ArticleScientific reports2016
Brain enhancer activities at the gene-poor 5p14.1 autism-associated locus.
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 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Regulatory Functions of Long Non-coding RNAs and Circular RNAs in the Molecular Pathogenesis of Autism Spectrum Disorder.Cellular and molecular neurobiology · 2025Review
- An Emerging Role for Enhancer RNAs in Brain Disorders.Neuromolecular medicine · 2024Review
- Of mice and human-specific long noncoding RNAs.Mammalian genome : official journal of the International Mammalian Genome Society · 2022Review
- Quantifying the tissue-specific regulatory information within enhancer DNA sequences.NAR genomics and bioinformatics · 2021Article
- Article
- Enhancer RNAs predict enhancer-gene regulatory links and are critical for enhancer function in neuronal systems.Nucleic acids research · 2020Article
- Chromatin Dynamics and Genetic Variation Combine to Regulate Innate Immune Memory.Journal of clinical & cellular immunology · 2020Article
- Genomic Enhancers in Brain Health and Disease.Genes · 2019Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Due to the vast clinical and genetic heterogeneity, identification of causal genetic determinants for autism spectrum disorder (ASD) has proven to be complex. Whereas several dozen 'rare' genetic variants for ASD susceptibility have been identified, studies are still underpowered to analyse 'common' variants for their subtle effects. A recent application of genome-wide association studies (GWAS) to ASD indicated significant associations with the single nucleotide polymorphisms (SNPs) on chromosome 5p14.1, located in a non-coding region between cadherin10 (CDH10) and cadherin9 (CDH9). Here we apply an in vivo bacterial artificial chromosome (BAC) based enhancer-trapping strategy in mice to scan the gene desert for spatiotemporal cis-regulatory activities. Our results show that the ASD-associated interval harbors the cortical area, striatum, and cerebellum specific enhancers for a long non-coding RNA, moesin pseudogene1 antisense (MSNP1AS) during the brain developing stages. Mouse moesin protein levels are not affected by exogenously expressed human antisense RNAs in our transgenic brains, demonstrating the difficulty in modeling rather smaller effects of common variants. Our first in vivo evidence for the spatiotemporal transcription of MSNP1AS however provides a further support to connect this intergenic variant with the ASD susceptibility.
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Registered trials
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