Figure 2
Figure 2. The effect of Rac1 inhibition on CXCR4 is reversible. (A) HL60 cells were incubated with the Rac1 inhibitory peptide and then surface CXCR4 (left) or total CXCR4 (right) were measured using mAb 44717 by flow cytometry (n = 3). (B) HL60 cells were incubated with the Rac1 inhibitory peptide, washed and placed at 37°C and CXCR4 surface signal (detected by mAb 12G5) was determined after different time periods by flow cytometry (n = 4). (C) One hour after washout of the Rac1 inhibitory peptide, HL60 cells were incubated again with the inhibitory peptide or with CXCL12 and the CXCR4 surface signal (as detected by mAb 12G5) was determined by flow cytometry (n = 3). Bars show the mean (A) and median (B-C) fluorescence intensity determined by flow cytometry and expressed as percentage ± SEM compared with untreated conditions (*P < .05, **P < .01).

The effect of Rac1 inhibition on CXCR4 is reversible. (A) HL60 cells were incubated with the Rac1 inhibitory peptide and then surface CXCR4 (left) or total CXCR4 (right) were measured using mAb 44717 by flow cytometry (n = 3). (B) HL60 cells were incubated with the Rac1 inhibitory peptide, washed and placed at 37°C and CXCR4 surface signal (detected by mAb 12G5) was determined after different time periods by flow cytometry (n = 4). (C) One hour after washout of the Rac1 inhibitory peptide, HL60 cells were incubated again with the inhibitory peptide or with CXCL12 and the CXCR4 surface signal (as detected by mAb 12G5) was determined by flow cytometry (n = 3). Bars show the mean (A) and median (B-C) fluorescence intensity determined by flow cytometry and expressed as percentage ± SEM compared with untreated conditions (*P < .05, **P < .01).

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