Dr. Kaufman is also Professor in the Departments of Biological Chemistry and Internal Medicine at the University of Michigan Medical School. He received his B.A. degree in Molecular, Cellular, and Developmental Biology from the University of Colorado.  Dr. Kaufman obtained his Ph.D. degree in Pharmacology from Stanford University where he studied gene amplification as a mechanism by which cells become resistant to anticancer agents. He was a Helen Hay Whitney fellow with Phillip Sharp at the Center for Cancer Research at the Massachusetts Institute of Technology where he developed gene transfer technologies based on gene amplification and expression in mammalian cells.  After post-doctoral studies, Dr. Kaufman became a founding scientist at Genetics Institute Inc., where he developed technologies for high-level mammalian cell expression of therapeutic proteins, such as clotting factors that are presently used to treat individuals with hemophilia. After moving to the University of Michigan Medical Center in 1994, Dr. Kaufman’s work has focused on mechanisms by which mammalian cells regulate protein folding and secretion and a cellular response known as the unfolded protein response (UPR). His current work extensively utilizes mouse models with deletion of UPR transducers to elucidate the physiological significance of the UPR in health and disease.

Selected publications among about 250 papers and more than 100 reviews:

1.     Wu, J., Rutkowski, D.T.,Dubois, M., Swathirajan, J., Saunders, T., Wang, J., Song, B., Yau, G. D-Y., Kaufman, R.J. (2007) ATF6 alpha optimizes long-term endoplasmic reticulum function to protect cells from chronic stress. Developmental Cell 13(3): 351-64.

2.     Zhou, J., Liu, C.Y., Back, S.H., Clark, R.L., Peisach, D., Xu, Z., Kaufman, R.J. (2006) The structure of an unfolded protein response sensor reveals a novel dimerization interface required for IRE1 and PERK activation. Proc. Natl. Acad. Sci. U.S.A. 103(39): 14343-14348.

3.     Back, S.H., Lee, K., Vink, E., Kaufman, R.J. (2006) Cytoplasmic IRE1α-mediated XBP1 mRNA splicing in the absence of nuclear processing and ER stress. (2006) J. Biol. Chem. 281(27): 18691-18706.

4.     Scheuner, D., Mierde, D.V., Song, B., Flamez, D., Creemers, J., Tsukamoto, K., Ribick, M., Schuit, F.C., Kaufman, R.J. (2005) Control of mRNA translation preserves endoplasmic reticulum function in beta cells and maintains glucose homeostasis. Nature Med. 11(7): 757-764.

5.     Zhang, K., Wong, H.N., Song, B., Miller, C.N., Scheuner, D., Kaufman, R.J. (2005) The unfolded protein response sensor IRE1α is required at two distinct steps in B cell lymphopoiesis. J. Clin. Invest. 115(2): 268-281.