Office: 302B Rowell
Phone: (802) 656-2506
Dr. Paula Deming received her B.S. and M.S. degrees in medical technology from the University of Vermont, and earned a doctoral degree in molecular pathology from the University of North Carolina at Chapel Hill. She is currently an associate professor and the program director for the Medical Laboratory Science program. She is actively involved with mentoring students in research and teaches a variety of courses in the biological and medical laboratory sciences.
Postdoctoral Training, Duke University Department of Pharmacology and Cancer Biology, Mentor: Dr. Sally Kornbluth
Postdoctoral Training, University of Vermont Department of Pharmacology, Mentor: Dr. Alan Howe
Ph.D, University of North Carolina-Chapel Hill, Dept. of Pathology and Laboratory Medicine, Mentor: Dr. William Kaufman
M.S., University of Vermont, Medical Technology
B.S., Medical Technology, University of Vermont
Dysfunctions of growth factor-mediated signaling pathways occur in a variety of human pathologies including cardiovascular disease and cancer, two leading causes of mortality worldwide. Research in my laboratory aims to impact these pandemic level diseases by actively exploring novel questions related to molecular signaling mechanisms in the hopes to identify new targets for therapeutic treatment. Specifically, projects are focused on understanding how cells relay signals from receptor tyrosine kinases (RTKs) to the cAMP-dependent protein kinase A (PKA) pathway, and how these various signaling networks communicate to orchestrate growth factor-mediated cellular responses. We utilize in vitro and cell culture model systems along with a variety of cell biological and biochemical techniques to address important and novel questions in the field.
We are presently elucidating the mechanism/s that link the platelet derived growth factor receptor (PDGFR) to the serine-threonine protein kinase, cyclic AMP-dependent protein kinase A (PKA). We have identified a novel interaction between PDGFR and the catalytic subunit of PKA, which appears to regulate PKA function. We are currently investigating whether this interaction influences growth factor mediated responses in fibroblasts and smooth muscle cells, two cell types found in the cardiovascular system. Another project in the laboratory is focused on elucidating a novel mechanism whereby the Src family of non-receptor tyrosine kinases can regulate the cAMP-dependent protein kinase A in a cancer cell model system. As deregulation of cellular signaling pathways is a characteristic of diseases such as cancer and atherosclerosis, we aim to reveal new mechanisms that may eventually be exploited to develop new therapeutic strategies and treatments.
The Deming Laboratory's research is currently funded in part by the American Heart Association. Projects have also been partially funded through a Vermont Cancer Center Pilot Award and College of Nursing and Health Sciences Incentive Grants.
Deming, PB, Campbell, SL, Stone, JB, Rivard, RL, Mercier, AL, Howe, AK "Anchoring of Protein Kinase A by ERM (ezrin-radixin-moesin) proteins is required for proper netrin signaling through DCC (deleted in colorectal cancer)” January 9, 2015, doi:10.1074/jbc. M114.628644 jbc.M114.628644.
Kwolek, S and Deming, PB “Warfarin-induced hypersensitivity due to gluten sensitive enteropathy: A case study”, Clinical Laboratory Science (2012) 25(2):78-80.
Caldwell, GB, Howe, AK, Nickl, CK, Dostmann, WG, Ballif, BA, Deming, PB “Direct modulation of the protein kinase A catalytic subunit a by growth factor receptor tyrosine kinases”Journal of Cellular Biochemistry (2012) 113(1):39-48
Deming Paula, Kornbluth Sally. Dismantling the Apoptotic Cell. Encyclopedia of Life Sciences (ELS). John Wiley&Sons, Ltd: Chichester, September 2009.
Deming PB, Campbell SC, Baldor LC, Howe AK. PKA regulates PDGF-induced membrane ruffling and phosphatidylinositol dynamics. The Journal of Biological Chemistry. (2008) Dec 12;283(50):35199-211 (Abstract)
Phalen T, Deming PB, Vikas A, Howe A, Jonsson T, Poole L, Neintz NH. Oxidation state governs structural transitions in peroxiredoxin II that correlate with cell cycle arrest and recovery. J. Cell Biol. (2007) 175:779-789. (Abstract)
Innes CL, Heinloth AN, Flores KG, Sieber SO, Deming PB, Bushel PR, Kaufmann WK, Paules RS. ATM Requirement in Gene Expression Responses to Ionizing Radiation in Human Lymphoblasts and Fibroblasts. Molecular Cancer Research. 2006; 4(3):197-207. (Abstract)
Deming PB, Rathmell JC. Mitochondria, cell death and B cell tolerance. Current Directions in Autoimmunity. 2006; 9:95-119. (Abstract)
Deming PB, Schafer ZT, Tashker JS, Potts MB, Deshmukh M, Kornbluth S. Bcr-Abl-mediated Protection from Apoposis Downstream of Mitochondrial Cytochrome C Release. Molecular and Cellular Biology. 2004; 24(23): 10289-10299. (Abstract)
Kaufmann WK, Campbell CB, Simpson DA, Deming PB, Filatov L., Galloway DA, Zhao XJ, Creighton AM, and Downes CS. Degradation of ATM-independent decatenation checkpoint function in human cells is secondary to inactivation of p53 and correlated with chro mosomal destabilization. Cell Cycle, 1. 2002; 210-219. (Abstract)
Deming PB, Flores KG, Downes CS, Paules RS, and Kaufmann WK. ATR enforces the topoisomerase II-dependent G2 checkpoint through inhibition of Plk1 kinase. J.Biol.Chem.. 2002; 277, 36832-36838. (Abstract)
Deming PB, Cistulli CA, Zhao H, Graves PR, Piwnica-Worms H, Paules RS, Downes CS, and Kaufmann WK. The human decatenation checkpoint. Proc.Natl.Acad.Sci.U.S.A. 2001; 98, 12044-12049.