ArticleScientific reports2016
Snord116 is critical in the regulation of food intake and body weight.
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 63 papers, 1 of them a synthesis that pooled it.
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Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.
- Hyperphagia in rare melanocortin-4 receptor pathway diseases: therapeutic options and assessing treatment response.Reviews in endocrine & metabolic disorders · 2025Pooled it
- Diazoxide Choline Extended-release Tablets in Prader-Willi Syndrome: A Randomized, Double-blind, Withdrawal Period Study.The Journal of clinical endocrinology and metabolism · 2026Trial
- Transcriptomic analysis reveals physiological adaptations and immune system modulation in Romanian Holstein cattle during heat stress exposure.International journal of biometeorology · 2026Article
- Altered neural electrophysiological properties in the anterior cingulate cortex in a mouse model of Prader-Willi syndrome.The Journal of physiology · 2026Article
- Review
- Magel2 deficiency promotes cardiac remodeling and increases arrhythmogenic susceptibility in a mouse model relevant to Prader-Willi and Schaaf-Yang syndromes.Clinical science (London, England : 1979) · 2026Article
- Neuroendocrinology and the Genetics of Obesity.Endocrinology · 2025Review
- Defining Hyperphagia for Improved Diagnosis and Management of MC4R Pathway-Associated Disease: A Roundtable Summary.Current obesity reports · 2025Review
- Sex dimorphic associations of Prader-Willi imprinted gene expressions in umbilical cord with prenatal and postnatal growth in healthy infants.World journal of pediatrics : WJP · 2025Article
- Article
- Impact of dcEF on microRNA profiles in glioblastoma and exosomes using a novel microfluidic bioreactor.Biomicrofluidics · 2024Article
- Newly developed oral bioavailable EHMT2 inhibitor as a potential epigenetic therapy for Prader-Willi syndrome.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- SNORA69 is up-regulated in the lateral habenula of individuals with major depressive disorder.Scientific reports · 2024Article
- SAGESDA: Multi-GraphSAGE networks for predicting SnoRNA-disease associations.Current research in structural biology · 2024Article
- A comprehensive review of genetic causes of obesity.World journal of pediatrics : WJP · 2024Review
- Accurate identification of snoRNA targets using variational graph autoencoder to advance the redevelopment of traditional medicines.Frontiers in pharmacology · 2024Article
- The Neural Progenitor Cell-Associated Transcription Factor FoxG1 Regulates Cardiac Epicardial Cell Proliferation.Stem cells international · 2024Article
- Endocrine features of Prader-Willi syndrome: a narrative review focusing on genotype-phenotype correlation.Frontiers in endocrinology · 2024Review
- The emerging role of snoRNAs in human disease.Genes & diseases · 2023Review
- Hormonal Imbalances in Prader-Willi and Schaaf-Yang Syndromes Imply the Evolution of Specific Regulation of Hypothalamic Neuroendocrine Function in Mammals.International journal of molecular sciences · 2023Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prader-Willi syndrome (PWS) is the predominant genetic cause of obesity in humans. Recent clinical reports have suggested that micro-deletion of the Snord116 gene cluster can lead to PWS, however, the extent of the contributions of the encoded snoRNAs is unknown. Here we show that mice lacking Snord116 globally have low birth weight, increased body weight gain, energy expenditure and hyperphagia. Consistent with this, microarray analysis of hypothalamic gene expression revealed a significant alteration in feeding related pathways that was also confirmed by in situ hybridisation. Importantly, selective deletion of Snord116 only from NPY expressing neurons mimics almost exactly the global deletion phenotype including the persistent low birth weight, increased body weight gain in early adulthood, increased energy expenditure and hyperphagia. Mechanistically, the lack of Snord116 in NPY neurons leads to the upregulation of NPY mRNA consistent with the hyperphagic phenotype and suggests a critical role of Snord116 in the control of NPY neuronal functions that might be dysregulated in PWS.
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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.