MICHAEL A BROWNLEE
Affiliation: Albert Einstein College of Medicine
- The pathobiology of diabetic complications: a unifying mechanismMichael Brownlee
Departments of Medicine and Pathology, Albert Einstein College of Medicine, F 531 1300 Morris Park Ave, Bronx, NY 10461 1602, USA
Diabetes 54:1615-25. 2005
- Hyperglycemia-induced reactive oxygen species increase expression of the receptor for advanced glycation end products (RAGE) and RAGE ligandsDachun Yao
Department of Medicine, Diabetes Research Center, Albert Einstein College of Medicine, Bronx, New York, USA
Diabetes 59:249-55. 2010..Since hyperglycemia-induced reactive oxygen species (ROS) activate many pathways of diabetic tissue damage, the effect of these ROS on RAGE and RAGE ligand expression was evaluated...
- Biochemistry and molecular cell biology of diabetic complicationsM Brownlee
Department of Medicine, Diabetes Research and Training Center, Albert Einstein College of Medicine, Bronx, New York, 10461, USA
Nature 414:813-20. 2001..This integrating paradigm provides a new conceptual framework for future research and drug discovery...
- A radical explanation for glucose-induced beta cell dysfunctionMichael Brownlee
Diabetes Research Center, Albert Einstein College of Medicine, 1300 Morris Park Avenue, New York, New York 10461, USA
J Clin Invest 112:1788-90. 2003....
- INTRACELLULAR GLYCATION AND DIABETIC COMPLICATIONSMichael Brownlee; Fiscal Year: 2006..Supershift experiments will use commercially available antibodies. IP-westerns of cell extracts will be immunoblotted with antibodies to glyoxalase I-substrate- derived advanced glycation endproducts. ..
- INTRACELLULAR GLYCATION AND DIABETIC COMPLICATIONSMichael Brownlee; Fiscal Year: 2007..Supershift experiments will use commercially availableantibodies. IP-westernsof cell extracts will be immunoblotted with antibodies to glyoxalase I-substrate-derived advanced glycationendproducts. ..
- Progenitor Cell Dysfunction and Impaired Vasculogenesis*Michael Brownlee; Fiscal Year: 2008..rational development of novel strategies to restore normal compensatory vasculogenesis in diabetes, thus preventing the poor outcome of cardiovascular events (Ml, stroke, amputation) associated with the disease [unreadable] [unreadable]..