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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 8. — Expression of the Cx31 skin disease mutants upregulate components of the UPR pathway. The UPR components ATF6 (E–H) and CHOP/GAAD153 (M–P) are upregulated in HeLa cells overexpressing (R42P)Cx31-EGFP (B and J) and (C86S)Cx31-EGFP (C and K) but not the (WT)Cx31-EGFP (A and I) nor the (66delD)Cx31-EGFP neuropathy mutant (D and L). Furthermore, the ATF6 staining (F and G) has a more nuclear localization in cells expressing (R42P)Cx31-EGFP (B) and (C86S)Cx31-EGFP (C) compared with untransfected cells and cells expressing (WT)Cx31-EGFP (A) and (66delD)Cx31-EGFP (D), indicating that the cleaved N-terminal portion has been translocated to the nucleus. The DAPI-stained nuclei are shown in blue.