Figure 6.
Receptor recycling or synthesis do not contribute to IGF1R retention at the cell surface on IGFBP7 treatment. RS4;11 or Jurkat cells were starved for 4 hours in serum-free RPMI medium and then left untreated or stimulated for 4 hours with insulin (500 ng/mL), IGFBP7 (100 ng/mL), and their combination. Receptor recycling, synthesis, and endocytosis were inhibited by concomitant addition of (A) primaquine (100 µM), (B) cycloheximide (20 µM), or (C) dansylcadaverine (DC; 10 µg/mL), respectively. The cell surface expression of IGF1R was measured by flow cytometry. (D) Proliferation of RS4;11 and Jurkat cells expressing shRNAs against IGFBP7 (sh.959) or scramble control (Scr) analyzed by the trypan blue exclusion technique after treatment with insulin (500 ng/mL), dansylcadaverine (DC; 10 µg/mL), or their combination. Results from a single experiment run in triplicate wells, using RPMI-3% FBS.

Receptor recycling or synthesis do not contribute to IGF1R retention at the cell surface on IGFBP7 treatment. RS4;11 or Jurkat cells were starved for 4 hours in serum-free RPMI medium and then left untreated or stimulated for 4 hours with insulin (500 ng/mL), IGFBP7 (100 ng/mL), and their combination. Receptor recycling, synthesis, and endocytosis were inhibited by concomitant addition of (A) primaquine (100 µM), (B) cycloheximide (20 µM), or (C) dansylcadaverine (DC; 10 µg/mL), respectively. The cell surface expression of IGF1R was measured by flow cytometry. (D) Proliferation of RS4;11 and Jurkat cells expressing shRNAs against IGFBP7 (sh.959) or scramble control (Scr) analyzed by the trypan blue exclusion technique after treatment with insulin (500 ng/mL), dansylcadaverine (DC; 10 µg/mL), or their combination. Results from a single experiment run in triplicate wells, using RPMI-3% FBS.

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