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. 2016 May 15;27(10):1650–1662. doi: 10.1091/mbc.E16-01-0033

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© 2016 Inoue and Tsai. 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 8. — Model depicting the role of the Grp170 nucleotide exchange factor during ERAD. During retrotranslocation of an ERAD-Ls client, the BiP–client complex is delivered to the Sel1L–Hrd1 membrane complex. When Grp170 is recruited to Sel1L, this nucleotide exchange factor triggers client release from BiP by converting ADP-BiP to ATP-BiP. This reaction enables the client to cross the postulated Hrd1 retrotranslocon, where it is extracted into the cytosol and targeted to the proteasome for degradation. An alternative scenario is possible in which Grp170 is first recruited to Sel1L, where it awaits the BiP–client complex.