ArticleeLife2016
Golgi self-correction generates bioequivalent glycans to preserve cellular homeostasis.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
48 citing papers in PubMed, 80 citations in OpenAlex.
- Effect of vitamin D supplementation on N-glycan branching and cellular immunophenotypes in MS.Annals of clinical and translational neurology · 2020Trial
- PA14 domain of glycosyltransferase B4GALNT3 is a lectin that binds to sulfated glycan ligands.The Journal of biological chemistry · 2026Article
- Article
- Chemoenzymatic Synthesis of Asymmetric Bisecting Bi-, Tri-, and Tetra-AntennaryJournal of the American Chemical Society · 2025Article
- Exploring the Impact of Mitoquinone Supplementation on Glycan Profiles in a Repeated Mild Traumatic Brain Injury Mouse Model.Neurotrauma reports · 2025Article
- N-Glycan Branching Regulates BTLA Opposite to PD-1 to Limit T Cell Hyperactivity Induced by Branching Deficiency.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Deletion ofFrontiers in cell and developmental biology · 2024Article
- Different glycosylation profiles of cystatin F alter the cytotoxic potential of natural killer cells.Cellular and molecular life sciences : CMLS · 2023Article
- Review
- Glycome dynamics in T and B cell development: basic immunological mechanisms and clinical applications.Trends in immunology · 2023Review
- Role of glycosphingolipid biosynthesis coregulators in malignant progression of thymoma.International journal of biological sciences · 2023Article
- N-glycosylation of cervicovaginal fluid reflects microbial community, immune activity, and pregnancy status.Scientific reports · 2022Article
- T cell senescence by N-glycan branching.Aging · 2022Article
- Shedding of N-acetylglucosaminyltransferase-V is regulated by maturity of cellular N-glycan.Communications biology · 2022Article
- Exploring serum glycome patterns after moderate to severe traumatic brain injury: A prospective pilot study.EClinicalMedicine · 2022Article
- The activation of PPARγ enhances Treg responses through up-regulating CD36/CPT1-mediated fatty acid oxidation and subsequent N-glycan branching of TβRII/IL-2Rα.Cell communication and signaling : CCS · 2022Article
- TMT-Based Multiplexed Quantitation ofACS omega · 2022Article
- Age-associated impairment of T cell immunity is linked to sex-dimorphic elevation of N-glycan branching.Nature aging · 2022Article
- Supply chain logistics - the role of the Golgi complex in extracellular matrix production and maintenance.Journal of cell science · 2022Review
- A general role for TANGO1, encoded by MIA3, in secretory pathway organization and function.Journal of cell science · 2021Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Essential biological systems employ self-correcting mechanisms to maintain cellular homeostasis. Mammalian cell function is dynamically regulated by the interaction of cell surface galectins with branched N-glycans. Here we report that N-glycan branching deficiency triggers the Golgi to generate bioequivalent N-glycans that preserve galectin-glycoprotein interactions and cellular homeostasis. Galectins bind N-acetyllactosamine (LacNAc) units within N-glycans initiated from UDP-GlcNAc by the medial-Golgi branching enzymes as well as the trans-Golgi poly-LacNAc extension enzyme β1,3-N-acetylglucosaminyltransferase (B3GNT). Marginally reducing LacNAc content by limiting N-glycans to three branches results in T-cell hyperactivity and autoimmunity; yet further restricting branching does not produce a more hyperactive state. Rather, new poly-LacNAc extension by B3GNT maintains galectin binding and immune homeostasis. Poly-LacNAc extension is triggered by redistribution of unused UDP-GlcNAc from the medial to trans-Golgi via inter-cisternal tubules. These data demonstrate the functional equivalency of structurally dissimilar N-glycans and suggest a self-correcting feature of the Golgi that sustains cellular homeostasis.
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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.