William Cain, Ph.D.
Assistant Professor
Cain
Phone: (302) 831-8098
Fax: (302) 831-2281
Email: will@udel.edu
Office: 215 McKinly Lab
Address:
Department of Biological Sciences
Wolf Hall
University of Delaware
Newark, DE 19716
Education
- B.S., Ph.D. - University of Delaware
Teaching
- BISC 208 - Introductory Biology II
- BISC 413 - Advanced Genetics Laboratory
- BISC 601 - Immunochemistry
- BISC 604 - Nucleic Acids Laboratory
Research Interests
I currently conduct research in close association with Dr. David Usher at the University of Delaware and Dr. Daniel Rader at the University of Pennsylvania. This research focuses on lipoprotein function in humans and other vertebrates. I have two main research interests:
- Metabolism of Lipoprotein(a). High plasma levels of lipoprotein(a) are considered a risk factor for coronary heart disease and yet we presently know very little about the mechanisms involved in it's plasma clearance. We are presently examining the mechanisms involved in the plasma clearance of Lp(a) in genetically modified mice.
- Evolution of Lipoproteins. We are examining lipoprotein metabolism in turtles with specific interest in the identification of apolipoproteins with homology to human apolipoproteins.
Selected Publications
- Chen X, Patel TP, Cain WJ, Duncan MK. Production of monoclonal antibodies against Prox1. Hybridoma (Larchmt). 2006;25(1):27–33.
- Cain WJ, Millar JS, Himebauch AS, et al. Lipoprotein [a] is cleared from the plasma primarily by the liver in a process mediated by apolipoprotein [a]. J Lipid Res. 2005;46(12):2681–2691.
- Ikewaki K, Cain W, Thomas F, et al. Abnormal in vivo metabolism of apoB-containing lipoproteins in human apoE deficiency. J Lipid Res. 2004;45(7):1302–1311.
- Cain W, Song L, Stephens G, Usher D. Characterization of lipoproteins from the turtle, Trachemys scripta elegans, in fasted and fed states. Comp Biochem Physiol A Mol Integr Physiol. 2003;134(4):783–794.
- Maugeais C, Tietge UJF, Broedl UC, et al. Dose-dependent acceleration of high-density lipoprotein catabolism by endothelial lipase. Circulation. 2003;108(17):2121–2126.
- Tietge UJF, Maugeais C, Cain W, Rader DJ. Acute inflammation increases selective uptake of HDL cholesteryl esters into adrenals of mice overexpressing human sPLA2. Am J Physiol Endocrinol Metab. 2003;285(2):E403–11.
- DiAngelo JR, Vasavada TK, Cain W, Duncan MK. Production of monoclonal antibodies against chicken Pop1 (BVES). Hybrid Hybridomics. 2001;20(5-6):377–381.
- Vaisman BL, Lambert G, Amar M, et al. ABCA1 overexpression leads to hyperalphalipoproteinemia and increased biliary cholesterol excretion in transgenic mice. J Clin Invest. 2001;108(2):303–309.
- Tietge UJ, Maugeais C, Cain W, et al. Overexpression of secretory phospholipase A(2) causes rapid catabolism and altered tissue uptake of high density lipoprotein cholesteryl ester and apolipoprotein A-I. J Biol Chem. 2000;275(14):10077–10084.
- Auerbach BJ, Cain W, Ansong M, Newton RS, Saxena U, Bisgaier CL. Lipoprotein lipase greatly enhances the retention of lipoprotein(a) to endothelial cell-matrix. Atherosclerosis. 1999;142(1):89–96.
- Bdeir K, Cane W, Canziani G, et al. Defensin promotes the binding of lipoprotein(a) to vascular matrix. Blood. 1999;94(6):2007–2019.
- Higazi AA, Lavi E, Bdeir K, et al. Defensin stimulates the binding of lipoprotein (a) to human vascular endothelial and smooth muscle cells. Blood. 1997;89(12):4290–4298.
- Wassmer GT, Cain W, Page TL. Photoperiodic regulation of hemolymph protein in the woodroach Parcoblatta pennsylvanica. J Insect Physiol. 1996;42(9):851–858.
- Rader DJ, Mann WA, Cain W, et al. The low density lipoprotein receptor is not required for normal catabolism of Lp(a) in humans. J Clin Invest. 1995;95(3):1403–1408.
- Rader DJ, Cain W, Ikewaki K, et al. The inverse association of plasma lipoprotein(a) concentrations with apolipoprotein(a) isoform size is not due to differences in Lp(a) catabolism but to differences in production rate. J Clin Invest. 1994;93(6):2758–2763.
- Rader DJ, Cain W, Zech LA, Usher D, Brewer HBJ. Variation in lipoprotein(a) concentrations among individuals with the same apolipoprotein (a) isoform is determined by the rate of lipoprotein(a) production. J Clin Invest. 1993;91(2):443–447.
