ArticleThe European journal of neuroscience2019
A Sam68-dependent alternative splicing program shapes postsynaptic protein complexes.
Article in The European journal of neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 17 citations in OpenAlex.
- Dysregulated nuclear Lamin B1 in DYT1 dystonia thickens nuclear lamina and disrupts 14-3-3 proteins.Cell death discovery · 2026Article
- Comparative Single-Cell Transcriptome Analysis of c-Met Receptor Expressing and Non-Expressing Projection Neurons in the Developing Frontal and Visual Cortices.Developmental neuroscience · 2025Article
- Release your inhibitions: The cell biology of GABAergic postsynaptic plasticity.Current opinion in neurobiology · 2025Review
- Variants in LRRC7 lead to intellectual disability, autism, aggression and abnormal eating behaviors.Nature communications · 2024Article
- Differential expression of paralog RNA binding proteins establishes a dynamic splicing program required for normal cerebral cortex development.Nucleic acids research · 2024Article
- A cell-type-specific alternative splicing regulator shapes synapse properties in a trans-synaptic manner.Cell reports · 2023Article
- Automated Image Analysis Reveals Different Localization of Synaptic Gephyrin C4 Splice Variants.eNeuro · 2023Article
- Regionally restricted modulation ofFrontiers in molecular neuroscience · 2022Article
- The Fine Art of Writing a Message: RNA Metabolism in the Shaping and Remodeling of the Nervous System.Frontiers in molecular neuroscience · 2021Review
- Sam68 splicing regulation contributes to motor unit establishment in the postnatal skeletal muscle.Life science alliance · 2020Article
- Deep Survey of GABAergic Interneurons: Emerging Insights From Gene-Isoform Transcriptomics.Frontiers in molecular neuroscience · 2019Article
- Cellular Mechanisms Contributing to the Functional Heterogeneity of GABAergic Synapses.Frontiers in molecular neuroscience · 2019Article
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 1 institution in 1 country.
Funding
Abstract
Alternative splicing is one of the key mechanisms to increase the diversity of cellular transcriptomes, thereby expanding the coding capacity of the genome. This diversity is of particular importance in the nervous system with its elaborated cellular networks. Sam68, a member of the Signal Transduction Associated RNA-binding (STAR) family of RNA-binding proteins, is expressed in the developing and mature nervous system but its neuronal functions are poorly understood. Here, we perform genome-wide mapping of the Sam68-dependent alternative splicing program in mice. We find that Sam68 is required for the regulation of a set of alternative splicing events in pre-mRNAs encoding several postsynaptic scaffolding molecules that are central to the function of GABAergic and glutamatergic synapses. These components include Collybistin (Arhgef9), Gephyrin (Gphn), and Densin-180 (Lrrc7). Sam68-regulated Lrrc7 variants engage in differential protein interactions with signalling proteins, thus, highlighting a contribution of the Sam68 splicing program to shaping synaptic complexes. These findings suggest an important role for Sam68-dependent alternative splicing in the regulation of synapses in the central nervous system.
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.