Fig. 4.
Fig. 4. Metabolic inhibitor profile for CD98-, CD29-, and CD43-induced aggregation. / (A) Aggregation was measured under standard conditions as described in “Materials and methods,” in the presence of CD98-AHN-18 (1.5 μg/mL), MEM 101A (CD29, 0.3 μg/mL), and 161-46 (CD43, 0.3 μg/mL). The inhibitors were added 1 hour prior to the antibody and remained in the culture. Results are expressed as aggregation relative to control cultures in the presence of each aggregating antibody, but in the absence of inhibitor (mean ± SEM, triplicate cultures). All values that differ significantly from controls (P < .05) are indicated by an asterisk. (B) As for panel A, but the deoxyglucose (10 mM) was added either before, simultaneously with, or after CD98-AHN-18. Aggregation in all cases was measured at 6 hours. Results are expressed as aggregation relative to control cultures in the presence of each aggregating antibody, but in the absence of inhibitor (mean ± SEM, triplicate cultures).

Metabolic inhibitor profile for CD98-, CD29-, and CD43-induced aggregation.

(A) Aggregation was measured under standard conditions as described in “Materials and methods,” in the presence of CD98-AHN-18 (1.5 μg/mL), MEM 101A (CD29, 0.3 μg/mL), and 161-46 (CD43, 0.3 μg/mL). The inhibitors were added 1 hour prior to the antibody and remained in the culture. Results are expressed as aggregation relative to control cultures in the presence of each aggregating antibody, but in the absence of inhibitor (mean ± SEM, triplicate cultures). All values that differ significantly from controls (P < .05) are indicated by an asterisk. (B) As for panel A, but the deoxyglucose (10 mM) was added either before, simultaneously with, or after CD98-AHN-18. Aggregation in all cases was measured at 6 hours. Results are expressed as aggregation relative to control cultures in the presence of each aggregating antibody, but in the absence of inhibitor (mean ± SEM, triplicate cultures).

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