ArticlePloS one2008
SnoRNA Snord116 (Pwcr1/MBII-85) deletion causes growth deficiency and hyperphagia in mice.
Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 146 papers, 1 of them a synthesis that pooled it.
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Who cites it
146 citing papers in PubMed, 1 synthesis or guideline pooled it, 287 citations in OpenAlex.
- Recommendations for the investigation of animal models of Prader-Willi syndrome.Mammalian genome : official journal of the International Mammalian Genome Society · 2013Guideline
- Article
- Altered neural electrophysiological properties in the anterior cingulate cortex in a mouse model of Prader-Willi syndrome.The Journal of physiology · 2026Article
- Neuroendocrinology and the Genetics of Obesity.Endocrinology · 2025Review
- Light and sex modifybioRxiv : the preprint server for biology · 2025Article
- Investigation of a mouse model of Prader-Willi Syndrome with combined disruption of Necdin and Magel2.JCI insight · 2025Article
- The Role of the Arcuate Nucleus in Regulating Hunger and Satiety in Prader-Willi Syndrome.Current issues in molecular biology · 2025Review
- Loss of Snord116 protects cardiomyocyte kinetics during ischemic stress.Journal of molecular and cellular cardiology plus · 2025Article
- Footprints in the Sno: investigating the cellular and molecular mechanisms of SNORD116.Open biology · 2025Review
- Common and Uncommon Mouse Models of Growth Hormone Deficiency.Endocrine reviews · 2024Review
- 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
- Truncated variants of MAGEL2 are involved in the etiologies of the Schaaf-Yang and Prader-Willi syndromes.American journal of human genetics · 2024Article
- Early psychomotor development and growth hormone therapy in children with Prader-Willi syndrome: a review.European journal of pediatrics · 2024Review
- Endocrine features of Prader-Willi syndrome: a narrative review focusing on genotype-phenotype correlation.Frontiers in endocrinology · 2024Review
- Coordinated evolution of the SNORD115 and SNORD116 tandem repeats at the imprinted Prader-Willi/Angelman locus.NAR molecular medicine · 2024Article
- The Neural Progenitor Cell-Associated Transcription Factor FoxG1 Regulates Cardiac Epicardial Cell Proliferation.Stem cells international · 2024Article
- 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
- Effects of thermoneutrality on food intake, body weight, and body composition in a Prader-Willi syndrome mouse model.Obesity (Silver Spring, Md.) · 2023Article
- Article
86 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prader-Willi syndrome (PWS) is the leading genetic cause of obesity. After initial severe hypotonia, PWS children become hyperphagic and morbidly obese, if intake is not restricted. Short stature with abnormal growth hormone secretion, hypogonadism, cognitive impairment, anxiety and behavior problems are other features. PWS is caused by lack of expression of imprinted genes in a approximately 4 mb region of chromosome band 15q11.2. Our previous translocation studies predicted a major role for the C/D box small nucleolar RNA cluster SNORD116 (PWCR1/HBII-85) in PWS. To test this hypothesis, we created a approximately 150 kb deletion of the > 40 copies of Snord116 (Pwcr1/MBII-85) in C57BL/6 mice. Snord116del mice with paternally derived deletion lack expression of this snoRNA. They have early-onset postnatal growth deficiency, but normal fertility and lifespan. While pituitary structure and somatotrophs are normal, liver Igf1 mRNA is decreased. In cognitive and behavior tests, Snord116del mice are deficient in motor learning and have increased anxiety. Around three months of age, they develop hyperphagia, but stay lean on regular and high-fat diet. On reduced caloric intake, Snord116del mice maintain their weight better than wild-type littermates, excluding increased energy requirement as a cause of hyperphagia. Normal compensatory feeding after fasting, and ability to maintain body temperature in the cold indicate normal energy homeostasis regulation. Metabolic chamber studies reveal that Snord116del mice maintain energy homeostasis by altered fuel usage. Prolonged mealtime and increased circulating ghrelin indicate a defect in meal termination mechanism. Snord116del mice, the first snoRNA deletion animal model, reveal a novel role for a non-coding RNA in growth and feeding regulation.
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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.