Found 32 results
Author Title [ Type(Desc)] Year
Filters: Author is Kerkvliet, Nancy I  [Clear All Filters]
Journal Article
W. H. Bisson, Koch, D. C., Donnell, E. F. ’, Khalil, S. M., Kerkvliet, N. I., Tanguay, R. L., Abagyan, R., and Kolluri, S., “Modeling of the Aryl Hydrocarbon Receptor (AhR) Ligand Binding Domain and Its Utility in Virtual Ligand Screening to Predict New AhR Ligands”, Journal of Medicinal Chemistry, vol. 52, no. 18, pp. 5635 - 5641, 2009.
W. H. Bisson, Koch, D. C., O'Donnell, E. F., Khalil, S. M., Kerkvliet, N. I., Tanguay, R. L., Abagyan, R., and Kolluri, S. Kumar, “Modeling of the aryl hydrocarbon receptor (AhR) ligand binding domain and its utility in virtual ligand screening to predict new AhR ligands.”, J Med Chem, vol. 52, no. 18, pp. 5635-41, 2009.
N. I. Kerkvliet, “Recent advances in understanding the mechanisms of TCDD immunotoxicity.”, Int Immunopharmacol, vol. 2, no. 2-3, pp. 277-91, 2002.
A. Perkins, Phillips, J. Lynne, Kerkvliet, N. I., Tanguay, R., Perdew, G. H., Kolluri, S., and Bisson, W. H., “A structural switch between agonist and antagonist bound conformations for a ligand-optimized model of the human aryl hydrocarbon receptor ligand binding domain”, Biology, vol. 3, pp. 645–669, 2014.
A. Perkins, Phillips, J. Lynne, Kerkvliet, N. I., Tanguay, R. L., Perdew, G. H., Kolluri, S. K., and Bisson, W. H., “A Structural Switch between Agonist and Antagonist Bound Conformations for a Ligand-Optimized Model of the Human Aryl Hydrocarbon Receptor Ligand Binding Domain.”, Biology (Basel), vol. 3, no. 4, pp. 645-69, 2014.
N. I. Kerkvliet, “T Lymphocytes Are Direct, Aryl Hydrocarbon Receptor (AhR)-Dependent Targets of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD): AhR Expression in Both CD4+ and CD8+ T Cells Is Necessary for Full Suppression of a Cytotoxic T Lymphocyte Response by TCDD”, Toxicology and Applied Pharmacology, vol. 185, no. 2, pp. 146 - 152, 2002.
A. K. Ehrlich, Pennington, J. M., Bisson, W. H., Kolluri, S., and Kerkvliet, N. I., “TCDD, FICZ, and other high affinity AhR ligands dose-dependently determine the fate of CD4+ T cell differentiation.”, Toxicol Sci, 2018.

Pages