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. 2016 Nov 7;27(22):3449–3458. doi: 10.1091/mbc.E16-06-0470

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© 2016 Jiang, Chen, 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 5: — Effects of tunicamycin treatment on CD16–hIgG1 binding. (A) The 2D affinities and (B) off-rates of CD16 isoforms expressed on CHO cell-surface and soluble CD16–Ig chimera for hIgG1 obtained from fitting Eq. 3 to specific adhesion frequencies measured at six contact durations ranging from 0.25 to 8 s (three RBC–CHO cell or RBC–RBC pairs with 50 or 100 contacts each per contact duration) as in Figure 2B. (C) Representative Scatchard plot analysis for saturation binding of CLBFcgran-1 to CD16a^TM. (D) The 3D affinities of CD16 isoforms expressed on CHO cell surface for CLBFcgran-1 obtained by Scatchard plot analysis as illustrated in C. In A, B, and D, data both without and with tunicamycin treatment are presented as mean ± SEM. Data values are below the plots; p-values from Student’s t test are above data bars.