Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
First Independent Research Support & Transition (FIRST) Awards (R29)
Project #
1R29HL058166-01
Application #
2235470
Study Section
Cardiovascular and Pulmonary Research A Study Section (CVA)
Project Start
1996-08-01
Project End
2000-06-30
Budget Start
1996-08-01
Budget End
1997-06-30
Support Year
1
Fiscal Year
1996
Total Cost
Indirect Cost
Name
University of Louisville
Department
Physiology
Type
Schools of Medicine
DUNS #
City
Louisville
State
KY
Country
United States
Zip Code
40292
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Li, R C; Ping, P; Zhang, J et al. (2000) PKCepsilon modulates NF-kappaB and AP-1 via mitogen-activated protein kinases in adult rabbit cardiomyocytes. Am J Physiol Heart Circ Physiol 279:H1679-89
Takeishi, Y; Ping, P; Bolli, R et al. (2000) Transgenic overexpression of constitutively active protein kinase C epsilon causes concentric cardiac hypertrophy. Circ Res 86:1218-23
Ping, P; Takano, H; Zhang, J et al. (1999) Isoform-selective activation of protein kinase C by nitric oxide in the heart of conscious rabbits: a signaling mechanism for both nitric oxide-induced and ischemia-induced preconditioning. Circ Res 84:587-604
Ping, P; Zhang, J; Zheng, Y T et al. (1999) Demonstration of selective protein kinase C-dependent activation of Src and Lck tyrosine kinases during ischemic preconditioning in conscious rabbits. Circ Res 85:542-50
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Qiu, Y; Ping, P; Tang, X L et al. (1998) Direct evidence that protein kinase C plays an essential role in the development of late preconditioning against myocardial stunning in conscious rabbits and that epsilon is the isoform involved. J Clin Invest 101:2182-98
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Ping, P; Zhang, J; Qiu, Y et al. (1997) Ischemic preconditioning induces selective translocation of protein kinase C isoforms epsilon and eta in the heart of conscious rabbits without subcellular redistribution of total protein kinase C activity. Circ Res 81:404-14