ReviewCells2020
Atg8-Family Proteins-Structural Features and Molecular Interactions in Autophagy and Beyond.
Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 95 citations in OpenAlex.
- Emerging mechanisms of ATG8-independent non-canonical autophagy.Journal of physiology and biochemistry · 2026Review
- CHCHD2 and CHCHD10 promoted autophagic clearance of protein aggregates via GABARAPs.Autophagy · 2026Article
- Discovering host-viral protein interactions in autophagy: A LIR discovery pipeline for identifying LC3-interacting region motifs in highly virulent viruses.PLoS pathogens · 2026Article
- A GABARAP-PtdIns3K-C1 positive feedback loop at the heart of the phagophore nucleation.Nature communications · 2026Article
- M1 macrophage-derived migrasomes ameliorate temporomandibular joint osteoarthritis via autophagy.Journal of nanobiotechnology · 2026Article
- PLETHORA-autophagy axis activates organ regeneration through ROS modulation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- A non-canonical ARMS-GABARAP interaction modulates dendritic spine formation and synaptic development.The EMBO journal · 2026Article
- Molecular cloning, characterization, and expression analysis of two GABAMolecular biology reports · 2026Article
- The modifier matrix: emerging roles of ubiquitin-like proteins in Alzheimer's disease.Molecular neurodegeneration advances · 2026Review
- Targeting autophagy in dysfunctional tumor vasculature.iScience · 2025Review
- AlphaFold2 SLiM screen for LC3-LIR interactions in autophagy.Autophagy · 2025Article
- Autophagy Dysfunction and Neurodegeneration: Where Does It Go Wrong?Journal of molecular biology · 2025Review
- The rapidly expanding role of LC3-interacting regions in autophagy.The Journal of cell biology · 2025Review
- Lipid Droplet Degradation Through Lipophagy in Aurantiochytrium limacinum mh0186.Marine biotechnology (New York, N.Y.) · 2025Article
- Lysosomal quality control Review.Autophagy · 2025Review
- Exploring human plasma proteomic variations in mucolipidosis type IV.Molecular therapy. Methods & clinical development · 2025Article
- A variant of the autophagic receptor NDP52 counteracts phospho-TAU accumulation and emerges as a protective factor for Alzheimer's disease.Cell death & disease · 2025Article
- Monitoring Autophagy in Human Aging: Key Cell Models and Insights.Frontiers in bioscience (Landmark edition) · 2025Review
- The autophagy component LC3 regulates lymphocyte adhesion via LFA1 transport in response to outside-in signaling.Nature communications · 2025Article
- Recycle, repair, recover: the role of autophagy in modulating skeletal muscle repair and post-exercise recovery.Bioscience reports · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.