ArticleProceedings of the National Academy of Sciences of the United States of America2013
RNA-binding protein Sam68 controls synapse number and local β-actin mRNA metabolism in dendrites.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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.
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Who cites it
34 citing papers in PubMed, 55 citations in OpenAlex.
- In Vivo Massively Parallel Reporter Assay Reveals Sequence Determinants of mRNA Localization in Astrocytes.bioRxiv : the preprint server for biology · 2026Article
- Sam68 is a druggable vulnerability point in cancer stem cells.Cancer metastasis reviews · 2024Review
- Article
- Muscleblind-1 interacts with tubulin mRNAs to regulate the microtubule cytoskeleton in C. elegans mechanosensory neurons.PLoS genetics · 2023Article
- Regionally restricted modulation ofFrontiers in molecular neuroscience · 2022Article
- Mouse Ataxin-2 Expansion Downregulates CamKII and Other Calcium Signaling Factors, Impairing Granule-Purkinje Neuron Synaptic Strength.International journal of molecular sciences · 2020Article
- The RNA binding protein Sam68 controls T helper 1 differentiation and anti-mycobacterial response through modulation of miR-29.Cell death and differentiation · 2019Article
- A Sam68-dependent alternative splicing program shapes postsynaptic protein complexes.The European journal of neuroscience · 2019Article
- 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
- Neuronal Porosome Complex: Secretory Machinery at the Nerve Terminal.Discoveries (Craiova, Romania) · 2017Review
- Expression of Sam68 Associates with Neuronal Apoptosis and Reactive Astrocytes After Spinal Cord Injury.Cellular and molecular neurobiology · 2017Article
- Imaging mRNA and protein interactions within neurons.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Neurexins 1-3 Each Have a Distinct Pattern of Expression in the Early Developing Human Cerebral Cortex.Cerebral cortex (New York, N.Y. : 1991) · 2017Article
- Sam68 promotes self-renewal and glycolytic metabolism in mouse neural progenitor cells by modulatingeLife · 2016Article
- The p53 status can influence the role of Sam68 in tumorigenesis.Oncotarget · 2016Article
- Molecular Pathophysiology of Fragile X-Associated Tremor/Ataxia Syndrome and Perspectives for Drug Development.Cerebellum (London, England) · 2016Review
- Single-Molecule Imaging Reveals the Activation Dynamics of Intracellular Protein Smad3 on Cell Membrane.Scientific reports · 2016Article
- Synaptonuclear messenger PRR7 inhibits c-Jun ubiquitination and regulates NMDA-mediated excitotoxicity.The EMBO journal · 2016Article
- Dissecting the expression relationships between RNA-binding proteins and their cognate targets in eukaryotic post-transcriptional regulatory networks.Scientific reports · 2016Article
- The neurogenetics of alternative splicing.Nature reviews. Neuroscience · 2016Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Proper synaptic function requires the spatial and temporal compartmentalization of RNA metabolism via transacting RNA-binding proteins (RBPs). Loss of RBP activity leads to abnormal posttranscriptional regulation and results in diverse neurological disorders with underlying deficits in synaptic morphology and transmission. Functional loss of the 68-kDa RBP Src associated in mitosis (Sam68) is associated with the pathogenesis of the neurological disorder fragile X tremor/ataxia syndrome. Sam68 binds to the mRNA of β-actin (actb), an integral cytoskeletal component of dendritic spines. We show that Sam68 knockdown or disruption of the binding between Sam68 and its actb mRNA cargo in primary hippocampal cultures decreases the amount of actb mRNA in the synaptodendritic compartment and results in fewer dendritic spines. Consistent with these observations, we find that Sam68-KO mice have reduced levels of actb mRNA associated with synaptic polysomes and diminished levels of synaptic actb protein, suggesting that Sam68 promotes the translation of actb mRNA at synapses in vivo. Moreover, genetic knockout of Sam68 or acute knockdown in vivo results in fewer excitatory synapses in the hippocampal formation as assessed morphologically and functionally. Therefore, we propose that Sam68 regulates synapse number in a cell-autonomous manner through control of postsynaptic actb mRNA metabolism. Our research identifies a role for Sam68 in synaptodendritic posttranscriptional regulation of actb and may provide insight into the pathophysiology of fragile X tremor/ataxia syndrome.
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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.