ArticleNature cell biology2025
Growth factor-triggered de-sialylation controls glycolipid-lectin-driven endocytosis.
Article in Nature cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 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
18 citing papers in PubMed.
- Galectin-3 Mediates TGF-β-Controlled Migration in Müller Glial Cells.International journal of molecular sciences · 2026Article
- Synergistic Regulation of Tumor Immunity by Integrins and Lectins: From Molecular Mechanisms to Dual-Targeted Therapy.International journal of molecular sciences · 2026Review
- Functional Specialization of Clathrin-Independent Endocytic Routes: Mechanisms and Cellular Roles.Traffic (Copenhagen, Denmark) · 2026Review
- Cis glycan-glycan interactions organize membrane nanodomains that tune receptor signaling.Nature communications · 2026Article
- From Glycocode to Precision Oncology: Therapeutic Strategies Targeting Aberrant O-GalNAc Glycosylation in Cancer.Chemical reviews · 2026Review
- Caveolae mechanics in cellular functions and disease.Nature reviews. Molecular cell biology · 2026Review
- Expression, Localization and Actions of Galectin-3: Implications in the Pathophysiology and Therapy of Cardiovascular Disease.International journal of molecular sciences · 2026Review
- The ligand preference of LRP1 is regulated by O-glycans.Science advances · 2026Article
- Sialylation in the nervous system: Functions and mechanisms.The Journal of biological chemistry · 2026Review
- From molecular mechanisms of glycosphingolipid function to bio-therapeutic applications.Cellular and molecular life sciences : CMLS · 2026Review
- pH sensing and inflammation: linking acidic microenvironments to immune reprogramming.Frontiers in immunology · 2026Review
- Article
- Ensemble Machine Learning Approaches Predict Survival in Lower-Grade Glioma Based on Glycosphingolipid Gene Expression and Metabolic Modeling.Computational and structural biotechnology journal · 2026Article
- Macropinocytosis fuels osteoclast differentiation in bone-related diseases.Journal of orthopaedic translation · 2025Article
- Spatial N-glycan rearrangement on αNature communications · 2025Article
- Article
- Proteostasis of immune checkpoint receptors.The Biochemical journal · 2025Review
- Galectin-3: Integrator of Signaling via Hexosamine Flux.Biomolecules · 2025Review
Corrections and comments
- Erratum issued
Authors and funding
27 authors.
Funding
Abstract
Glycolipid-lectin-driven endocytosis controls the formation of clathrin-independent carriers and the internalization of various cargos such as β1 integrin. Whether this process is regulated in a dynamic manner remained unexplored. Here we demonstrate that, within minutes, the epidermal growth factor triggers the galectin-driven endocytosis of cell-surface glycoproteins, such as integrins, that are key regulators of cell adhesion and migration. The onset of this process-mediated by the Na
Indexed as
Identifiers
39984654What Socratic 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 Socratic graph.