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. 2016 Feb 15;27(4):716–730. doi: 10.1091/mbc.E15-08-0547

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© 2016 Amsalem et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 7: — Clathrin-mediated endocytosis attenuates the cell surface expression of BMPRII-LF. HEK293T cells were transfected with myc-BMPRII-LF or myc-BMPRII-LF-AA. At 24 h posttransfection, the steady-state expression of the transfected receptors (A, B) and their expression levels at the plasma membrane (C, D) were measured as in Figures 1 and 4, respectively. (A) A representative gel. (B) Quantification of the steady-state expression levels of myc-BMPRII-LF and myc-BMPRII-LF-AA from multiple experiments (n = 6). Results (mean ± SEM) were normalized relative to β-actin, taking the expression level of myc-BMPRII-LF as 100%. (C) A representative immunoblot with or without proteinase K digestion. (D) Quantification of cell surface–localized myc-BMPRII-LF and myc-BMPRII-LF-AA. Results (mean ± SEM, n = 6) were derived from the difference between proteinase K–treated and untreated samples, as in Figure 4. The asterisk indicates a significant increase (p < 0.05) in cell surface level of myc-BMPRII-LF-AA relative to that of myc-BMPRII-LF (taken as 100%).