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Advancements in Genetic Engineering

Advancements in Genetic Engineering
Open Access

ISSN: 2169-0111

+44 20 3868 9735

Randal J Kaufman

Randal J Kaufman

Randal J Kaufman
Director, Degenerative Disease Research, Center for Neuroscience, Aging, and Stem Cell Research, Sanford-Burnham Medical Research Institute
USA

Biography

Born: May 22, 1951, Denver, CO. B.A. Molecular, Cellular, and Developmental Biology, University of Colorado, Boulder, CO 1969-1972. Ph.D. Pharmacology, Stanford University, Palo Alto, CA 1974-1979. Senior Scientist, Genetics Institute, Cambridge, MA 1982-1986. Director, Molecular and Cellular Genetics, Genetics Institute, Cambridge MA 1986-1993. Investigator, Howard Hughes Medical Institute, University of Michigan Medical Center, Ann Arbor, MI 1993-2010. Professor, Department of Biological Chemistry, University of Michigan Medical Center, Ann Arbor, MI 1993-2011. Warner-Lambert/Parke Davis Professor of Internal Medicine and Biological Chemistry, University of Michigan Medical Center, Ann Arbor, MI 2006-2011. Director & Professor, Degenerative Disease Research, Center For Neuroscience, Aging and Stem Cell Research, Sanford-Burnham Medical Research Institute, La Jolla, Ca 2011-Present. Post-doctoral Fellow, Helen Hay Whitney, Mass. Inst. Tech. Cambridge, MA 1979-1982. Dr. Murray Thelin Award, National Hemophilia Foundation (NHF, 1993). “Prix Henri Chaigneau” International Association Francaise Des Hemophiles (1998). Investigator Recognition Award, International Society for Thrombosis and Haemostasis (ISTH, 1999). Van Wezel Prize, European Society of Animal Cell Technology (ESACT, 2003). Medical & Scientific Advisory Board (NHF, 1996-2005). AAAS Fellow (2006). NIH MERIT (2007).

Research Interest

My research focuses on three signaling pathways that emanate from the ER that orchestrate survival and death responses. More recently, our studies have discovered that ER protein misfolding leads to oxidative stress, calcium mobilization, and inflammatory responses. These findings are central to the defect in intestinal epithelial cells that encounter a necessity to increase protein secretion to produce antimicrobial peptides.

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