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. 2015 Apr 15;26(8):1532–1542. doi: 10.1091/mbc.E14-12-1615

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© 2015 Merulla et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 6: — The chimeras analyzed in this study and their fate. (A) The chimeras with the misfolded ectodomain (NHKc_D6A and NHKc) are retained in the ER by the conventional quality control relying on UGGT1, CNX, and BiP intervention. These proteins are eventually destined to ERAD. (B) The chimera with the native ectodomain, characterized by an ionizable residue in the TM (α1ATc), fulfills the quality control requirement for release from CNX and BiP, but its transport to the Golgi is halted upon p97 and UGGT1 intervention. This protein quality checkpoint is bypassed upon pharmacologic inhibition of p97 or silencing of p97 or UGGT1 expression. (C) The folding-competent chimera (α1ATc_D6A) is efficiently transported to the Golgi compartment.