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|CREATE Sustainable Synthesis Program||DETAILS »|
|Rodrigues Laboratory PhD Student Position||DETAILS »|
We are actively seeking an individual who can join our laboratory as a PhD Student. Personnel specifications of the candidate include:
• A Masters degree
• Interest in biological research
• Excellent organizational ability and strong communication skills
• Experience in cell isolation, cell culture, Western Blotting, rtPCR and enzymology
Heart has a limited potential to synthesize fatty acid (FA) and therefore FA is supplied from several sources: lipolysis of endogenous cardiac triglyceride (TG) stores, or from exogenous sources in the blood. Lipoprotein lipase (LPL), synthesized in cardiomyocytes, catalyzes the breakdown of the TG component of lipoproteins to provide FA to the heart. It is the vascular endothelial-bound LPL that determines the rate of plasma TG clearance and hence, it is also called heparin releasable (HR) "functional" LPL. Functional LPL is regulated by numerous dietary and hormonal factors, and is sensitive to pathophysiological alterations like those observed during diabetes. In this condition, absolute or relative lack of insulin impairs cardiac glucose transport and oxidation, resulting in FA becoming the preferred means of energy supply. To make available this increased requirement of the heart for FA, diabetic heart upregulates its luminal LPL activity by posttranslational mechanisms. Chronically elevated cardiac LPL can result in abnormal FA supply and utilization by the heart tissue that could potentially initiate and sustain cardiac dysfunction during diabetes. The student recruited will be expected to examine the regulation of cardiac LPL in an attempt to piece together how early metabolic changes could instigate diabetic heart disease.
1. Kim, M.S., Wang, F., Puthanveetil, P., Kewalramani, G., Hosseini-Beheshti, E., Ng, N., Wang, Y., Kumar, U., Innis, S., Proud, C.G., Abrahani, A., and Rodrigues, B. Protein kinase D is a key regulator of cardiomyocyte lipoprotein lipase secretion after diabetes. Circ. Res. 103: 252-260, 2008.
2. Kim, M.S., Kewalramani, G., Puthanveetil, P., Lee, V., Kumar, U., An, D., Abrahani, A, and Rodrigues, B. Acute diabetes moderates trafficking of cardiac lipoprotein lipase through p38 MAPK dependent actin cytoskeleton organization. Diabetes 57: 64-76, 2008.
3. Kim, M., Wang, F., Puthanveetil, P., Kewalramani, G., Marzban, L., Steinberg, S.F., Webber, T.D., Kieffer, T.J., Abrahani, A., and Rodrigues, B. Cleavage of protein kinase D following acute hypoinsulinemia prevents excessive LPL-mediated triglyceride accumulation. Diabetes 58: 2464-2475, 2009.
4. Wang, Y., Puthanveetil, P., Wang. F., Kim, M. S., Abrahani, A., and Rodrigues, B. The severity of diabetes governs vascular LPL by affecting enzyme dimerization and disassembly. Diabetes. 60:2041-2050, 2011.
5. Wang, F., Wang, Y., Zhang, D., Puthanveetil, P., Johnson, J.D., Abrahani, A., and Rodrigues, B. Fatty acid-induced nuclear translocation of heparanase uncoupels glucose metabollism in endothelial cells. Arterioscler. Thromb. Vasc. Biol 32: 406-414, 2012.
Interested individuals are requested to submit a letter of research interests and current CV to:
Dr. Brian Rodrigues
Faculty of Pharmaceutical Sciences
The University of British Columbia
2405 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3