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 #
5P01HL080101-09
Application #
8697105
Study Section
Heart, Lung, and Blood Initial Review Group (HLBP)
Project Start
Project End
Budget Start
2014-06-01
Budget End
2015-05-31
Support Year
9
Fiscal Year
2014
Total Cost
$222,938
Indirect Cost
$65,579
Name
University of California Davis
Department
Type
DUNS #
047120084
City
Davis
State
CA
Country
United States
Zip Code
95618
Hoeker, Gregory S; Hanafy, Mohamed A; Oster, Robert A et al. (2016) Reduced Arrhythmia Inducibility With Calcium/Calmodulin-dependent Protein Kinase II Inhibition in Heart Failure Rabbits. J Cardiovasc Pharmacol 67:260-5
Panama, Brian K; Korogyi, Adam S; Aschar-Sobbi, Roozbeh et al. (2016) Reductions in the Cardiac Transient Outward K+ Current Ito Caused by Chronic β-Adrenergic Receptor Stimulation Are Partly Rescued by Inhibition of Nuclear Factor κB. J Biol Chem 291:4156-65
Lu, Xiyuan; Kwong, Jennifer Q; Molkentin, Jeffery D et al. (2016) Individual Cardiac Mitochondria Undergo Rare Transient Permeability Transition Pore Openings. Circ Res 118:834-41
Uchinoumi, Hitoshi; Yang, Yi; Oda, Tetsuro et al. (2016) CaMKII-dependent phosphorylation of RyR2 promotes targetable pathological RyR2 conformational shift. J Mol Cell Cardiol 98:62-72
Kanaporis, Giedrius; Blatter, Lothar A (2016) Calcium-activated chloride current determines action potential morphology during calcium alternans in atrial myocytes. J Physiol 594:699-714
Miyamoto, Shigeki; Brown, Joan Heller (2016) Drp1 and Mitochondrial Autophagy Lend a Helping Hand in Adaptation to Pressure Overload. Circulation 133:1225-7
Bossuyt, Julie; Bers, Donald M (2015) Assessing GPCR and G protein signaling to the nucleus in live cells using fluorescent biosensors. Methods Mol Biol 1234:149-59
Grimm, Michael; Ling, Haiyun; Willeford, Andrew et al. (2015) CaMKIIδ mediates β-adrenergic effects on RyR2 phosphorylation and SR Ca(2+) leak and the pathophysiological response to chronic β-adrenergic stimulation. J Mol Cell Cardiol 85:282-91
Hohendanner, Felix; Maxwell, Joshua T; Blatter, Lothar A (2015) Cytosolic and nuclear calcium signaling in atrial myocytes: IP3-mediated calcium release and the role of mitochondria. Channels (Austin) 9:129-38
Erickson, Jeffrey R; Nichols, C Blake; Uchinoumi, Hitoshi et al. (2015) S-Nitrosylation Induces Both Autonomous Activation and Inhibition of Calcium/Calmodulin-dependent Protein Kinase II δ. J Biol Chem 290:25646-56

Showing the most recent 10 out of 194 publications