ArticleAutophagy2018
Systematic analysis of ATG13 domain requirements for autophagy induction.
Article in Autophagy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed.
- ATG13 promotes K63-linked polyubiquitination of MAVS via ASB1 to restrict influenza A virus replication.Emerging microbes & infections · 2026Article
- The human autophagy-initiating complexes ULK1C and PI3KC3-C1.The Journal of biological chemistry · 2025Review
- The triad interaction of ULK1, ATG13, and FIP200 is required for ULK complex formation and autophagy.eLife · 2025Article
- Different types of cell death and their interactions in myocardial ischemia-reperfusion injury.Cell death discovery · 2025Review
- Autophagy/Mitophagy Regulated by Ubiquitination: A Promising Pathway in Cancer Therapeutics.Cancers · 2023Review
- Hyperoside Attenuates Sepsis-Induced Acute Lung Injury (ALI) through Autophagy Regulation and Inflammation Suppression.Mediators of inflammation · 2023Article
- Neuroinflammation and Autophagy in Parkinson's Disease-Novel Perspectives.International journal of molecular sciences · 2022Review
- Autophagy and beyond: Unraveling the complexity of UNC-51-like kinase 1 (ULK1) from biological functions to therapeutic implications.Acta pharmaceutica Sinica. B · 2022Review
- Review
- Article
- Regulation of neuronal autophagy and the implications in neurodegenerative diseases.Neurobiology of disease · 2022Review
- TNF-induced necroptosis initiates early autophagy events via RIPK3-dependent AMPK activation, but inhibits late autophagy.Autophagy · 2021Article
- BioID reveals an ATG9A interaction with ATG13-ATG101 in the degradation of p62/SQSTM1-ubiquitin clusters.EMBO reports · 2021Article
- FIP200 controls the TBK1 activation threshold at SQSTM1/p62-positive condensates.Scientific reports · 2021Article
- Atlastin 2/3 regulate ER targeting of the ULK1 complex to initiate autophagy.The Journal of cell biology · 2021Article
- Autophagosome biogenesis comes out of the black box.Nature cell biology · 2021Review
- Simultaneous ZnNature communications · 2021Article
- Target of Rapamycin in Control of Autophagy: Puppet Master and Signal Integrator.International journal of molecular sciences · 2020Review
- ULK complex organization in autophagy by a C-shaped FIP200 N-terminal domain dimer.The Journal of cell biology · 2020Article
- Non-Apoptotic Cell Death Signaling Pathways in Melanoma.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macroautophagy/autophagy is an evolutionarily conserved cellular process whose induction is regulated by the ULK1 protein kinase complex. The subunit ATG13 functions as an adaptor protein by recruiting ULK1, RB1CC1 and ATG101 to a core ULK1 complex. Furthermore, ATG13 directly binds both phospholipids and members of the Atg8 family. The central involvement of ATG13 in complex formation makes it an attractive target for autophagy regulation. Here, we analyzed known interactions of ATG13 with proteins and lipids for their potential modulation of ULK1 complex formation and autophagy induction. Targeting the ATG101-ATG13 interaction showed the strongest autophagy-inhibitory effect, whereas the inhibition of binding to ULK1 or RB1CC1 had only minor effects, emphasizing that mutations interfering with ULK1 complex assembly do not necessarily result in a blockade of autophagy. Furthermore, inhibition of ATG13 binding to phospholipids or Atg8 proteins had only mild effects on autophagy. Generally, the observed phenotypes were more severe when autophagy was induced by MTORC1/2 inhibition compared to amino acid starvation. Collectively, these data establish the interaction between ATG13 and ATG101 as a promising target in disease-settings where the inhibition of autophagy is desired.
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.