Bruce K.Walcheck, Ph.D. Associate Professor Department of Veterinary Pathobiology Montana State University, 1994, Ph.D. walch003@umn.edu 612-624-2282 office 612-624-9741 lab

Research Interests:

Cell adhesion: leukocyte migration

Our research focus pertains to the mechanisms of leukocyte migration from the blood into lymphoid organs and sites of inflammation. Leukocytes disciminate between tissue sites, in part, by adhesion molecules expressed on the leukocyte cell surface and on the endothelial cell lining of the vascular wall. Our work primarily focuses on the selectin and integrin families of adhesion proteins and their ligands. These adhesion molecules perform more than just a passive role of adhesion, they also regulate their affinity, expression levels, and numerous intracellular events. For instance, L-selectin receptors are rapidly cleaved (within seconds to minutes) from the cell surface of leukocytes following cell activation and ligand interaction. We are investigating the intermolecular interactions within the cell that participate in this process. In our research, we use state-of-art equipment an techniques, including flow cytometry and sorting, videomicroscopy and comptuer-based image analysis, molecular biology, protein biochemistry, and monoclonal antibody production.

Walcheck lab

Selected Recent Publications:

• Schaff U, Mattila PE, Simon SI, Walcheck B. 2007. Neutrophil adhesion to E- selectin under shear promotes the redistribution and co-clustering of ADAM17 and its proteolytic substrate L-selectin. J Leukoc Biol. In press.

• Bell J., Herrera AH. Li, Y., and Walcheck B. 2007. Role of ADAM17 in the ectodomain shedding of TNF-alpha and its receptors by neutrophils and macrophages. J. Leuko. Biol. 82:173-176.

• Ni, Z. and Walcheck, B. 2007. Varied levels of reactivity by different E-selectin/Fc constructs with cutaneous lymphocyte-associated antigen (CLA)+ CD4+ T cells. Immunol. Lett. 108:179.

• Li, Y., Brazzell, JL., Herrera, AH., Walcheck, B. 2006. ADAM17 deficiency by
  mature neutrophils has differential effects on L-selectin shedding. Blood 108(7):2275-9.

• Ni Z, Campbell JJ, Niehans G, Walcheck B. 2006. The Monoclonal Antibody CHO-131 Identifies a Subset of CutaneousLymphocyte-Associated Antigen T Cells Enriched in P-Selectin-Binding Cells. J Immunol. 177(7):4742-8.
  

• Walcheck, B., Herrera, A.H., St. Hill, C.A., Mattila, P., Whitney, A.R., and DeLeo, F.R. 2006. ADAM17 activity during human neutrophil activation and apoptosis. Eur. J. Immunol. 36:968-76.

• Mattila, P., Green, C.E., Schaff, U., Simon, S.I., and Walcheck, B. 2005. L-selectin clustering involves altered lipid phase partitioning and is regulated by cytoskeletal anchorage. Amer. J. Physiol. Cell Physiol. 289:323.

• St. Hill, C.A., Bullard, K.M. and Walcheck, B. 2005. Expression of the high-affinity selectin glycan ligand C2-O-sLeX by colon carcinoma cells. Cancer Lett. 217:105.

• Walcheck, B., Alexander, S.R., St. Hill, C.A., and Matala, E. 2003. ADAM-17-independent shedding of L-selectin. J. Leukoc. Biol. 74:389.

• Catherine St. Hill, Shelia R. Alexander, and Bruce Walcheck. 2003. Indirect capture augments leukocyte accumulation on P-selectin in flowing whole blood. J. Leukoc. Biol. 73: 464.

• Walcheck, B., Leppanen, A., Cummings, RD., Knibbs, RN., Stoolman, LM., Alexander, SR., Mattila, PE., and McEver, RP. 2002. 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 99:4064.

• Matala, E., Alexander, S.R., Kishimoto T.K., and Walcheck B. 2001. The cytoplasmic domain of L-selectin participates in regulating L-selectin endoproteolysis. J. Immunol. 167:1617.

• Alexander, S.R., Kishimoto, T.K., and Walcheck, B. 2000. Effects of selective protein kinase C inhibitors on the proteolytic downregulation of L-selectin from chemoattractant-activated neutrophils. J. Leuk. Biol. 67:415.

• Kahn, J., B. Walcheck, G. Migaki, M.A. Jutila, and T.K. Kishimoto. (1998) Calmodulin regulates L-selection adhesion molecule expression and function through a protease-dependent mechansim. Cell 92:809.
  

• Walcheck, B., J. Kahn, J.M. Fisher, B.B. Wang, R.S. Fisk, D.G. Payan, C. Feehan, R. Betageri, K. Darlak, A.F. Spatola, and T.K. Kishimoto. (1996) Neutophil rolling altered by inhibition of L-selectin shedding in vitro. Nature 380:720.
  

• Walcheck, B., K.L. Moore, R.P. McEver, and T.K. Kishimoto. (1996) Neutrophil-neutrophil interactions under hydrodynamic shear stress involve L-selectin and PSGL-1: A mechanism that amplifies initial leukocyte accumulation on P-selectin in vitro. J. Clin. Invest. 98:1081.

Last modified on: November 15, 2007