ArticleThe EMBO journal2023
The disulfide catalyst QSOX1 maintains the colon mucosal barrier by regulating Golgi glycosyltransferases.
Article in The EMBO journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 33 citations in OpenAlex.
- LC-MS/MS Profiling of Blood Serum Reveals Disease-Enriched Peptides in Metabolic Syndrome.Journal of personalized medicine · 2026Article
- The RNA-binding protein Imp1 promotes a Spdef transcriptional program and mucus fucosylation during necrotizing enterocolitis.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- Electric Field-Induced Release and Measurement Liquid Biopsy of Urinary Transcriptomics and Key Proteins from Normal and High-risk Pregnant Women.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- Zinc-redox crosstalk regulates proteostasis in the endoplasmic reticulum.Nature communications · 2026Article
- Regulating the dormancy of cancer stem cells: a novel approach to preventing cancer relapse.Cell death & disease · 2026Review
- Limosilactobacillus reuteri metabolites modulate immune pathways and intestinal barrier repair after 5 fluorouracil exposure.Scientific reports · 2026Article
- The RNA-binding protein Imp1 promotes a Spdef transcriptional program and mucus fucosylation during necrotizing enterocolitis.bioRxiv : the preprint server for biology · 2026Article
- QSOX1: A Mysterious Golgi-Localized Disulfide Bond Catalyst and an Emerging Cancer Regulator.Cancers · 2026Article
- Molecular Modeling and Gene Ontology Implicate SLC35F4 and SLC35F5 as Golgi-Associated Importers of Flavin-Adenine-Dinucleotide.International journal of molecular sciences · 2026Article
- Hypoxia-Induced TGFBI Promotes Bladder Cancer Progression by Creating a Stemness Regulation Loop through Stabilizing the Disulfide Bonds of GDF15.Research (Washington, D.C.) · 2026Article
- Crosstalk between the circadian clock, intestinal stem cell niche, and epithelial cell fate decision.Genes & diseases · 2025Review
- QSOX2-Mediated Disulfide Bond Modification Enhances Tumor Stemness and Chemoresistance by Activating TSC2/mTOR/c-Myc Feedback Loop in Esophageal Squamous Cell Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Identification of common diagnostic genes and molecular pathways in endometriosis and systemic lupus erythematosus by machine learning approach and in vitro experiment.International journal of medical sciences · 2025Article
- Emerging cell and molecular targets for treating mucus hypersecretion in asthma.Allergology international : official journal of the Japanese Society of Allergology · 2024Review
- The gut commensal Blautia maintains colonic mucus function under low-fiber consumption through secretion of short-chain fatty acids.Nature communications · 2024Article
- Site-specific immobilization of the endosialidase reveals QSOX2 is a novel polysialylated protein.Glycobiology · 2024Article
- Crosstalk between hypoxia-inducible factor-1α and short-chain fatty acids in inflammatory bowel disease: key clues toward unraveling the mystery.Frontiers in immunology · 2024Review
- Barrett's Esophagus Epithelial Stem Cells Have Distinct Gene Signatures.Gastro hep advances · 2024Review
- Intestinal mucus and their glycans: A habitat for thriving microbiota.Cell host & microbe · 2023Review
- Trans-Golgi protein TVP23B regulates host-microbe interactions via Paneth cell homeostasis and Goblet cell glycosylation.Nature communications · 2023Article
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Authors and funding
14 authors at 2 institutions in 2 countries.
Funding
Abstract
Mucus is made of enormous mucin glycoproteins that polymerize by disulfide crosslinking in the Golgi apparatus. QSOX1 is a catalyst of disulfide bond formation localized to the Golgi. Both QSOX1 and mucins are highly expressed in goblet cells of mucosal tissues, leading to the hypothesis that QSOX1 catalyzes disulfide-mediated mucin polymerization. We found that knockout mice lacking QSOX1 had impaired mucus barrier function due to production of defective mucus. However, an investigation on the molecular level revealed normal disulfide-mediated polymerization of mucins and related glycoproteins. Instead, we detected a drastic decrease in sialic acid in the gut mucus glycome of the QSOX1 knockout mice, leading to the discovery that QSOX1 forms regulatory disulfides in Golgi glycosyltransferases. Sialylation defects in the colon are known to cause colitis in humans. Here we show that QSOX1 redox control of sialylation is essential for maintaining mucosal function.
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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.