ArticlePLoS pathogens2022
TBK1 is part of a galectin 8 dependent membrane damage recognition complex and drives autophagy upon Adenovirus endosomal escape.
Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Review
- Autophagy machinery as exploited by viruses.Autophagy reports · 2025Article
- GSK3A promotes human adenovirus replication and phosphorylates viral L4-22K protein.Life science alliance · 2025Article
- Chemically engineered antibodies for autophagy-based receptor degradation.Nature chemical biology · 2025Article
- Linear ubiquitination at damaged lysosomes induces local NFKB activation and controls cell survival.Autophagy · 2025Article
- Activation of lysophagy by a TBK1-SCFNature communications · 2025Article
- Calcium signaling from damaged lysosomes induces cytoprotective stress granules.The EMBO journal · 2024Article
- In Silico Insights: QSAR Modeling of TBK1 Kinase Inhibitors for Enhanced Drug Discovery.Journal of chemical information and modeling · 2024Article
- Lysosomal TBK1 responds to amino acid availability to relieve Rab7-dependent mTORC1 inhibition.The EMBO journal · 2024Article
- Galectin-8 modulates human osteoclast activity partly through isoform-specific interactions.Life science alliance · 2024Article
- A mechanism that transduces lysosomal damage signals to stress granule formation for cell survival.bioRxiv : the preprint server for biology · 2024Article
- Lysophagy protects against propagation of α-synuclein aggregation through ruptured lysosomal vesicles.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Identification of TBK1 inhibitors against breast cancer using a computational approach supported by machine learning.Frontiers in pharmacology · 2024Article
- Lysosomal TBK1 Responds to Amino Acid Availability to Relieve Rab7-Dependent mTORC1 Inhibition.bioRxiv : the preprint server for biology · 2023Article
- Autophagy induced by human adenovirus B7 structural protein VI inhibits viral replication.Virologica Sinica · 2023Article
- Galectins and galectin-mediated autophagy regulation: new insights into targeted cancer therapy.Biomarker research · 2023Review
- TheAutophagy reports · 2022Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intracellular pathogens cause membrane distortion and damage as they enter host cells. Cells perceive these membrane alterations as danger signals and respond by activating autophagy. This response has primarily been studied during bacterial invasion, and only rarely in viral infections. Here, we investigate the cellular response to membrane damage during adenoviral entry. Adenoviruses and their vector derivatives, that are an important vaccine platform against SARS-CoV-2, enter the host cell by endocytosis followed by lysis of the endosomal membrane. We previously showed that cells mount a locally confined autophagy response at the site of endosomal membrane lysis. Here we describe the mechanism of autophagy induction: endosomal membrane damage activates the kinase TBK1 that accumulates in its phosphorylated form at the penetration site. Activation and recruitment of TBK1 require detection of membrane damage by galectin 8 but occur independently of classical autophagy receptors or functional autophagy. Instead, TBK1 itself promotes subsequent autophagy that adenoviruses need to take control of. Deletion of TBK1 reduces LC3 lipidation during adenovirus infection and restores the infectivity of an adenovirus mutant that is restricted by autophagy. By comparing adenovirus-induced membrane damage to sterile lysosomal damage, we implicate TBK1 in the response to a broader range of types of membrane damage. Our study thus highlights an important role for TBK1 in the cellular response to adenoviral endosome penetration and places TBK1 early in the pathway leading to autophagy in response to membrane damage.
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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 Socratic graph.