
Masonic Cancer Center, University of Minnesota

Research Program: Immunology
Associate Professor, Department of Veterinary and Biomedical Sciences, and Department of Lab Medicine and Pathology (Adjunct)
walch003@umn.edu
612-624-2282 — office
612-624-9741 — lab
Preferred contact method: e-mail
Lab Web site
Research Interests
Tumor development and progression are strongly linked to inflammation. My research group is examining various aspects of inflammation regulation. A key white blood cell (leukocyte) involved in the early inflammatory response is the neutrophil, which is the most predominant leukocyte in the peripheral blood and at sites of acute inflammation. The expression of various inflammatory mediators produced by neutrophils is regulated by a process referred to as ectodomain shedding. This process is primarily mediated by the protease ADAM17 (also referred to as TACE). Among other lines of research, my lab is actively involved in understanding the function and regulation of this protease in order to manipulate inflammation for therapeutic purposes.
Selected Publications
Matala E, Alexander SR, Kishimoto TK, Walcheck B. The cytoplasmic domain of L-selectin participates in regulating L-selectin endoproteolysis. J Immunol. 2001;167:1617.
Walcheck B, Leppanen A, Cummings RD, Knibbs RN, Stoolman LM, Alexander SR, Mattila PE, McEver RP. The monoclonal antibody CHO-131 binds to a core 2 O-glycan terminated with sialyl-Lewis x, which is a functional glycan ligand for P-selectin. Blood. 2002;99:4063.
St. Hill CA, Alexander SR, Walcheck B. Indirect capture augments leukocyte accumulation on P-selectin in flowing whole blood. J Leukoc Biol. 2003;73:464.
Walcheck B, Alexander SR, St. Hill CA, Matala E. ADAM-17-independent shedding of L-selectin. J Leukoc Biol. 2003;74:389-394.
St. Hill, CA, Bullard, KM, and Walcheck B. 2005. Expression of the high-affinity selectin glycan ligand C2-O-sLeX by colon carcinoma cells. Cancer Lett. 217:105.
Mattila P, Green CE, Schaff U, Simon SI, Walcheck B. Cytoskeletal interactions regulate inducible L-selectin clustering. Am J Physiol Cell Physiol. 2005;289:C323-332.
Li Y, Brazzell JL, Herrera AH, Walcheck B. ADAM17 deficiency by mature neutrophils has differential effects on L-selectin shedding. Blood 2006;108:2275-2279.
Ni Z, Campbell JJ, Niehans G, Walcheck B. 2006. The monoclonal antibody CHO-131 identifies a subset of cutaneous lymphocyte-associated antigen T cells enriched in P-selectin-binding cells. J Immunol. 177:4742-4748.
Walcheck B, Herrera AH, St. Hill CA, Mattila P, Whitney AR, DeLeo FR. ADAM17 activity during human neutrophil activation and apoptosis. Eur J Immunol. 2006;36:968-976.
Ni Z, Walcheck B. Varied levels of reactivity by different E-selectin/Fc constructs with cutaneous lymphocyte-associated antigen (CLA)+ CD4+ T cells. Immunol Lett. 2007;108:179-182.
Bell J, Herrera AH, Li L, Walcheck B.Role of ADAM17 in the ectodomain shedding of TNF-alpha and its receptors by neutrophils and macrophages. J Leukoc Biol. 2007;82:173-176.
Schaff U, Mattila P, Simon SI, Walcheck B. Neutrophil adhesion to E-selectin under shear promotes the redistribution and co-clustering of ADAM17 and its proteolytic substrate L-selectin. J Leukoc Biol. 2008;83:99-105.
Wang Y., Herrera, AH., Li, Y., and Walcheck, B. 2009. Regulation of ADAM17-mediated ectodomain shedding through conformational changes in its extracellular region. J. Immunol. 182:2449-57
St Hill, C.A., Farooqui, M., Mitcheltree, G., Gulbahce, H.E., Jessurun, J., Cao, Q., Walcheck, B. 2009. The high affinity selectin glycan ligand C2-O-sLex and mRNA transcripts of the core 2 beta-1,6-N- acetylglusaminyltransferase (C2GnT1) gene are highly expressed in human colorectal adenocarcinomas. BMC Cancer 9:79.