ArticleCell host & microbe2012
The autophagy regulator Rubicon is a feedback inhibitor of CARD9-mediated host innate immunity.
Article in Cell host & microbe, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
What it found
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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.
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Who cites it
71 citing papers in PubMed, 106 citations in OpenAlex.
- Platelet Rubicon Bidirectional Regulation of GPVI and Integrin αIIbβ3 Signaling Mitigates Stroke Infarction Without Compromising Hemostasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- PMA1-containing extracellular vesicles ofGut microbes · 2025Article
- ENKD1 attenuates antibacterial immunity by facilitating TRIM21-mediated RUBCN degradation to suppress LC3-associated phagocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Circulating autophagy regulator Rubicon is linked to increased myocardial infarction risk.Journal of molecular and cellular cardiology plus · 2025Article
- MYC is in the CARDs: CBM complexes coordinate immune and MYC-dependent cellular function.Frontiers in molecular medicine · 2025Article
- Highly Efficient Methods with a Generalized Linear Mixed Model for the Quantitative Trait Locus Mapping of Resistance to Columnaris Disease in Rainbow Trout (International journal of molecular sciences · 2024Article
- Innate immune signal transduction pathways to fungal infection: Components and regulation.Cell insight · 2024Review
- MALT-1 shortens lifespan by inhibiting autophagy in the intestine ofAutophagy reports · 2023Article
- Reduction in Rubicon by cigarette smoke is associated with impaired phagocytosis and occurs through lysosomal degradation pathway.Clinical and experimental medicine · 2023Article
- Genetic inhibition of CARD9 accelerates the development of atherosclerosis in mice through CD36 dependent-defective autophagy.Nature communications · 2023Article
- Article
- A ZFYVE21-Rubicon-RNF34 signaling complex promotes endosome-associated inflammasome activity in endothelial cells.Nature communications · 2023Article
- Meloxicam inhibits STING phosphorylation and alleviates intracellular DNA-mediated autoimmune responses.Cell & bioscience · 2023Article
- The role of autophagy in viral infections.Journal of biomedical science · 2023Review
- You are what you eat and how you digest it! A discussion on inflammatory efferocytosis.Frontiers in cell and developmental biology · 2023Review
- Plasma levels of autophagy regulator Rubicon are inversely associated with acute coronary syndrome.Frontiers in cardiovascular medicine · 2023Article
- LC3-associated endocytosis and the functions of Rubicon and ATG16L1.Science advances · 2022Review
- Beyond autophagy: LC3-associated phagocytosis and endocytosis.Science advances · 2022Review
- DJ-1 binds to Rubicon to Impair LC-3 Associated Phagocytosis.Cell death and differentiation · 2022Article
- The molecular regulation of autophagy in antimicrobial immunity.Journal of molecular cell biology · 2022Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Assembly of a scaffold consisting of CARD9, BCL10, and MALT1 (CBM complex) is critical for effective signaling by multiple pattern recognition receptors (PRRs) including Dectin and RIG-I. The RUN domain Beclin-1-interacting cysteine-rich-containing Rubicon protein associates constitutively with the Beclin-UVRAG-Vps34 complex under normal conditions to regulate autophagy. Rubicon also interacts with the phagocytic NADPH-oxidase complex upon TLR stimulation to induce potent antimicrobial responses. Here, we show Rubicon is a physiological feedback inhibitor of CBM-mediated PRR signaling, preventing unbalanced proinflammatory responses. Upon Dectin-1- or RIG-I-mediated activation, Rubicon dynamically exchanges binding partners from 14-3-3β to CARD9 in a stimulation-specific and phosphorylation-dependent manner, disassembling the CBM signaling complex and ultimately terminating PRR-induced cytokine production. Remarkably, Rubicon's actions in the autophagy complex, phagocytosis complex, and CBM complex are functionally and genetically separable. Rubicon thus differentially targets signaling complexes, depending on environmental stimuli, and may function to coordinate various immune responses against microbial infection.
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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.