Development of genetically engineered mouse models is crucial to understanding the roles of specific genes in cardiac function and disease. The PPG makes extensive use of a variety of genetic approaches to study the role of several genes in cardiac function and disease. The purpose of the mouse core is to provide services for the generation and management of gene-targeted and transgenic mice. Founder mice will be identified, bred, and maintained in a Core animal facility at UCSD. The Core will also be responsible for maintaining and distributing mouse lines to each individual project. In addition, the Core will also cryopreserve critical lines in case of a disaster (e.g. natural disasters, infectious outbreaks, etc.).

Public Health Relevance

This PPG application is proposing many new studies with innovative experimental tools and genetically modified animal models, to answer significant fundamental mechanistic questions, as well as translational questions related to cardiac hypertrophy, failure and arrhythmia. The mouse core will provide services for the generation and management of gene-targeted and transgenic mice for all four projects in the PPG. Thus it is essential for the success of the PPG.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
2P01HL080101-06A1
Application #
8207385
Study Section
Heart, Lung, and Blood Initial Review Group (HLBP)
Project Start
Project End
Budget Start
2011-08-01
Budget End
2012-05-31
Support Year
6
Fiscal Year
2011
Total Cost
$253,275
Indirect Cost
Name
University of California Davis
Department
Type
DUNS #
047120084
City
Davis
State
CA
Country
United States
Zip Code
95618
Hegyi, Bence; Bossuyt, Julie; Ginsburg, Kenneth S et al. (2018) Altered Repolarization Reserve in Failing Rabbit Ventricular Myocytes: Calcium and ?-Adrenergic Effects on Delayed- and Inward-Rectifier Potassium Currents. Circ Arrhythm Electrophysiol 11:e005852
Yan, Jiajie; Zhao, Weiwei; Thomson, Justin K et al. (2018) Stress Signaling JNK2 Crosstalk With CaMKII Underlies Enhanced Atrial Arrhythmogenesis. Circ Res 122:821-835
Hegyi, Bence; Bossuyt, Julie; Griffiths, Leigh G et al. (2018) Complex electrophysiological remodeling in postinfarction ischemic heart failure. Proc Natl Acad Sci U S A 115:E3036-E3044
Willeford, Andrew; Suetomi, Takeshi; Nickle, Audrey et al. (2018) CaMKII?-mediated inflammatory gene expression and inflammasome activation in cardiomyocytes initiate inflammation and induce fibrosis. JCI Insight 3:
Wood, Brent M; Simon, Mitchell; Galice, Samuel et al. (2018) Cardiac CaMKII activation promotes rapid translocation to its extra-dyadic targets. J Mol Cell Cardiol 125:18-28
Maxwell, Joshua T; Blatter, Lothar A (2017) A novel mechanism of tandem activation of ryanodine receptors by cytosolic and SR luminal Ca2+ during excitation-contraction coupling in atrial myocytes. J Physiol 595:3835-3845
Burel, Sophie; Coyan, Fabien C; Lorenzini, Maxime et al. (2017) C-terminal phosphorylation of NaV1.5 impairs FGF13-dependent regulation of channel inactivation. J Biol Chem 292:17431-17448
Surdo, Nicoletta C; Berrera, Marco; Koschinski, Andreas et al. (2017) FRET biosensor uncovers cAMP nano-domains at ?-adrenergic targets that dictate precise tuning of cardiac contractility. Nat Commun 8:15031
Ma, Xiaolong; Chen, Chao; Veevers, Jennifer et al. (2017) CRISPR/Cas9-mediated gene manipulation to create single-amino-acid-substituted and floxed mice with a cloning-free method. Sci Rep 7:42244
Lang, Di; Sato, Daisuke; Jiang, Yanyan et al. (2017) Calcium-Dependent Arrhythmogenic Foci Created by Weakly Coupled Myocytes in the Failing Heart. Circ Res 121:1379-1391

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