John B. Lowe, M.D.
Professor of Pathology
johnlowe@mmg.im.med.umich.edu
Campus Address:
Howard Hughes Medical Inst
3510 MSRBI 0605
1301 Catherine Street
Ann Arbor, Michigan 48109-0602
Phone: 734/647-4779
Annual Report | Biography | Research Interests | Selected Publications
Departmental Annual Report
Brief Biography
Dr. Lowe received his M.D. from the University of Utah College of Medicine in 1980. He trained as a resident in clinical pathology at Washington University in St. Louis from 1980-1984, and completed postdoctoral research training in bacterial genetics and mammalian gene expression at Washington University during the same period. Dr. Lowe is a diplomat of the American Board of Pathology (Clinical Pathology). He has conducted research funded by the NIH and by the Howard Hughes Medical Institute in areas pertaining to nflammation and leukocyte trafficking, and molecular analysis of mammalian glycosylation pathways, continuously since 1984. Dr. Lowe was an Assistant Professor of Pathology and Internal Medicine at Washington University in St. Louis until becoming a faculty member at the University of Michigan in 1986. Dr. Lowe also holds the Warner-Lambert/Parke-Davis endowed Professorship in Medicine at the University of Michigan, and is an Investigator of the Howard Hughes Medical Institute.
Research Interests
Regulation and function of mammalian glycosylation.
Our laboratory has in the past years focused on the molecular genetics
of mammalian genes that determine expression of cell surface glycoproteins
implicated in cell adhesion and embryonic development. These genes include
those that encode glycosyltransferases. In past years, we have used gene
transfer cloning methods to isolate and characterize mammalian glycosyltransferase
genes that include the human H, Secretor, and Lewis blood group loci.
More recently, we are exploring glycosyltransferases that determine adhesive
interactions essential to leukocyteendothelial cell communications during
inflammation. Current efforts include ablation of glycosyltransferase
genes that participate in this process, using gene "knock-out"
technologies, in the mouse. This work is extending to genes that participate
in the synthesis of nucleotide sugar substrates for these enzymes, together
with an analysis of the immune system defects in these mutant mice.
Selected Publications
Lowe JB. Glycosylation, Immunity, and Autoimmunity. Cell 104:809-812, 2001.
Domino S, Zhang L, and Lowe JB. Molecular cloning, genomic mapping, and expression of two Secretor blood group alpha-(1,2) fucosyltransferase genes differentially regulted in mouse uterine epithelium and gastrointestinal tract. J Biol Chem, 2001, in press.
Homeister JH, Thall A, Petryniak B, Maly P, Rogers CE, Smith PL, Kelly RJ, Gersten KM, Misra A, Chen G, Askari S, Smithson G, Marks RM, Hindsgaul O, von Adrian UH, and Lowe JB. The alpha-(1,3) fucosyltransferases Fuc-TIV and Fuc-TVII collaborate in the control of selectin ligand activities on leukocytes and high endothelial venules. Immunity, 2001, in press.
Yeh J-C, Hiraoka N, Petryniak B, Nakayama J, Ellies LG, Rabuka D, Hindsgaul O, Marth JD, Lowe JB, and Fukuda M. Noval sulfated lymphocyte homing receptors and their control by a new core 1 extension beta-1, 3-N-acetylglucosaminyltransferase. Cell, 2001, in press.
Smithson G, Rogers CE, Smith PL, Scheidegger EP, Petryniak B, Myers JT, Kim DSL, Homeister JW, and Lowe JB. Fuc-TVII is required for Th1 and Tc1 lymphocyte selectin ligand expression and recruitment in inflammation, and together with Fuc-TIV regulates naive T cell trafficking to lymph nodes. J Exp Med, 2001, in press.