Transgenic and ES Cell Core The Transgenic and ES Cell Core of the Washington University Diabetes Research Center (DRC) provides services for efficient and cost-effective development of genetically altered mouse models to elucidate the pathogenesis of diabetes and related metabolic disorders. Importantly, in vivo models allow analysis of gene function in the context of complex intercellular and integrative systemic responses needed for the study of diabetes, a polygenic disorder involving multiple tissue types and environmental influences. Current molecular genetic techniques allow spatially and temporally restricted analysis of gene effects (both inactivation and over- expression) in mice, leading to previously unprecedented creativity and analytical resolution. The concepts involved in generating transgenic (Tg) or knockout/knockin (KO/KI) animals are straightforward. However, it is impractical and too expensive for most labs to maintain the requisite equipment, facilities, and highly skilled personnel for making genetically altered mice. Given the substantial demand by the Washington University community for assistance in the generation of these mouse models, the DRC Transgenic and ES Cell Core will continue to provide the necessary advice, expertise, facilities, equipment, and personnel to efficiently generate Tg and KO/KI mice for DRC members using state-of-the-art techniques, such as CRISPR/Cas9 nuclease- mediated genome editing in ES cells and in mouse zygotes. The Core will also assist in propagating poorly breeding animals, and in achieving transient Cre or FLP recombinase expression in zygotes by microinjection of expression plasmids. By making specialized, state-of-the-art services accessible to DRC investigators, the Core facilitates translation of basic research advances toward improvements in the diagnosis, treatment and cure of diabetes.
Transgenic and ES Cell Core Diabetes is a growing health problem in the United States and worldwide. Generation and analysis of small animal models to study diabetes and its complications has provided a better understanding of the disease in humans. These insights have led to the development of therapies for human diabetes that have improved quality of life. Research facilitated by the services of the DRC Transgenic and ES Cell Core at Washington University has considerable potential to identify mechanisms that may lead to novel approaches for treating people with diabetes.
|Musselman, Laura Palanker; Fink, Jill L; Maier, Ezekiel J et al. (2018) Seven-Up Is a Novel Regulator of Insulin Signaling. Genetics 208:1643-1656|
|Riek, Amy E; Oh, Jisu; Darwech, Isra et al. (2018) Vitamin D3 supplementation decreases a unique circulating monocyte cholesterol pool in patients with type 2 diabetes. J Steroid Biochem Mol Biol 177:187-192|
|Bittel, Adam J; Bohnert, Kathryn L; Reeds, Dominic N et al. (2018) Reduced Muscle Strength in Barth Syndrome May Be Improved by Resistance Exercise Training: A Pilot Study. JIMD Rep :|
|Peterson, Linda R; Xanthakis, Vanessa; Duncan, Meredith S et al. (2018) Ceramide Remodeling and Risk of Cardiovascular Events and Mortality. J Am Heart Assoc 7:|
|Ferguson, Daniel; Blenden, Mitchell; Hutson, Irina et al. (2018) Mouse Embryonic Fibroblasts Protect ob/ob Mice From Obesity and Metabolic Complications. Endocrinology 159:3275-3286|
|Hampton, Kaia K; Anderson, Katie; Frazier, Hilaree et al. (2018) Insulin Receptor Plasma Membrane Levels Increased by the Progesterone Receptor Membrane Component 1. Mol Pharmacol 94:665-673|
|Warren, Junco S; Tracy, Christopher M; Miller, Mickey R et al. (2018) Histone methyltransferase Smyd1 regulates mitochondrial energetics in the heart. Proc Natl Acad Sci U S A 115:E7871-E7880|
|Samovski, Dmitri; Dhule, Pallavi; Pietka, Terri et al. (2018) Regulation of Insulin Receptor Pathway and Glucose Metabolism by CD36 Signaling. Diabetes 67:1272-1284|
|Adams, Melissa T; Gilbert, Jennifer M; Hinojosa Paiz, Jesus et al. (2018) Endocrine cell type sorting and mature architecture in the islets of Langerhans require expression of Roundabout receptors in ? cells. Sci Rep 8:10876|
|Funk, Steven D; Bayer, Raymond H; Malone, Andrew F et al. (2018) Pathogenicity of a Human Laminin ?2 Mutation Revealed in Models of Alport Syndrome. J Am Soc Nephrol 29:949-960|
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