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. 2015 Apr 13;209(1):23–32. doi: 10.1083/jcb.201407059

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© 2015 Juanes-Garcia et al.

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Figure 3. — Ser1935 regulates the stability of NMII-B in actomyosin bundles and controls its ability to locally suppress protrusion during front–back polarization. (A) FRAP curves of wild-type and single mutation S1935A, S1938A, and S1939A GFP–MHCII-B constructs. (B) FRAP curves of wild-type and single mutation S1935D, S1938D, and S1939D GFP–MHCII-B proteins. (C) FRAP curves of wild-type GFP–MHCII-B and DAAAA and ADDDD mutants. (A–C) Data are the means ± SEM of 24 individual measurements per condition in four independent experiments. (D and E) Snapshots of TIRF microscopy time-lapse videos of MHCII-B–depleted CHO.K1 cells cotransfected with shRNA-resistant wild-type GFP–MHCII-B (D) or GFP–1935D-MHCII-B (E) and mCherry-vinculin. Arrows point to protrusive areas of the cell. Arrowheads point to regions decorated with NMII-B filaments. Bars, 10 µm. Images extracted from Videos 4 and 5.