Angiotensin II, the central regulator of the renin-angiotensin system, mediates a series of complex biological responses to maintain homeostasis. Angiotensin II also mediates growth stimulatory responses, which may play a role in the development of atherosclerosis, hypertension, and cardiac hypertrophy. These responses are predominately generated through the action of a single receptor, the AT1 receptor. The signaling mechanisms activated by angiotensin II binding to its receptor include both calcium-mediated and tyrosine kinase-mediated events. The proposal focuses on understanding the signaling mechanisms and functional outcomes of angiotensin II-mediated tyrosine kinase signaling.

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
5F32DK065410-02
Application #
6827388
Study Section
Special Emphasis Panel (ZRG1-F10 (20))
Program Officer
Rankin, Tracy L
Project Start
2003-12-01
Project End
2005-11-30
Budget Start
2004-12-01
Budget End
2005-11-30
Support Year
2
Fiscal Year
2005
Total Cost
$48,148
Indirect Cost
Name
Emory University
Department
Pathology
Type
Schools of Medicine
DUNS #
066469933
City
Atlanta
State
GA
Country
United States
Zip Code
30322
Frenzel, Kristen; Wallace, Tiffany A; McDoom, Issam et al. (2006) A functional Jak2 tyrosine kinase domain is essential for mouse development. Exp Cell Res 312:2735-44
Fuchs, Sebastien; Frenzel, Kristen; Hubert, Christine et al. (2005) Male fertility is dependent on dipeptidase activity of testis ACE. Nat Med 11:1140-2; author reply 1142-3
Bernstein, Kenneth E; Xiao, Hong D; Frenzel, Kristen et al. (2005) Six truisms concerning ACE and the renin-angiotensin system educed from the genetic analysis of mice. Circ Res 96:1135-44
Bernstein, Kenneth E; Xiao, Hong D; Adams, Jon W et al. (2005) Establishing the role of angiotensin-converting enzyme in renal function and blood pressure control through the analysis of genetically modified mice. J Am Soc Nephrol 16:583-91