ArticlePloS one2016
Altered mRNA Splicing in SMN-Depleted Motor Neuron-Like Cells.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
17 citing papers in PubMed, 22 citations in OpenAlex.
- Widespread intron retention and exon skipping characterise alternative splicing changes in a C. elegans model of spinal muscular atrophy.Human molecular genetics · 2026Article
- Review
- IL-1ra and CCL5, but not IL-10, are promising targets for treating SMA astrocyte-driven pathology.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- COPI coatomer subunit α-COP interacts with the RNA binding protein Nucleolin via a C-terminal dilysine motif.Human molecular genetics · 2023Article
- PRMT inhibitor promotes SMN2 exon 7 inclusion and synergizes with nusinersen to rescue SMA mice.EMBO molecular medicine · 2023Article
- Mitochondrial Dysfunction in Spinal Muscular Atrophy.International journal of molecular sciences · 2022Review
- Splicing efficiency of minor introns in a mouse model of SMA predominantly depends on their branchpoint sequence and can involve the contribution of major spliceosome components.RNA (New York, N.Y.) · 2022Article
- Mitochondrial defects in the respiratory complex I contribute to impaired translational initiation via ROS and energy homeostasis in SMA motor neurons.Acta neuropathologica communications · 2020Article
- Ultrasensitive single-cell proteomics workflow identifies >1000 protein groups per mammalian cell.Chemical science · 2020Article
- Muscle regulates mTOR dependent axonal local translation in motor neurons via CTRP3 secretion: implications for a neuromuscular disorder, spinal muscular atrophy.Acta neuropathologica communications · 2019Article
- AAV9-mediated delivery of miR-23a reduces disease severity in Smn2B/-SMA model mice.Human molecular genetics · 2019Article
- mRNP assembly, axonal transport, and local translation in neurodegenerative diseases.Brain research · 2018Review
- Unraveling the Pathways to Neuronal Homeostasis and Disease: Mechanistic Insights into the Role of RNA-Binding Proteins and Associated Factors.International journal of molecular sciences · 2018Review
- Targeting RNA structure in SMN2 reverses spinal muscular atrophy molecular phenotypes.Nature communications · 2018Article
- Neurochondrin interacts with the SMN protein suggesting a novel mechanism for spinal muscular atrophy pathology.Journal of cell science · 2018Article
- The Survival of Motor Neuron Protein Acts as a Molecular Chaperone for mRNP Assembly.Cell reports · 2017Article
- Alternative Splicing and CaV-Associated Channelopathies.Wiley interdisciplinary reviews. RNAReview
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Spinal muscular atrophy (SMA) is an intractable neurodegenerative disease afflicting 1 in 6-10,000 live births. One of the key functions of the SMN protein is regulation of spliceosome assembly. Reduced levels of the SMN protein that are observed in SMA have been shown to result in aberrant mRNA splicing. SMN-dependent mis-spliced transcripts in motor neurons may cause stresses that are particularly harmful and may serve as potential targets for the treatment of motor neuron disease or as biomarkers in the SMA patient population. We performed deep RNA sequencing using motor neuron-like NSC-34 cells to screen for SMN-dependent mRNA processing changes that occur following acute depletion of SMN. We identified SMN-dependent splicing changes, including an intron retention event that results in the production of a truncated Rit1 transcript. This intron-retained transcript is stable and is mis-spliced in spinal cord from symptomatic SMA mice. Constitutively active Rit1 ameliorated the neurite outgrowth defect in SMN depleted NSC-34 cells, while expression of the truncated protein product of the mis-spliced Rit1 transcript inhibited neurite extension. These results reveal new insights into the biological consequence of SMN-dependent splicing in motor neuron-like cells.
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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.