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. 2021 Aug 2;9(8):e002443. doi: 10.1136/jitc-2021-002443

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© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See http://creativecommons.org/licenses/by-nc/4.0/.

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Targeting thyroid adenoma associated gene (THADA) blocks programmed death-ligand 1 (PD-L1) trafficking to Golgi while induces endoplasmic reticulum (ER) retention of PD-L1 and ER-associated degradation (ERAD). THADA mediates the interaction of PD-L1 and Sec24A, driving PD-L1 export from the ER by coat protein complex II (COPII) trafficking vesicles. THADA depletion significantly blocks PD-L1 binding to Sec24A, thereby causing ER retention of PD-L1 and exhaustion of both Golgi and cytomembrane resident PD-L1. Aberrant aggregation of PD-L1 proteins trigger ERAD, which are recognized and retrotranslocated by HRD1 ERAD complex, and ultimately eliminated by ubiquitin-proteasome pathway in the cytoplasm.