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Cell Death Differ. 2019 Oct 28. doi: 10.1038/s41418-019-0444-0. [Epub ahead of print]

ER-phagy and human diseases.

Author information

1
Institute of Human Genetics, University Hospital Jena, Friedrich-Schiller-Universität Jena, Jena, Germany. Christian.Huebner@med.uni-jena.de.
2
Institute of Biochemistry II, Goethe University School of Medicine, Frankfurt, Germany. dikic@biochem2.uni-frankfurt.de.
3
Buchmann Institute for Molecular Life Sciences, Goethe University Frankfurt, Frankfurt, Germany. dikic@biochem2.uni-frankfurt.de.
4
Max Planck Institute for Biophysics, Frankfurt, Germany. dikic@biochem2.uni-frankfurt.de.

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.

PMID:
31659280
DOI:
10.1038/s41418-019-0444-0

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