Author:
Resnick JL, Nicholls RD, Wevrick R.
Scientific Notation:
Mamm Genome. 2013 Jun;24(5-6):165-78. doi: 10.1007/s00335-013-9454-2. Epub 2013 Apr 23.
Publication Link:
http://www.ncbi.nlm.nih.gov/pubmed/23609791
Resnick JL, Nicholls RD, Wevrick R.
Mamm Genome. 2013 Jun;24(5-6):165-78. doi: 10.1007/s00335-013-9454-2. Epub 2013 Apr 23.
http://www.ncbi.nlm.nih.gov/pubmed/23609791
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.
The Foundation for Prader-Willi Research (federal tax id 31-1763110) is a nonprofit corporation with federal tax exempt status as a public charity under section 501(c)(3).
The mission of FPWR is to eliminate the challenges of Prader-Willi syndrome through the advancement of research and therapeutic development.
Foundation for Prader-Willi Research
Phone: 888-322-5487
Email: info@fpwr.org
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Covina, CA 91723
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