ArticleCell reports2019
Overlapping Activities of Two Neuronal Splicing Factors Switch the GABA Effect from Excitatory to Inhibitory by Regulating REST.
Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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Who cites it
31 citing papers in PubMed, 56 citations in OpenAlex.
- CASZ1 regulates the maturation of outer hair cells and is required for hearing in mice.iScience · 2026Article
- Neuronal microexons modulate arousal via the cAMP-PKA-CREB pathway in zebrafish.Science advances · 2026Article
- Imbalance of Excitatory and Inhibitory Neurotransmitter Systems in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.International journal of molecular sciences · 2026Review
- Restoring early postnatal synaptic dysregulation rescues motor neuron degeneration in a mouse model of Spinal and Bulbar Muscular Atrophy.Nature communications · 2026Article
- Heterozygous loss of SRRM1 may be associated with neurodevelopmental phenotypes and anomalies in cell growth and neurite morphology.European journal of human genetics : EJHG · 2026Article
- Ethanol selectively disrupts neuronal microexon regulation and chromatin marks in PC12 cells.Frontiers in cellular neuroscience · 2026Article
- Article
- Phenotypic impact of individual conserved neuronal microexons and their master regulators in zebrafish.eLife · 2025Article
- Core splicing architecture and early spliceosomal recognition determine microexon sensitivity to SRRM3/4.Nature structural & molecular biology · 2025Article
- Mutations in the microexon splicing regulator srrm4 have minor phenotypic effects on zebrafish neural development.G3 (Bethesda, Md.) · 2025Article
- A highly conserved neuronal microexon in DAAM1 controls actin dynamics, RHOA/ROCK signaling, and memory formation.Nature communications · 2025Article
- The potential causes of myasthenia and fasciculations in severely ill ME/CFS patients: the role of disturbed electrophysiology.Frontiers in physiology · 2025Article
- Exploratory study on autoantibodies to arginine-rich human peptides mimicking Epstein-Barr virus in women with post-COVID and myalgic encephalomyelitis/chronic fatigue syndrome.Frontiers in immunology · 2025Article
- Conserved role for spliceosomal component PRPF40A in microexon splicing.RNA (New York, N.Y.) · 2024Article
- Abnormality in GABAergic postsynaptic transmission associated with anxiety inIBRO neuroscience reports · 2024Article
- SRRM2 splicing factor modulates cell fate in early development.Biology open · 2024Article
- Unique transcriptomes of sensory and non-sensory neurons: insights from Splicing Regulatory States.Molecular systems biology · 2024Review
- The cause of Jones syndrome put to REST: a mutation in the REST gene causes gingival fibromatosis and hearing loss.European journal of human genetics : EJHG · 2023Article
- Pancreatic microexons regulate islet function and glucose homeostasis.Nature metabolism · 2023Article
- Specialization of the photoreceptor transcriptome byProceedings of the National Academy of Sciences of the United States of America · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
A truncating mutation in the mouse Srrm4 gene, which encodes a neuronal splicing factor, causes alternative splicing defects selectively in the ear. The mechanism by which splicing is preserved in the brain of these mice is not known. Here, we show that SRRM3 limits the Srrm4 mutation-associated defects to the ear and that, in cortical neurons, overlapping SRRM3-SRRM4 activity regulates the development of interneuronal inhibition. In vitro, SRRM3 and SRRM4 regulate the same splicing events, but a mutation in mouse Srrm3 causes tremors and mild defects in neuronal alternative splicing, demonstrating unique SRRM3 roles in vivo. Mice harboring mutations in both Srrm3 and Srrm4 die neonatally and exhibit severe splicing defects. In these mice, splicing alterations prevent inactivation of the gene repressor REST, which maintains immature excitatory GABAergic neurotransmission by repressing K-Cl cotransporter 2. Thus, our data reveal that SRRM3 and SRRM4 act redundantly to regulate GABAergic neurotransmission by inactivating REST.
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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 Socratic graph.