TY  - JOUR
A1  - Wesch, Nicole
A1  - Kirkin, Vladimir
A1  - Rogov, Vladimir V.
T1  - Atg8-family proteins - structural features and molecular interactions in autophagy and beyond
T2  - Cells
N2  - Autophagy is a common name for a number of catabolic processes, which keep the cellular homeostasis by removing damaged and dysfunctional intracellular components. Impairment or misbalance of autophagy can lead to various diseases, such as neurodegeneration, infection diseases, and cancer. A central axis of autophagy is formed along the interactions of autophagy modifiers (Atg8-family proteins) with a variety of their cellular counter partners. Besides autophagy, Atg8-proteins participate in many other pathways, among which membrane trafficking and neuronal signaling are the most known. Despite the fact that autophagy modifiers are well-studied, as the small globular proteins show similarity to ubiquitin on a structural level, the mechanism of their interactions are still not completely understood. A thorough analysis and classification of all known mechanisms of Atg8-protein interactions could shed light on their functioning and connect the pathways involving Atg8-proteins. In this review, we present our views of the key features of the Atg8-proteins and describe the basic principles of their recognition and binding by interaction partners. We discuss affinity and selectivity of their interactions as well as provide perspectives for discovery of new Atg8-interacting proteins and therapeutic approaches to tackle major human diseases.
KW  - Atg8
KW  - LC3
KW  - GABARAP
KW  - LIR motif
KW  - SAR
KW  - UBL
KW  - autophagy
Y1  - 2020
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/55940
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-559407
SN  - 2073-4409
N1  - © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
VL  - 9
IS  - 9, art. 2008
SP  - 1
EP  - 25
PB  - MDPI
CY  - Basel
ER  -