Abstract
Autophagy regulates the degradation of unnecessary or dysfunctional cellular components. This catabolic process requires the formation of a double-membrane vesicle, the autophagosome, that engulfs the cytosolic material and delivers it to the lysosome. Substrate specificity is achieved by autophagy receptors, which are characterized by the presence of at least one LC3-interaction region (LIR) or GABARAP-interaction motif (GIM). Only recently, several receptors that mediate the specific degradation of endoplasmic reticulum (ER) components via autophagy have been identified (the process known as ER-phagy or reticulophagy). Here, we give an update on the current knowledge about the role of ER-phagy receptors in health and disease.
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Acknowledgements
We are grateful to Paolo Grumati, Andrea Gubas, Ingo Kurth, and Antje-Kathrin Huebner for critical comments and insightful discussions. This work was partially supported by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation)—Project number 259130777—SFB 1177 and DFG-funded Research Unit FOR 2625 on Mechanisms of Lysosomal Homeostasis, the European Research Council (ERC) grant 742720 UbBAC, Cardio-Pulmonary Institute (CPI), EXC 2026, Project ID: 390649896, and the LOEWE program on Ubiquitin Networks (Ub-Net), State of Hesse, Germany to ID and by German Research Foundation HU 800/6–2, HU 800/13–1, the DFG-funded Research Unit FOR 2625 on Mechanisms of Lysosomal Homeostasis and the SP6 within the DFG-funded research training group 1715 to CAH. CAH and ID envisioned and wrote the manuscript.
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Hübner, C.A., Dikic, I. ER-phagy and human diseases. Cell Death Differ 27, 833–842 (2020). https://doi.org/10.1038/s41418-019-0444-0
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DOI: https://doi.org/10.1038/s41418-019-0444-0
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