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Fig. 5. ER stress induces downregulation of E-cadherin and formation of stress fibers in PC Cl3 cells. (A) PC Cl3 cells were grown on glass coverslips for 48 hours, then were vehicle treated (i) or treated with 0.5 µg/ml TN for 30 minutes, followed by 24 hours in medium without TN (ii). Cells were stained with antibodies against E-cadherin. Following TN treatment, the signal for E-cadherin decreased. Arrows in (ii) indicate residual E-cadherin localized at the remaining cell-cell contacts. Bars, 15 µm. (B) PC Cl3 cells were grown and treated as above. Cells were double stained with antibodies against TG and rhodamine-conjugated phalloidin. Bars, 30 µm (i, ii, iii), 15 µm (iv, v, vi). In control cells, rhodaminated phalloidin staining is mainly at the level of cortical actin. Following TN treatment, the signal for TG decreased and stress fibers were formed. Arrows indicate: the few cells expressing various amounts of residual TG (iv), the correlation between residual TG expression and partially formed, not fully formed, stress fibers (v) and, consequently, the lack of overlap between TG and actin signals (vi). A greater magnification for TN-treated cells was intentionally used to show better the coordinate variations of TG, cortical actin and stress fibers.
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