The overall objective of the Viral Vector and Transgenic Mouse Core is to provide Diabetes Research Center affiliate investigators at the University of Washington with state-of-the-art vectors necessary to overexpress, knockdown, knockout, or otherwise alter expression of RNAs and proteins of interest in cultured cells, isolated fissues, and animals. The Core has considerably evolved since the last competifive renewal. New services to generate genetically engineered mice have been added, and under-ufilized and standard molecular biology methods that are now increasingly performed in individual investigator's labs have been removed.
The specific aims of the Core are to provide the following services to affiliate invesfigators: (1) Producfion of lentiviral, adenoviral and retroviral vectors for use in animals, fissues, and cells;(2) Producfion of vectors for generation of transgenic, knockout, and knockin mice;(3) Specialized molecular biology methods not routinely performed in affiliate investigators'laboratories;(4) Cost-effective production of genefically engineered mice through the University of Washington Transgenic Resources Program;and (5) Consultafion and training.. The Core has been highly productive in the current funding period and has added new services that are expected to significantly increase producfivity and usability for Diabetes Research Center affiliate investigators to meet the Center's goal to enhance research in diabetes, obesity and related disorders in the Greater Seattle area and beyond.

Public Health Relevance

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Center Core Grants (P30)
Project #
5P30DK017047-38
Application #
8635328
Study Section
Special Emphasis Panel (ZDK1-GRB-S)
Project Start
Project End
Budget Start
2013-12-01
Budget End
2014-11-30
Support Year
38
Fiscal Year
2014
Total Cost
$163,634
Indirect Cost
$69,592
Name
University of Washington
Department
Type
DUNS #
605799469
City
Seattle
State
WA
Country
United States
Zip Code
98195
Kursan, Shams; McMillen, Timothy S; Beesetty, Pavani et al. (2017) The neuronal K+Cl- co-transporter 2 (Slc12a5) modulates insulin secretion. Sci Rep 7:1732
Lee, Crystal Man Ying; Woodward, Mark; Pandeya, Nirmala et al. (2017) Comparison of relationships between four common anthropometric measures and incident diabetes. Diabetes Res Clin Pract 132:36-44
Han, Seung Jin; Boyko, Edward J; Fujimoto, Wilfred Y et al. (2017) Low Plasma Adiponectin Concentrations Predict Increases in Visceral Adiposity and Insulin Resistance. J Clin Endocrinol Metab 102:4626-4633
Den Hartigh, Laura J; Omer, Mohamed; Goodspeed, Leela et al. (2017) Adipocyte-Specific Deficiency of NADPH Oxidase 4 Delays the Onset of Insulin Resistance and Attenuates Adipose Tissue Inflammation in Obesity. Arterioscler Thromb Vasc Biol 37:466-475
Kanter, Jenny E (2017) Monocyte Recruitment Versus Macrophage Proliferation in Atherosclerosis. Circ Res 121:1109-1110
Morton, Gregory J; Muta, Kenjiro; Kaiyala, Karl J et al. (2017) Evidence That the Sympathetic Nervous System Elicits Rapid, Coordinated, and Reciprocal Adjustments of Insulin Secretion and Insulin Sensitivity During Cold Exposure. Diabetes 66:823-834
Kanow, Mark A; Giarmarco, Michelle M; Jankowski, Connor Sr et al. (2017) Biochemical adaptations of the retina and retinal pigment epithelium support a metabolic ecosystem in the vertebrate eye. Elife 6:
Anderson, Lindsey J; Tamayose, Jamie M; Garcia, Jose M (2017) Use of growth hormone, IGF-I, and insulin for anabolic purpose: Pharmacological basis, methods of detection, and adverse effects. Mol Cell Endocrinol :
Hogan, Meghan F; Hull, Rebecca L (2017) The islet endothelial cell: a novel contributor to beta cell secretory dysfunction in diabetes. Diabetologia 60:952-959
Douglass, John D; Dorfman, Mauricio D; Thaler, Joshua P (2017) Glia: silent partners in energy homeostasis and obesity pathogenesis. Diabetologia 60:226-236

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