Figure 4
Figure 4. Rabaptin-5 deficiency decreases FcϵRIα half-life. (A) FcϵRIα half-life was measured in control (shC) or Rabaptin-5 (shR) shRNA-treated BMCMCs by exposing cells to 100 μg/mL of brefeldin A (BFA), or 1.5 μg/mL of cycloheximide (CHX) for the indicated times. Surface FcϵRIα was then assessed by flow cytometry. Expression relative to time 0 was calculated for the indicated time points. Data from 3 separate pairs of shC- or shR-treated BMCMCs were pooled and fit to exponential decay curves. (B) Bar graph indicates shR-treated BMCMC surface FcϵRIα levels relative to shC-treated BMCMCs at the indicated times from data pooled from 3 separate pairs of shC- or shR-treated BMCMCs (*P < .05, **P < .01 by Student t test compared with percentage difference at time 0).

Rabaptin-5 deficiency decreases FcϵRIα half-life. (A) FcϵRIα half-life was measured in control (shC) or Rabaptin-5 (shR) shRNA-treated BMCMCs by exposing cells to 100 μg/mL of brefeldin A (BFA), or 1.5 μg/mL of cycloheximide (CHX) for the indicated times. Surface FcϵRIα was then assessed by flow cytometry. Expression relative to time 0 was calculated for the indicated time points. Data from 3 separate pairs of shC- or shR-treated BMCMCs were pooled and fit to exponential decay curves. (B) Bar graph indicates shR-treated BMCMC surface FcϵRIα levels relative to shC-treated BMCMCs at the indicated times from data pooled from 3 separate pairs of shC- or shR-treated BMCMCs (*P < .05, **P < .01 by Student t test compared with percentage difference at time 0).

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