ReviewFrontiers in molecular biosciences2017
Spinal Muscular Atrophy: From Defective Chaperoning of snRNP Assembly to Neuromuscular Dysfunction.
Review in Frontiers in molecular biosciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 32 citations in OpenAlex.
- RNA biomarkers in spinal muscular atrophy: enhancing pathogenesis understanding and guiding precision medicine.Cellular and molecular life sciences : CMLS · 2026Review
- Co-translational determination of quaternary structures in chaperone factories.Nature communications · 2026Article
- Neurodegenerative spliceosomopathies.Frontiers in cell and developmental biology · 2026Review
- SNUPN deficiency causes a recessive muscular dystrophy due to RNA mis-splicing and ECM dysregulation.Nature communications · 2024Article
- Molecular Mechanisms of Medicinal PlantCurrent pharmaceutical design · 2024Article
- Review
- Functional Implications of Protein Arginine Methyltransferases (PRMTs) in Neurodegenerative Diseases.Biology · 2023Review
- Cajal bodies: Evolutionarily conserved nuclear biomolecular condensates with properties unique to plants.The Plant cell · 2023Review
- SMN regulates GEMIN5 expression and acts as a modifier of GEMIN5-mediated neurodegeneration.Acta neuropathologica · 2023Article
- SMN complex member Gemin3 self-interacts and has a functional relationship with ALS-linked proteins TDP-43, FUS and Sod1.Scientific reports · 2019Article
- Binding of the protein ICln to α-integrin contributes to the activation of IClScientific reports · 2019Article
- Bridging human chaperonopathies and microbial chaperonins.Communications biology · 2019Review
- Genetic screen identifies a requirement for SMN in mRNA localisation within the Drosophila oocyte.BMC research notes · 2018Article
- Post-transcriptional regulation of gene expression and human disease.Current opinion in cell biology · 2018Review
- From phenologs to silent suppressors: Identifying potential therapeutic targets for human disease.Molecular reproduction and development · 2017Review
- Plant snRNP Biogenesis: A Perspective from the Nucleolus and Cajal Bodies.Frontiers in plant science · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal Muscular Atrophy (SMA) is a neuromuscular disorder that results from decreased levels of the survival motor neuron (SMN) protein. SMN is part of a multiprotein complex that also includes Gemins 2-8 and Unrip. The SMN-Gemins complex cooperates with the protein arginine methyltransferase 5 (PRMT5) complex, whose constituents include WD45, PRMT5 and pICln. Both complexes function as molecular chaperones, interacting with and assisting in the assembly of an Sm protein core onto small nuclear RNAs (snRNAs) to generate small nuclear ribonucleoproteins (snRNPs), which are the operating components of the spliceosome. Molecular and structural studies have refined our knowledge of the key events taking place within the crowded environment of cells and the numerous precautions undertaken to ensure the faithful assembly of snRNPs. Nonetheless, it remains unclear whether a loss of chaperoning in snRNP assembly, considered as a "housekeeping" activity, is responsible for the selective neuromuscular phenotype in SMA. This review thus shines light on
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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.