GuidelineMammalian genome : official journal of the International Mammalian Genome Society2013
Recommendations for the investigation of animal models of Prader-Willi syndrome.
Guideline in Mammalian genome : official journal of the International Mammalian Genome Society, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 44 citations in OpenAlex.
- Low dose systemic AAV-exendin-4 gene therapy for Prader-Willi syndrome and dietary obesity.Molecular therapy. Advances · 2026Article
- Footprints in the Sno: investigating the cellular and molecular mechanisms of SNORD116.Open biology · 2025Review
- Environmental Enrichment Normalizes Metabolic Function in the Murine Model of Prader-Willi Syndrome Magel2-Null Mice.Endocrinology · 2025Article
- Article
- MAGEL2 (patho-)physiology and Schaaf-Yang syndrome.Developmental medicine and child neurology · 2025Review
- AAV-BDNF gene therapy ameliorates a hypothalamic neuroinflammatory signature in theMolecular therapy. Methods & clinical development · 2023Article
- 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
- Novel epigenetic molecular therapies for imprinting disorders.Molecular psychiatry · 2023Review
- Effects of thermoneutrality on food intake, body weight, and body composition in a Prader-Willi syndrome mouse model.Obesity (Silver Spring, Md.) · 2023Article
- Hypothalamic AAV-BDNF gene therapy improves metabolic function and behavior in theMolecular therapy. Methods & clinical development · 2022Article
- Article
- Review
- Review
- The necdin interactome: evaluating the effects of amino acid substitutions and cell stress using proximity-dependent biotinylation (BioID) and mass spectrometry.Human genetics · 2020Article
- Temple syndrome and Kagami-Ogata syndrome: clinical presentations, genotypes, models and mechanisms.Human molecular genetics · 2020Review
- Epigenetics meets GPCR: inhibition of histone H3 methyltransferase (G9a) and histamine HScientific reports · 2020Article
- 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
- Ghrelin Receptor Agonist Rescues Excess Neonatal Mortality in a Prader-Willi Syndrome Mouse Model.Endocrinology · 2018Article
- A Transcriptomic Signature of the Hypothalamic Response to Fasting and BDNF Deficiency in Prader-Willi Syndrome.Cell reports · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prader-Willi syndrome (PWS) occurs in about 1 in 15,000 individuals and is a contiguous gene disorder causing developmental disability, hyperphagia usually with obesity, and behavioral problems, including an increased incidence of psychiatric illness. The genomic imprinting that regulates allele-specific expression of PWS candidate genes, the fact that multiple genes are typically inactivated, and the presence of many genes that produce functional RNAs rather than proteins has complicated the identification of the underlying genetic pathophysiology of PWS. Over 30 genetically modified mouse strains that have been developed and characterized have been instrumental in elucidating the genetic and epigenetic mechanisms for the regulation of PWS genes and in discovering their physiological functions. In 2011, a PWS Animal Models Working Group (AMWG) was established to generate discussions and facilitate exchange of ideas regarding the best use of PWS animal models. Here, we summarize the goals of the AMWG, describe current animal models of PWS, and make recommendations for strategies to maximize the utility of animal models and for the development and use of new animal models of 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.