|Department:||Experimental & Systems Pharmacology; WSU Spokane|
|Credentials:||2005 - Ph.D., The University of Queensland; Human Movement Studies|
College of Pharmacy
|Web Site:||Click here|
Protein O-GlcNAcylation and chromatin regulation; Cell signaling events in the heart in response to high fat diet, diabetes and/or exercise
My laboratory investigates post-translational O-GlcNAc protein modification in the heart in response to exercise, dietary manipulation and diabetes. Our current work is focused on the role of the O-GlcNAc pathway in modulation of cardiac chromatin regulation, gene transcription and downstream signaling pathways. Experimental techniques include in vivo mouse model (including forced and voluntary exercise training), cell culture, isolated heart perfusion, fluorescent microscopy, western blotting and PCR.
Medford HM, Cox EJ, Miller LE, Marsh SA. Consuming a Western diet for two weeks suppresses fetal genes in mouse hearts. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. In Press, 2014
Cox EJ, Marsh SA. A systemic review of fetal genes as biomarkers of cardiac hypertrophy in rodent models of diabetes. PLoS ONE. 9(3):e92903, 2014.
Cox EJ, Marsh SA. Exercise and diabetes have opposite effects on the assembly and O-GlcNAc modification of the mSin3A/HDAC1/2 complex in the heart. Cardiovascular Diabetology. 12:101, 2013.
Medford HM, Porter K, Marsh SA. Immediate effects of a single exercise bout on protein O-GlcNAcylation and chromatin regulation of cardiac hypertrophy. American Journal of Physiology – Heart and Circulatory Physiology. 305(1):H114-123, 2013.
Medford HM, Chatham JC, Marsh SA. Chronic ingestion of a western diet increases O-linked-β-N-acetylglucosamine (O-GlcNAc) protein modification in the heart. Life Sciences. 90(23-24): 883-8, 2012.
Porter K, Medford HM, McIntosh CM, Marsh SA. Cardioprotection requires flipping the ‘posttranslational modification’ switch. Life Sciences. 90(3-4): 89-98, 2012.