ArticleScience signaling2018
The interaction between IKKα and LC3 promotes type I interferon production through the TLR9-containing LAPosome.
Article in Science signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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51 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
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- NFκB signalling in colorectal cancer: Examining the central dogma of IKKα and IKKβ signalling.Heliyon · 2024Review
- Integrin αvβ3 Limits Cytokine Production by Plasmacytoid Dendritic Cells and Restricts TLR-Driven Autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
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- A possible role for proinflammatory activation via cGAS-STING pathway in atherosclerosis induced by accumulation of DNA double-strand breaks.Scientific reports · 2023Article
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- The role of mtDAMPs in the trauma-induced systemic inflammatory response syndrome.Frontiers in immunology · 2023Review
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- LC3-Associated Phagocytosis in Bacterial Infection.Pathogens (Basel, Switzerland) · 2022Review
- APOBEC3A regulates transcription from interferon-stimulated response elements.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
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3 authors at 2 institutions in 1 country.
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Abstract
Toll-like receptor 9 (TLR9) recognizes DNA in endosomes and activates distinct signaling pathways to stimulate the production of proinflammatory cytokines and type I interferons (IFNs). The assembly of signaling platforms on microtubule-associated proteins 1A/1B-light chain 3 (LC3)-decorated endosomal vesicles is required to transduce TLR9 signals that stimulate the production of IFN but not interleukin-12 p40 (IL-12p40). LC3-associated phagocytosis (LAP), a form of noncanonical autophagy, is critical for the activation of interferon regulatory factor 7 (IRF7) and for IFN synthesis. We showed that after the stimulation of TLR9 by CpG oligonucleotides, the autophagy protein LC3 and the kinase IKKα were recruited to endosomes that contained TLR9. The recruitment of IKKα and LC3 to such signaling endosomes was not stimulated by catalysts of classical autophagosome formation but involved LAP formation, which required ATG5 but not FIP200. In addition, we found that the LC3-IKKα complex further associated with both TRAF3 and IRF7. We identified three putative LC3-interacting regions (LIRs) in IKKα, and mutagenesis suggested that two of these were critical for direct binding to LC3. Moreover, mutation of the same LIR sequences failed to rescue type I IFN production in IKKα-deficient dendritic cells upon reconstitution. Together, these data suggest a direct link between LAP formation and IKKα recruitment downstream of TLR9 activation that is necessary to facilitate type I IFN production.
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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 OpenQuestion graph.