ArticleImmunity2016
ARC Syndrome-Linked Vps33B Protein Is Required for Inflammatory Endosomal Maturation and Signal Termination.
Article in Immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- VPS33B regulates MHC class II antigen presentation in dendritic cells to drive CD4 T cell immunity.iScience · 2026Article
- Evaluation of the Antifungal Activity of the Polyphenol FormulationAntibiotics (Basel, Switzerland) · 2026Article
- Article
- Staphylococcus aureus induces mitophagy via the HDAC11/IL10 pathway to sustain intracellular survival.Journal of translational medicine · 2025Article
- E3 Ubiquitin Ligase RNF13 Suppresses TLR Lysosomal Degradation by Promoting LAMP-1 Proteasomal Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Two novel mutations in theWorld journal of clinical cases · 2022Article
- Compromised mitochondrial quality control triggers lipin1-related rhabdomyolysis.Cell reports. Medicine · 2021Article
- TLR4 and CD14 trafficking and its influence on LPS-induced pro-inflammatory signaling.Cellular and molecular life sciences : CMLS · 2021Review
- TLR signaling adapter BCAP regulates inflammatory to reparatory macrophage transition by promoting histone lactylation.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Hypersensitivity of Vps33B mutant flies to non-pathogenic infections is dictated by aberrant activation of p38b MAP kinase.Traffic (Copenhagen, Denmark) · 2020Article
- Mutual editing of alternative splicing between breast cancer cells and macrophages.Oncology reports · 2019Article
- The road to lysosome-related organelles: Insights from Hermansky-Pudlak syndrome and other rare diseases.Traffic (Copenhagen, Denmark) · 2019Review
- Metabolomics and Lipidomics Reveal the Effect of HepaticFrontiers in pharmacology · 2019Article
- Proteomic and Biochemical Comparison of the Cellular Interaction Partners of Human VPS33A and VPS33B.Journal of molecular biology · 2018Article
- VPS33B and VIPAR are essential for epidermal lamellar body biogenesis and function.Biochimica et biophysica acta. Molecular basis of disease · 2018Article
- Human Adenoviruses, Cholesterol Trafficking, and NF-κB Signaling.Journal of immunological sciences · 2018Article
- The Vici syndrome protein EPG5 regulates intracellular nucleic acid trafficking linking autophagy to innate and adaptive immunity.Autophagy · 2018Article
- Article
- Isolation and Infection ofBio-protocol · 2017Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Toll-like receptors (TLRs) and other pattern-recognition receptors (PRRs) sense microbial ligands and initiate signaling to induce inflammatory responses. Although the quality of inflammatory responses is influenced by internalization of TLRs, the role of endosomal maturation in clearing receptors and terminating inflammatory responses is not well understood. Here, we report that Drosophila and mammalian Vps33B proteins play critical roles in the maturation of phagosomes and endosomes following microbial recognition. Vps33B was necessary for clearance of endosomes containing internalized PRRs, failure of which resulted in enhanced signaling and expression of inflammatory mediators. Lack of Vps33B had no effect on trafficking of endosomes containing non-microbial cargo. These findings indicate that Vps33B function is critical for determining the fate of signaling endosomes formed following PRR activation. Exaggerated inflammatory responses dictated by persistence of receptors in aberrant endosomal compartments could therefore contribute to symptoms of ARC syndrome, a disease linked to loss of Vps33B.
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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.