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. 2009 Sep 14;18(24):4734–4745. doi: 10.1093/hmg/ddp436

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© The Author 2009. Published by Oxford University Press

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.5/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 6. — Expression of Cx31 skin disease mutants disrupts the ER marker BiP/GRP78. The ER marker BiP/GRP78 (E–H) is upregulated/disrupted in HeLa cells overexpressing (R42P)Cx31-EGFP (B) and (C86S)Cx31-EGFP (C) but not (WT)Cx31-EGFP (A) or (66delD)Cx31-EGFP (D). Note the exposure settings have been optimized for each field of view, the surrounding non-transfected control cells in (F and G) have a similar level of BiP/GRP78 expression as the cells in (E and H). The KDEL antibody also shows a marked upregulation in cells expressing the (R42P)Cx31-EGFP and (C86S)Cx31-EGFP construct (data not shown). The DAPI-stained nuclei are shown in blue.