Cargo recognition and trafficking in selective autophagy
Abstract
Selective autophagy is a quality control pathway through which cellular components are sequestered into double-membrane vesicles and delivered to specific intracellular compartments. This process requires autophagy receptors that link cargo to growing autophagosomal membranes. Selective autophagy is also implicated in various membrane trafficking events. Here we discuss the current view on how cargo selection and transport are achieved during selective autophagy, and point out molecular mechanisms that are congruent between autophagy and vesicle trafficking pathways.
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Recent evidence demonstrates a strong selectivity for autophagy.
“Recent evidence demonstrates a strong selectivity for autophagy28.”
From Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration (2020) · cites this paper as [28]
OPTN is an autophagy receptor that binds ubiquitinated cargo via its UBAN domain and LC3 via its LIR domain, although it can also act independently of target ubiquitination.
“OPTN is an autophagy receptor that binds ubiquitinated cargo (via its UBAN domain) and LC3 (via its LIR domain) [194,254,255], although it can also act independently of target ubiquitination [254].”
From Autophagy and ALS: mechanistic insights and therapeutic implications (2022) · cites this paper as [255]
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A brief history of autophagy from cell biology to physiology and disease
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AUTACs: Cargo-Specific Degraders Using Selective Autophagy
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Receptor-mediated selective autophagy degrades the endoplasmic reticulum and the nucleus
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Microglia clear neuron-released α-synuclein via selective autophagy and prevent neurodegeneration
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Dual role of autophagy in hallmarks of cancer
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Galectin-3 Coordinates a Cellular System for Lysosomal Repair and Removal
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Autophagy in acute kidney injury
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Autophagy in liver diseases: Time for translation?
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Recent Advances in Understanding of Pathogenesis of Alcohol-Associated Liver Disease
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Human TBK1: A Gatekeeper of Neuroinflammation
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Regulation of YAP by mTOR and autophagy reveals a therapeutic target of tuberous sclerosis complex
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- Authors
- Stolz, A., Ernst, A., & Dikic, I.
- Affiliations
- Goethe University Frankfurt (DE)
- Venue
- Nature Cell Biology
- Published
- 2014-05-30
- Volume
- 16
- Issue
- 6
- Pages
- 495-501
- ISSN
- 1465-7392 (ISSN-L)
- 1476-4679
- OpenAlex
- W2077757969
- Cited by
- 1,207
- References
- 112
- Citations by year
- 2026: 42 · 2025: 79 · 2024: 75 · 2023: 66 · 2022: 99 · 2021: 144 · 2020: 136 · 2019: 129 · 2018: 129 · 2017: 108 · 2016: 108 · 2015: 73 · 2014: 18
- FWCI
- 13.66
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Keywords
- selective autophagy, cargo recognition, cargo delivery, autophagy receptors, membrane trafficking, vesicle trafficking, autophagosome formation, protein degradation, organelle degradation, quality control
- MeSH terms
- Animals, Autophagy, Humans, Intracellular Membranes, Receptors, Cytoplasmic and Nuclear, Protein Transport, Transport Vesicles
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