{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,12]],"date-time":"2026-03-12T06:25:03Z","timestamp":1773296703880,"version":"3.50.1"},"reference-count":41,"publisher":"American Society for Cell Biology (ASCB)","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["MBoC"],"published-print":{"date-parts":[[2010,4]]},"abstract":"<jats:p>Cholera toxin (CT) is transported from the plasma membrane of host cells to the endoplasmic reticulum (ER) where the catalytic CTA1 subunit retro-translocates to the cytosol to induce toxicity. Our previous analyses demonstrated that the ER oxidoreductase protein disulfide isomerase (PDI) acts as a redox-dependent chaperone to unfold CTA1, a reaction postulated to initiate toxin retro-translocation. In its reduced state, PDI binds and unfolds CTA1; subsequent oxidation of PDI by Ero1\u03b1 enables toxin release. Whether this in vitro model describes events in cells that control CTA1 retro-translocation is unknown. Here we show that down-regulation of Ero1\u03b1 decreases retro-translocation of CTA1 by increasing reduced PDI and blocking efficient toxin release. Overexpression of Ero1\u03b1 also attenuates CTA1 retro-translocation, an effect due to increased PDI oxidation, which prevents PDI from engaging the toxin effectively. Interestingly, Ero1\u03b1 down-regulation increases interaction between PDI and Derlin-1, an ER membrane protein that is a component of the retro-translocation complex. These findings demonstrate that an appropriate Ero1\u03b1-PDI ratio is critical for regulating the binding\u2013release cycle of CTA1 by PDI during retro-translocation, and implicate PDI's redox state in targeting it to the retro-translocon.<\/jats:p>","DOI":"10.1091\/mbc.e09-09-0826","type":"journal-article","created":{"date-parts":[[2010,2,4]],"date-time":"2010-02-04T02:11:14Z","timestamp":1265249474000},"page":"1305-1313","source":"Crossref","is-referenced-by-count":32,"title":["The Ero1\u03b1-PDI Redox Cycle Regulates Retro-Translocation of Cholera Toxin"],"prefix":"10.1091","volume":"21","author":[{"given":"Paul","family":"Moore","sequence":"first","affiliation":[{"name":"Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI 48109"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kaleena M.","family":"Bernardi","sequence":"additional","affiliation":[{"name":"Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI 48109"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Billy","family":"Tsai","sequence":"additional","affiliation":[{"name":"Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI 48109"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"1076","reference":[{"key":"B1","doi-asserted-by":"crossref","first-page":"55","DOI":"10.1089\/ars.2007.1837","volume":"10","author":"Appenzeller-Herzog C.","year":"2008","journal-title":"Antioxid. 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