Frontiers in molecular neuroscience · 2020Review
- Review
- 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
- Stasimon/Tmem41b localizes to mitochondria-associated ER membranes and is essential for mouse embryonic development.Biochemical and biophysical research communications · 2018Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Spinal muscular atrophy (SMA), a heritable neurodegenerative disease, results from insufficient levels of the survival motor neuron (SMN) protein. α-COP binds to SMN, linking the COPI vesicular transport pathway to SMA. Reduced levels of α-COP restricted development of neuronal processes in NSC-34 cells and primary cortical neurons. Remarkably, heterologous expression of human α-COP restored normal neurite length and morphology in SMN-depleted NSC-34 cells in vitro and zebrafish motor neurons in vivo. We identified single amino acid mutants of α-COP that selectively abrogate SMN binding, retain COPI-mediated Golgi-ER trafficking functionality, but were unable to support neurite outgrowth in cellular and zebrafish models of SMA. Taken together, these demonstrate the functional role of COPI association with the SMN protein in neuronal development.
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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.