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Sami Noujaim, PhD


Overview

Training + Education SUNY Upstate Medical University; University of Michigan
Gender Male

Publications + National Presentations

Park HJ, Georgescu SP, Du C, Madias C, Aronovitz MJ, Welzig CM, Wang B, Begley U, Zhang Y, Blaustein RO, Patten RD, Karas RH, Van Tol HH, Osborne TF, Shimano H, Liao R, Link MS, Galper JB. Parasympathetic response in chick myocytes and mouse heart is controlled by SREBP. Journal of Clinical Investigation 2008;118(1):259-271.

Park HJ, Zhang Y, Georgescu SP, Johnson KL, Kong D, Galper JB. Human umbilical vein endothelial cells and human dermal microvascular endothelial cells offer new insights into the relationship between lipid metabolism and angiogenesis. Stem Cell Reviews 2006;2(2):93-102.

Park HJ, Ward SM, Desgrosellier JS, Georgescu SP, Papageorge AG, Zhuang X, Barnett JV, Galper JB. Transforming growth factor β regulates the expression of the M² muscarinic receptor in atrial myocytes via an effect on RhoA and p190RhoGAP. Journal of Biological Chemistry 2006;281(29):19995-20002.

Tang D, Park HJ, Georgescu SP, Sebti SM, Hamilton AD, Galper JB. Simvastatin potentiates tumor necrosis factor β-mediated apoptosis of human vascular endothelial cells via the inhibition of the geranylgeranylation of RhoA. Life Sciences 2006;79(15):1484-1492.

Welzig CM*, Shin DG*, Park HJ*, Kim YJ, Saul JP and Galper JB. Lipid Lowering by Pravastatin Increases Parasympathetic Modulation of Heart Rate: Gαi2, a Possible Molecular Marker for Parasympathetic Responsiveness. *WCM, SDG and PHJ contributed equally to this work. Circulation 2003; 108: 2743-6.

Park HJ, Kong D, Iruela-Arispe L, Begley U, Tang D and Galper JB. 3-Hydroxy-3-Methylglutaryl CoA Reductase Inhibitors Interfere with Angiogenesis by Inhibiting Geranylgeranylation of RhoA. Circ. Res. 2002; 91: 143-150.

Park HJ, Begley U, Kong D, Yu H, Osborne T, and Galper JB. Role of Sterol Regulatory Element Binding Protein in the Regulation of Gai2 Expression in Cultured Heart Cells. Circ. Res. 2002; 91: 32-37.

Park HJ, Galper JB. 3-Hydroxy-3-Methylglutaryl CoA Reductase Inhibitors Upregulate Transforming Growth Factor b Signaling via Inhibition of Geranylgeranylation of RhoA GTPase in Cultured Heart Cells. Proc. Nat. Acad. Sci. 1999; 96: 11525-11530.

Park HJ, RajBhandary UL. Tetracycline-Regulated Suppression of Amber Codons in Mammalian Cells. Mol. Cell. Biol. 1998; 18:4418-4425.

Hecht HJ, Erdmann H, Park HJ, Sprinzl M, Schmid RD. Crystal structure of NADH oxidase from Thermus thermophilus. Nature Structural Biology 1995; 2:1109-1114.

Biography

Dr. Noujaim obtained his PhD in Pharmacology from the SUNY Upstate Medical University in 2007. Subsequently, he completed his postdoctoral training at the University of Michigan (2008-2012), in the Laboratory of Dr. Jose Jalife. Dr. Noujaim’s research focuses on the study of cardiac fibrillation mechanisms. Specifically, he is interested in the role that inward rectifiers play in atrial fibrillation (AF).

AF is the most prevalent arrhythmia in the clinic and a major cause of stroke. Pharmacological treatment of AF is inadequate. This is in part due to the relatively poor understanding of AF mechanisms and of the structural and molecular bases of drug-ion channel interactions. The Noujaim laboratory uses technological, and conceptual advances from the fields of structural biology and ion channel trafficking in order to explore the electrophysiological details of the contribution of inward rectifiers, and specifically the acetylcholine sensitive potassium current (IKACh) to arrhythmogenesis in the atria. The laboratory also studies functional and trafficking aspects of drug-ion channels interactions.

Research Interests

Dr. Noujaim’s research focuses on the study of cardiac fibrillation mechanisms. Specifically, he is interested in the role that inward rectifiers play in atrial fibrillation (AF). AF is the most prevalent arrhythmia in the clinic and a major cause of stroke. Pharmacological treatment of AF is inadequate. This is in part due to the relatively poor understanding of AF mechanisms and of the structural and molecular bases of drug-ion channel interactions.

The Noujaim laboratory uses technological, and conceptual advances from the fields of structural biology and ion channel trafficking in order to explore the electrophysiological details of the contribution of inward rectifiers, and specifically the acetylcholine sensitive potassium current (IKACh) to arrhythmogenesis in the atria. The laboratory also studies functional and trafficking aspects of drug-ion channels interactions.

Contact Information

Phone: 617-636-5190

Email: SNoujaim@tuftsmedicalcenter.org

Molecular Cardiology Research Institute
Tufts Medical Center
800 Washington Street, Box #5045
Boston, MA 02111