期刊
TRENDS IN CELL BIOLOGY
卷 26, 期 1, 页码 6-16出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tcb.2015.08.010
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资金
- Corona Stiftung
- Deutsche Forschungsgemeinschaft (Collaborative Research Center 1080 grant)
- Deutsche Forschungsgemeinschaft, the Cluster of Excellence 'Macromolecular Complexes' [EXC115]
- LOEWE Centrum for Cell and Gene Therapy Frankfurt
- European Research Council Advanced Grant
Selective autophagy regulates the abundance of specific cellular components via a specialized arsenal of factors, termed autophagy receptors, that target protein complexes, aggregates, and whole organelles into lysosomes. Autophagy receptors bind to LC3/GABARAP proteins on phagophore and autophagosome membranes, and recognize signals on cargoes to deliver them to autophagy. Ubiquitin (Ub), a well-known signal for the degradation of polypeptides in the proteasome, also plays an important role in the recognition of cargoes destined for selective autophagy. In addition, a variety of cargoes are committed to selective autophagy pathways by Ub-independent mechanisms employing protein-protein interaction motifs, Ub-like modifiers, and sugar- or lipid-based signals. In this article we summarize Ub-dependent and independent selective autophagy pathways, and discuss regulatory mechanisms and challenges for future studies.
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