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. 2017 Oct 5;12(10):e0185992. doi: 10.1371/journal.pone.0185992

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© 2017 Lu et al

This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Fig 4 — A. Co-localization of MEX3C-2 (GFP-tagged) with an endogenous AP-2 α subunit. Endogenous AP-2 α was immunostained by specific antibody. The boxed area was shown at high magnification in the following row. Co-localized signals were marked by *. B. Co-localization of transiently expressed MEX3C variants (Flag-tagged, stained by anti-Flag antibody) with transiently expressed AP-2 μ2 (mCherry-tagged). The boxed area was shown at high magnification in the following row. Co-localized signals are marked by *. C. GTP binding defective dynamin^K44A mutant trapped wild-type MEX3C-1, but not MEX3C-1 mutants unable to interact with AP-2, at dynamin^K44A enriched foci. K44A: Dynamin^K44A mutant; 1ΔC: MEX3C-1ΔC, MEX3C-1 C-terminal 247AA deleted; 1ΔKH: MEX3C-1ΔKH, MEX3C-1 KH domains (AA 206–407) deleted. Shown are representative images of multiple double-positive cells. Quantitative data are presented in Fig A in S1 File.