ER-phagy and human diseases

被引:85
作者
Huebner, Christian A. [1 ]
Dikic, Ivan [2 ,3 ,4 ]
机构
[1] Friedrich Schiller Univ Jena, Univ Hosp Jena, Inst Human Genet, Jena, Germany
[2] Goethe Univ, Inst Biochem 2, Sch Med, Frankfurt, Germany
[3] Goethe Univ Frankfurt, Buchmann Inst Mol Life Sci, Frankfurt, Germany
[4] Max Planck Inst Biophys, Frankfurt, Germany
基金
欧洲研究理事会;
关键词
ENDOPLASMIC-RETICULUM TURNOVER; AUTOPHAGY RECEPTOR; SENSORY NEUROPATHY; CARGO RECEPTOR; FAM134B; PROTEIN; MUTATIONS; SEC62; GENE; MECHANISMS;
D O I
10.1038/s41418-019-0444-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:833 / 842
页数:10
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