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. 2020 Jul 31;9(7):bio054304. doi: 10.1242/bio.054304

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© 2020. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Fig. 4. — Isoform-mediated differences in human Arp2/3 complexes. (A) Left, location of non-conserved sequence variation between human ARPC1A and ARPC1B (green spheres) and location of disease-causing ARPC1B point mutations (purple spheres) mapped onto ARPC1B; right, cross section through ARPC1B; (B) left, density corresponding to ARPC5L, showing the incomplete density for this subunit apart from helix-α7 adjacent to ARPC4; right, density corresponding to ARPC5, showing the near complete density for this subunit (C) left, 90° rotated view compared to B, left of ARPC5L showing the incomplete density for this subunit and lack of connectivity to Arp2; right, 90° rotated view compared to B, right of ARPC5, showing the clear density for most of the subunit, including its N-terminal tether to Arp2.