ArticleHuman molecular genetics2013
A Prader-Willi locus lncRNA cloud modulates diurnal genes and energy expenditure.
Article in Human molecular genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 1 of them a synthesis that pooled it.
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
87 citing papers in PubMed, 1 synthesis or guideline pooled it, 170 citations in OpenAlex.
- Integrated multi-cohort transcriptional meta-analysis of neurodegenerative diseases.Acta neuropathologica communications · 2014Pooled it
- Epigenetic Insights and Exosome-Based Therapeutics for Insomnia: Bridging Sleep Biology and Precision Medicine.Molecular neurobiology · 2026Review
- Altered neural electrophysiological properties in the anterior cingulate cortex in a mouse model of Prader-Willi syndrome.The Journal of physiology · 2026Article
- Widespread DNA off-targeting confounds RNA chromatin occupancy studies.Nature biotechnology · 2026Article
- A scoping review of dietary interventions to treat obesity among Prader-Willi syndrome individuals.Intractable & rare diseases research · 2025Review
- Light and sex modifybioRxiv : the preprint server for biology · 2025Article
- Footprints in the Sno: investigating the cellular and molecular mechanisms of SNORD116.Open biology · 2025Review
- Loss of Snord116 protects cardiomyocyte kinetics during ischemic stress.Journal of molecular and cellular cardiology plus · 2025Article
- Identifying key underlying regulatory networks and predicting targets of orphan C/D box SNORD116 snoRNAs in Prader-Willi syndrome.Nucleic acids research · 2024Article
- Roles of SNORD115 and SNORD116 ncRNA clusters during neuronal differentiation.Nature communications · 2024Article
- Truncated variants of MAGEL2 are involved in the etiologies of the Schaaf-Yang and Prader-Willi syndromes.American journal of human genetics · 2024Article
- The Importance of Sleep in Overcoming Childhood Obesity and Reshaping Epigenetics.Biomedicines · 2024Review
- RNA-Chrom: a manually curated analytical database of RNA-chromatin interactome.Database : the journal of biological databases and curation · 2023Article
- What has single-cell transcriptomics taught us about long non-coding RNAs in the ventricular-subventricular zone?Stem cell reports · 2023Article
- Diagnosis and management of sleep disorders in Prader-Willi syndrome.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2022Review
- Building a model for predicting metabolic syndrome using artificial intelligence based on an investigation of whole-genome sequencing.Journal of translational medicine · 2022Article
- Review
- Dysregulated CRMP Mediates Circadian Deficits in a Drosophila Model of Fragile X Syndrome.Neuroscience bulletin · 2021Article
- A Comprehensive Review of Genetically Engineered Mouse Models for Prader-Willi Syndrome Research.International journal of molecular sciences · 2021Review
- Epigenetics in Prader-Willi Syndrome.Frontiers in genetics · 2021Review
27 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Prader-Willi syndrome (PWS), a genetic disorder of obesity, intellectual disability and sleep abnormalities, is caused by loss of non-coding RNAs on paternal chromosome 15q11-q13. The imprinted minimal PWS locus encompasses a long non-coding RNA (lncRNA) transcript processed into multiple SNORD116 small nucleolar RNAs and the spliced exons of the host gene, 116HG. However, both the molecular function and the disease relevance of the spliced lncRNA 116HG are unknown. Here, we show that 116HG forms a subnuclear RNA cloud that co-purifies with the transcriptional activator RBBP5 and active metabolic genes, remains tethered to the site of its transcription and increases in size in post-natal neurons and during sleep. Snord116del mice lacking 116HG exhibited increased energy expenditure corresponding to the dysregulation of diurnally expressed Mtor and circadian genes Clock, Cry1 and Per2. These combined genomic and metabolic analyses demonstrate that 116HG regulates the diurnal energy expenditure of the brain. These novel molecular insights into the energy imbalance in PWS should lead to improved therapies and understanding of lncRNA roles in complex neurodevelopmental and metabolic disorders.
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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 OpenQuestion graph.