Maria L. Valencik, Ph.D.
Department: Department of Biochemistry and Molecular Biology
Academic Unit: College of Medicine
Title: Assistant Professor
Ph.D. University of California Los Angeles (1991)
Mail Stop: 330
Phone: (775) 784-1389
Fax: (775) 784-1419
In the United States 79.4 million adults have cardiovascular disease (CVD) and in 2004 CVD was responsible for 1 in every 2.8 deaths. Therefore, CVD claims more lives than cancer, chronic lower respiratory diseases, accidents and diabetes combined. To devise more effective treatment strategies, it is necessary to understand (at the molecular level) how the heart responds to high blood pressure and heart attacks. Our lab uses state of the art molecular genetics to examine two different proteins that regulate the response of individual heart muscle cells to stress (Integrins and ANP receptors). By altering these proteins and reintroducing them into a mouse, we can dissect how they function. After their reintroduction, we examine whole heart function by electrocardiographs (ECGs) and echocardiography. Then biochemical and molecular analysis allows us to dissect how individual genes/proteins respond to the altered protein. Understanding these processes will help us to develop better therapies for treatment of CVD. Our research is funded by two NIH grants.
Current Graduate Students
Other Lab Members
Nick Tschernia, Biochemistry
Valencik ML, and McDonald JA. Cardiac expression of a gain-of-function alpha(5)-integrin results in perinatal lethality. Am. J. Physiol. Heart Circ. Physiol. 280H, 361-7, (2001).
Keller RS, Shai SY, Babbitt CJ, Pham CG, Solaro RJ, Valencik ML, Loftus JC and Ross RS. Disruption of integrin function in the murine myocardium leads to perinatal lethality, fibrosis and abnormal cardiac performance. Am. J. Pathol. 158, 1079-90 (2001).
Valencik ML, and McDonald JA. Codon optimization markedly improves doxycycline regulated gene expression in the mouse heart. Transgenic Res. 10, 269-75 (2001).
Valencik ML, Keller RS, Loftus JC, and McDonald JA. A lethal perinatal cardiac
phenotype resulting from altered integrin function in cardiomyocytes. J. Card.
Fail. 84, 262-72 (2002).
Faculty by research area
- Mastick, C
- Mastick C.
- Mastick G.
- Van der Linden
- von Bartheld
- von Bartheld