ArticleScientific reports2014
Differential regulation of non-protein coding RNAs from Prader-Willi Syndrome locus.
Article in Scientific reports, 2014. 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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Who cites it
34 citing papers in PubMed, 52 citations in OpenAlex.
- Article
- The superpowers of imprinting control regions.Genome research · 2026Review
- Footprints in the Sno: investigating the cellular and molecular mechanisms of SNORD116.Open biology · 2025Review
- Epigenetic regulation of sex dimorphism in cardiovascular health.Canadian journal of physiology and pharmacology · 2024Review
- The emerging role of snoRNAs in human disease.Genes & diseases · 2023Review
- Analysis ofGenes · 2022Review
- Reference Genes across Nine Brain Areas of Wild Type and Prader-Willi Syndrome Mice: Assessing Differences inInternational journal of molecular sciences · 2022Article
- Small but strong: Pivotal roles and potential applications of snoRNAs in hematopoietic malignancies.Frontiers in oncology · 2022Review
- Transcriptomic Analysis of Cardiomyocyte Extracellular Vesicles in Hypertrophic Cardiomyopathy Reveals Differential snoRNA Cargo.Stem cells and development · 2021Article
- Small but Mighty-The Emerging Role of snoRNAs in Hematological Malignancies.Non-coding RNA · 2021Review
- A Comprehensive Review of Genetically Engineered Mouse Models for Prader-Willi Syndrome Research.International journal of molecular sciences · 2021Review
- Influence of pentoxifylline on gene expression of PAG1/ miR-1206/ SNHG14 in ischemic heart disease.Biochemistry and biophysics reports · 2021Article
- SPMLMI: predicting lncRNA-miRNA interactions in humans using a structural perturbation method.PeerJ · 2021Article
- Emerging Classes of Small Non-Coding RNAs With Potential Implications in Diabetes and Associated Metabolic Disorders.Frontiers in endocrinology · 2021Review
- Identifying Transcription Factor Combinations to Modulate Circadian Rhythms by Leveraging Virtual Knockouts on Transcription Networks.iScience · 2020Article
- Prader-Willi syndrome: reflections on seminal studies and future therapies.Open biology · 2020Review
- The 15q11.2 BP1-BP2 Microdeletion (International journal of molecular sciences · 2020Review
- Preclinical Testing in Translational Animal Models of Prader-Willi Syndrome: Overview and Gap Analysis.Molecular therapy. Methods & clinical development · 2019Review
- Epigenetic therapy of Prader-Willi syndrome.Translational research : the journal of laboratory and clinical medicine · 2019Review
- Ectopic expression of Snord115 in choroid plexus interferes with editing but not splicing of 5-Ht2c receptor pre-mRNA in mice.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prader-Willi Syndrome (PWS) is a neurogenetic disorder caused by the deletion of imprinted genes on the paternally inherited human chromosome 15q11-q13. This locus harbours a long non-protein-coding RNA (U-UBE3A-ATS) that contains six intron-encoded snoRNAs, including the SNORD116 and SNORD115 repetitive clusters. The 3'-region of U-UBE3A-ATS is transcribed in the cis-antisense direction to the ubiquitin-protein ligase E3A (UBE3A) gene. Deletion of the SNORD116 region causes key characteristics of PWS. There are few indications that SNORD115 might regulate serotonin receptor (5HT2C) pre-mRNA processing. Here we performed quantitative real-time expression analyses of RNAs from the PWS locus across 20 human tissues and combined it with deep-sequencing data derived from Cap Analysis of Gene Expression (CAGE-seq) libraries. We found that the expression profiles of SNORD64, SNORD107, SNORD108 and SNORD116 are similar across analyzed tissues and correlate well with SNORD116 embedded U-UBE3A-ATS exons (IPW116). Notable differences in expressions between the aforementioned RNAs and SNORD115 together with the host IPW115 and UBE3A cis-antisense exons were observed. CAGE-seq analysis revealed the presence of potential transcriptional start sites originated from the U-UBE3A-ATS spanning region. Our findings indicate novel aspects for the expression regulation in the PWS locus.
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