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. 2010 Mar 19;285(21):15906–15915. doi: 10.1074/jbc.M110.104349

FIGURE 6.

FIGURE 6.

Expression of full-length wild-type and mutant ICAM-1 in HEK-293 and COS-7 cells. A, shown is immunofluorescence staining of HeLa and HEK-293 cells that were transfected with the wild-type ICAM-1 and ICAM-1 with the mutations in D1.v2 with P38R (ICAM-1*) after incubation with mAb LB2, HRV14, and HRV16. Non-transfected HEK-293 cells were indicated as None. Histograms in thin open line are of antibody binding to cells without the primary antibody or viruses used as a control. B, shown is a CPE assay of HeLa and HEK-293 cells in a 96-well plate after incubation with HRV16 for 48 h, quantified by crystal violet staining of adherent cells. The data represent the average values of the absorbance at 570 nm, normalized to the control well with no virus added as 100%. The CPE assay was carried out in triplicate, and the error bars indicate S.D. (*, versus matching control, p < 0.05 by Student's t test). PFU, plaque-forming units. C, shown is immunofluorescence staining of HeLa and COS-7 cells that were transfected with the wild-type ICAM-1 and ICAM-1 with the mutations in D1.v2 with P38R (ICAM-1*) after incubation with mAb LB2, HRV14, and HRV16. Histograms in thin open lines are of antibody binding to cells without the primary antibody or viruses used as a control. D, shown is a CPE assay of HeLa and COS-7 cells in a 96-well plate after incubation with HRV16 for 96 h, quantified by crystal violet staining of adherent cells. The data represent the average values of the absorbance at 570 nm, normalized to the control well with no virus added as 100%. The CPE assay was carried out in triplicate, and the error bars indicate S.D. (*, versus matching control, p < 0.05 by Student's t test).