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.
|Rusconi, B; Jiang, X; Sidhu, R et al. (2018) Gut Sphingolipid Composition as a Prelude to Necrotizing Enterocolitis. Sci Rep 8:10984|
|Chen, Yana; McCommis, Kyle S; Ferguson, Daniel et al. (2018) Inhibition of the Mitochondrial Pyruvate Carrier by Tolylfluanid. Endocrinology 159:609-621|
|Zhang, Yan; Rohatgi, Nidhi; Veis, Deborah J et al. (2018) PGC1? Organizes the Osteoclast Cytoskeleton by Mitochondrial Biogenesis and Activation. J Bone Miner Res 33:1114-1125|
|Xu, Wei; Mukherjee, Sumit; Ning, Yu et al. (2018) Cyclopropane fatty acid synthesis affects cell shape and acid resistance in Leishmania mexicana. Int J Parasitol 48:245-256|
|Hughes, Jing W; Bao, Yicheng K; Salam, Maamoun et al. (2018) Late-Onset T1DM and Older Age Predict Risk of Additional Autoimmune Disease. Diabetes Care :|
|Zhang, Xiangyu; Evans, Trent D; Jeong, Se-Jin et al. (2018) Classical and alternative roles for autophagy in lipid metabolism. Curr Opin Lipidol 29:203-211|
|Ban, Norimitsu; Lee, Tae Jun; Sene, Abdoulaye et al. (2018) Disrupted cholesterol metabolism promotes age-related photoreceptor neurodegeneration. J Lipid Res 59:1414-1423|
|Ban, Norimitsu; Lee, Tae Jun; Sene, Abdoulaye et al. (2018) Impaired monocyte cholesterol clearance initiates age-related retinal degeneration and vision loss. JCI Insight 3:|
|Mayer, Allyson L; Zhang, Yiming; Feng, Emily H et al. (2018) Enhanced Hepatic PPAR? Activity Links GLUT8 Deficiency to Augmented Peripheral Fasting Responses in Male Mice. Endocrinology 159:2110-2126|
|Weber, Kassandra J; Sauer, Madeline; He, Li et al. (2018) PPAR? Deficiency Suppresses the Release of IL-1? and IL-1? in Macrophages via a Type 1 IFN-Dependent Mechanism. J Immunol 201:2054-2069|
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