ReviewNature reviews. Neuroscience2009
Spinal muscular atrophy: why do low levels of survival motor neuron protein make motor neurons sick?
Review in Nature reviews. Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 426 papers, 3 of them syntheses that pooled it.
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
426 citing papers in PubMed, 3 syntheses or guidelines pooled it, 711 citations in OpenAlex.
- Systematic literature review of the impact of spinal muscular atrophy therapies on bulbar function.Journal of neuromuscular diseases · 2025Pooled it
- Drug treatment for spinal muscular atrophy types II and III.The Cochrane database of systematic reviews · 2020Pooled it
- Drug treatment for spinal muscular atrophy type I.The Cochrane database of systematic reviews · 2019Pooled it
- From optical control to translational readiness: an evidence-tiered framework for optogenetics in neuromuscular and neurological disorders.Materials today. Bio · 2026Review
- Biphasic SMN condensates safeguard stress-induced cytoplasmic mislocalization of splicing RNPs.Cellular and molecular life sciences : CMLS · 2026Article
- Are components of the histone gene expression machinery functionally repurposed in terminally differentiated cells?Biology open · 2026Article
- Clinical Characterization of Patients With 5q Spinal Muscular Atrophy Types 2 and 3 in Brazil: A Cross-Sectional Observational Study.Clinical genetics · 2026Observational
- Antisense oligonucleotides treatment uncovers differences in the modulation of dysregulated intracellular pathways in Spinal Muscular Atrophy motoneurons.Cell death & disease · 2026Article
- Temperature-induced symptoms in adolescents and adults with spinal muscular atrophy.Journal of neuromuscular diseases · 2026Article
- Onasemnogene abeparvovec gene therapy for treatment of patients with spinal muscular atrophy: Updated real-world practical considerations.Journal of neuromuscular diseases · 2026Review
- Motor function score changes in severe 5q spinal muscular atrophy during risdiplam treatment: an observational longitudinal nationwide cohort study.EClinicalMedicine · 2026Article
- A stand-alone ICln release module revealed by deconstructing the SMN complex with engineered Brr1.Nucleic acids research · 2026Article
- Characterizing SMN1 hybrid and deletion alleles using large-scale SNP array-based SMA carrier screening.BMC medical genomics · 2026Article
- Long-term comparative analysis of AAV9-mediated gene replacement therapies for spinal muscular atrophy in mice.Nature communications · 2026Article
- RNA-binding protein family diversification correlates with neural complexity across metazoan evolution.iScience · 2026Article
- RNA-binding proteins TDP-43 and FUS promote R-loop resolution and regulate transcription termination.The Journal of biological chemistry · 2026Article
- Linking rare variants to cell-type function in profound autism with brain transcriptomics and foundation models.Cell genomics · 2026Review
- RNA biomarkers in spinal muscular atrophy: enhancing pathogenesis understanding and guiding precision medicine.Cellular and molecular life sciences : CMLS · 2026Review
- Immaturity of the neuromuscular junction in spinal muscular atrophy mouse models.Frontiers in cellular neuroscience · 2026Review
- Neurodegenerative spliceosomopathies.Frontiers in cell and developmental biology · 2026Review
366 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Many neurogenetic disorders are caused by the mutation of ubiquitously expressed genes. One such disorder, spinal muscular atrophy, is caused by loss or mutation of the survival motor neuron1 gene (SMN1), leading to reduced SMN protein levels and a selective dysfunction of motor neurons. SMN, together with partner proteins, functions in the assembly of small nuclear ribonucleoproteins (snRNPs), which are important for pre-mRNA splicing. It has also been suggested that SMN might function in the assembly of other ribonucleoprotein complexes. Two hypotheses have been proposed to explain the molecular dysfunction that gives rise to spinal muscular atrophy (SMA) and its specificity to a particular group of neurons. The first hypothesis states that the loss of SMN's well-known function in snRNP assembly causes an alteration in the splicing of a specific gene (or genes). The second hypothesis proposes that SMN is crucial for the transport of mRNA in neurons and that disruption of this function results in SMA.
Indexed as
Identifiers
What OpenQuestion holds
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.