ArticleScientific reports2016
The autism-related gene SNRPN regulates cortical and spine development via controlling nuclear receptor Nr4a1.
Article in Scientific reports, 2016. 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
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
31 citing papers in PubMed, 70 citations in OpenAlex.
- Trial
- Article
- Spatial Changes in Hippocampal Transcriptomic Profiles Following Limbic Non-convulsive Status Epilepticus: Insights into Long-Term Inflammation and Cognitive Deficits.Molecular neurobiology · 2026Article
- Article
- 3,3'-Diindolylmethane improves pathology and neurological outcome following traumatic brain injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Activation of the imprinted Prader-Willi syndrome locus by CRISPR-based epigenome editing.Cell genomics · 2025Article
- Microglial type I interferon signaling mediates chronic stress-induced synapse loss and social behavior deficits.Molecular psychiatry · 2025Article
- Article
- Characterization of Circulating Protein Profiles in Individuals with Prader-Willi Syndrome and Individuals with Non-Syndromic Obesity.Journal of clinical medicine · 2024Article
- Activation of the imprinted Prader-Willi Syndrome locus by CRISPR-based epigenome editing.bioRxiv : the preprint server for biology · 2024Article
- Neural EGFL-like 1, a craniosynostosis-related osteochondrogenic molecule, strikingly associates with neurodevelopmental pathologies.Cell & bioscience · 2023Article
- Genome-wide identification and phenotypic characterization of seizure-associated copy number variations in 741,075 individuals.Nature communications · 2023Article
- N-Acetylglucosamine Kinase-Small Nuclear Ribonucleoprotein Polypeptide N Interaction Promotes Axodendritic Branching in Neurons via Dynein-Mediated Microtubule Transport.International journal of molecular sciences · 2023Article
- Multi-omics analysis reveals multiple mechanisms causing Prader-Willi like syndrome in a family with a X;15 translocation.Human mutation · 2022Article
- Molecular and behavioral consequences of Ube3a gene overdosage in mice.JCI insight · 2022Article
- Paternal preconceptional diet enriched with n-3 polyunsaturated fatty acids affects offspring brain function in mice.Frontiers in nutrition · 2022Article
- Dual imaging of dendritic spines and mitochondriaNeurobiology of stress · 2021Article
- Genetic dissection identifies Necdin as a driver gene in a mouse model of paternal 15q duplications.Nature communications · 2021Article
- The Diagnostic Journey of a Patient with Prader-Willi-Like Syndrome and a Unique HomozygousGenes · 2021Review
- Distinctive gene expression patterns and imprinting signatures revealed in reciprocal crosses between cattle sub-species.BMC genomics · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The small nuclear ribonucleoprotein polypeptide N (SNRPN) gene, encoding the RNA-associated SmN protein, duplications or deletions of which are strongly associated with neurodevelopmental disabilities. SNRPN-coding protein is highly expressed in the brain. However, the role of SNRPN protein in neural development remains largely unknown. Here we showed that the expression of SNRPN increased markedly during postnatal brain development. Overexpression or knockdown of SNRPN in cortical neurons impaired neurite outgrowth, neuron migration, and the distribution of dendritic spines. We found that SNRPN regulated the expression level of Nr4a1, a critical nuclear receptor during neural development, in cultured primary cortical neurons. The abnormal spine development caused by SNRPN overexpression could be fully rescued by Nr4a1 co-expression. Importantly, we found that either knockdown of Nr4a1 or 3, 3'- Diindolylmethane (DIM), an Nr4a1 antagonist, were able to rescue the effects of SNRPN knockdown on neurite outgrowth of embryonic cortical neurons, providing the potential therapeutic methods for SNRPN deletion disorders. We thus concluded that maintaining the proper level of SNRPN is critical in cortical neurodevelopment. Finally, Nr4a1 may serve as a potential drug target for SNRPN-related neurodevelopmental disabilities, including Prader-Willi syndrome (PWS) and autism spectrum disorders (ASDs).
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.