The Transgenic Mouse/ES Cell Shared Resource (TMESCSR) facilitates the generation, maintenance, and storage of genetically modified mice, thereby providing useful animal models for the study of diabetes, obesity, and the mechanisms controlling carbohydrate, fat, and protein homeostasis. This facility has been in operation and supported by the VDRTC for nearly 18 years and currently provides six different service clusters related to the production and maintenance of genetically modified mice. During its history, the TMESCSR has served 182 different investigators by generating over 2400 transgenic founder mice from 660 distinct DNA constructs and 4100 chimeric mice from 700 different ES cell clones. The Shared Resource has further assisted in the generation of at least 101 different genetically modified mice using homologous recombination in mouse embryonic stem cells (mESCs). Many of the genetically modified mice have been used by investigators at Vanderbilt and other institutions to gain insight into the function and development of pancreatic islets, the liver, skeletal muscle, and fat and to study complications of diabetes such as diabetic nephropathy. The resource has developed several new services over the past funding cycle, including the ability to perform Recombinase-mediated Cassette Exchange (RMCE) and BAC Recombineering. By providing state-of-the-art, cost-effective and quality-controlled services this resource continues to be an important asset for both DTRC-affiliated investigators and others who indirectly benefit from this resource.
Transgenic and gene knock-out mice have been and continue to be highly useful in the study of diabetes. This core facility provides a means for VDRTC members to make new lines of genetically-modified mice, and thus is very relevant to both the ongoing operations and scientific impact of the Vanderbilt Diabetes Research and Training Center.
|Mani, Bharath K; Osborne-Lawrence, Sherri; Vijayaraghavan, Prasanna et al. (2016) Î²1-Adrenergic receptor deficiency in ghrelin-expressing cells causes hypoglycemia in susceptible individuals. J Clin Invest 126:3467-78|
|King-Morris, Kelli R; Deger, Serpil Muge; Hung, Adriana M et al. (2016) Measurement and Correlation of Indices of Insulin Resistance in Patients on Peritoneal Dialysis. Perit Dial Int 36:433-41|
|(2016) Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition). Autophagy 12:1-222|
|Gamboa, Jorge L; Billings 4th, Frederic T; Bojanowski, Matthew T et al. (2016) Mitochondrial dysfunction and oxidative stress in patients with chronic kidney disease. Physiol Rep 4:|
|Beavers, Kelsey R; Werfel, Thomas A; Shen, Tianwei et al. (2016) Porous Silicon and Polymer Nanocomposites for Delivery of Peptide Nucleic Acids as Anti-MicroRNA Therapies. Adv Mater 28:7984-7992|
|Crowder, Spencer W; Balikov, Daniel A; Boire, Timothy C et al. (2016) Copolymer-Mediated Cell Aggregation Promotes a Proangiogenic Stem Cell Phenotype In Vitro and In Vivo. Adv Healthc Mater 5:2866-2871|
|Shaffer, Carrie L; Good, James A D; Kumar, Santosh et al. (2016) Peptidomimetic Small Molecules Disrupt Type IV Secretion System Activity in Diverse Bacterial Pathogens. MBio 7:e00221-16|
|Conrad, Elizabeth; Dai, Chunhua; Spaeth, Jason et al. (2016) The MAFB transcription factor impacts islet Î±-cell function in rodents and represents a unique signature of primate islet Î²-cells. Am J Physiol Endocrinol Metab 310:E91-E102|
|Leamy, Alexandra K; Hasenour, Clinton M; Egnatchik, Robert A et al. (2016) Knockdown of triglyceride synthesis does not enhance palmitate lipotoxicity or prevent oleate-mediated rescue in rat hepatocytes. Biochim Biophys Acta 1861:1005-14|
|Delong, Thomas; Wiles, Timothy A; Baker, Rocky L et al. (2016) Pathogenic CD4 T cells in type 1 diabetes recognize epitopes formed by peptide fusion. Science 351:711-4|
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