ArticlemBio2017
Galectin-3 Inhibits Galectin-8/Parkin-Mediated Ubiquitination of Group A Streptococcus.
Article in mBio, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 45 citations in OpenAlex.
- The role of E3 ubiquitin ligases in selective types of macroautophagy.EMBO reports · 2026Review
- A Narrative Review on the Multifaceted Roles of Galectins in Host-Pathogen Interactions DuringInternational journal of molecular sciences · 2025Review
- Capsule-deficient group AmBio · 2024Article
- Group AInfection and immunity · 2024Article
- Interplay between group AMicrobiology and molecular biology reviews : MMBR · 2024Review
- Galectins in Equine Placental Disease.Veterinary sciences · 2023Article
- Manipulating autophagic degradation in human diseases: from mechanisms to interventions.Life medicine · 2022Review
- Activated leukocyte cell adhesion molecule/cluster of differentiation 166 rs10933819 (G>A) variant is associated with familial intracranial aneurysms.Biomedical reports · 2022Article
- A patatin-like phospholipase mediates Rickettsia parkeri escape from host membranes.Nature communications · 2022Article
- Article
- Galectin-3: a new biomarker for differentiating periodic fever, adenitis, pharyngitis, aphthous stomatitis (PFAPA) syndrome from familial Mediterranean fever?Rheumatology international · 2022Observational
- The ubiquitin ligation machinery in the defense against bacterial pathogens.EMBO reports · 2021Review
- Glycans in autophagy, endocytosis and lysosomal functions.Glycoconjugate journal · 2021Review
- Intracellular galectins sense cytosolically exposed glycans as danger and mediate cellular responses.Journal of biomedical science · 2021Review
- Review
- Galectins in the Pathogenesis of Common Retinal Disease.Frontiers in pharmacology · 2021Review
- Article
- A MicroRNA Network ControlsmBio · 2020Article
- AMPK, a Regulator of Metabolism and Autophagy, Is Activated by Lysosomal Damage via a Novel Galectin-Directed Ubiquitin Signal Transduction System.Molecular cell · 2020Article
- TBC1D9 regulates TBK1 activation through CaNature communications · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Group A streptococcus (GAS) is an important human pathogen that causes a wide variety of cutaneous and systemic infections. Although originally thought to be an extracellular bacterium, numerous studies have demonstrated that GAS can trigger internalization into nonimmune cells to escape from immune surveillance or antibiotic-mediated killing. Epithelial cells possess a defense mechanism involving autophagy-mediated targeting and killing of GAS within lysosome-fused autophagosomes. In endothelial cells, in contrast, we previously showed that autophagy is not sufficient for GAS killing. In the present study, we showed higher galectin-3 (Gal-3) expression and lower Gal-8 expression in endothelial cells than in epithelial cells. The recruitment of Gal-3 to GAS is higher and the recruitment of Gal-8 to GAS is lower in endothelial cells than in epithelial cells. We further showed that Gal-3 promotes GAS replication and diminishes the recruitment of Gal-8 and ubiquitin, the latter of which is a critical protein for autophagy sequestration. After knockdown of Gal-3 in endothelial cells, the colocalization of Gal-8, parkin, and ubiquitin-decorated GAS is significantly increased, as is the interaction of Gal-8 and parkin, an E3 ligase. Furthermore, inhibition of Gal-8 in epithelial cells attenuates recruitment of parkin; both Gal-8 and parkin contribute to ubiquitin recruitment and GAS elimination. Animal studies confirmed that Gal-3-knockout mice develop less-severe skin damage and that GAS replication can be detected only in the air pouch and not in organs and endothelial cells. These results demonstrate that Gal-3 inhibits ubiquitin recruitment by blocking Gal-8 and parkin recruitment, resulting in GAS replication in endothelial cells.
Indexed as
Identifiers
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.