ArticleBlood2012
Galectin-3 binds to CD45 on diffuse large B-cell lymphoma cells to regulate susceptibility to cell death.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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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
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 96 citations in OpenAlex.
- A systematic investigation of clear cell renal cell carcinoma using meta-analysis and systems biology approaches.Molecular genetics and genomics : MGG · 2024Pooled it
- The protein tyrosine phosphatase CD45 promotes PMN transepithelial migration, antimicrobial function, and colonic mucosal repair.JCI insight · 2026Article
- CD45 as a multifunctional target in immune regulation and therapeutic delivery.Journal of translational medicine · 2026Review
- Glycobiology-driven therapeutic targeting of glycan-binding proteins: mechanisms, diseases, and clinical translation.Signal transduction and targeted therapy · 2026Review
- CD28 is Not Required for T cell Activation.Journal of cellular signaling · 2026Article
- The Role of Galectin-3 in Liver Inflammation and Fibrosis.Journal of inflammation research · 2026Review
- HLA-A drives diabetic retinopathy pathogenesis: multi-omics integration reveals resveratrol's therapeutic potential via immunomodulation.Journal of translational medicine · 2025Article
- Review
- Galectin-3 Release in the Bone Marrow Microenvironment Promotes Drug Resistance and Relapse in Acute Myeloid Leukemia.Life (Basel, Switzerland) · 2025Review
- Tumor-secreted galectin-3 suppresses antitumor response by inducing IL-10Journal for immunotherapy of cancer · 2025Article
- Implications of Mucin-TypeMolecules (Basel, Switzerland) · 2025Review
- Galectins-1, -3 and -9 in leukemia: mechanistic insights and therapeutic translation.Frontiers in immunology · 2025Review
- Glycosylation: mechanisms, biological functions and clinical implications.Signal transduction and targeted therapy · 2024Review
- Membrane organization by tetraspanins and galectins shapes lymphocyte function.Nature reviews. Immunology · 2024Review
- Transcriptome Analysis of Diffuse Large B-Cell Lymphoma Cells Inducibly Expressing MyD88 L265P Mutation Identifies Upregulated CD44, LGALS3, NFKBIZ, and BATF as Downstream Targets of Oncogenic NF-κB Signaling.International journal of molecular sciences · 2023Article
- Decoding Strategies to Evade Immunoregulators Galectin-1, -3, and -9 and Their Ligands as Novel Therapeutics in Cancer Immunotherapy.International journal of molecular sciences · 2022Review
- T-helper cell regulation of CD45 phosphatase activity by galectin-1 and CD43 governs chronic lymphocytic leukaemia proliferation.British journal of haematology · 2022Article
- Galectin Family Members: Emerging Novel Targets for Lymphoma Therapy?Frontiers in oncology · 2022Review
- Analysis of Galectin-Binding Receptors on B Cells.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Diffuse large B-cell lymphoma (DLBCL) is the most common non-Hodgkin lymphoma and an aggressive malignancy. Galectin-3 (gal-3), the only antiapoptotic member of the galectin family, is overexpressed in DLBCL. While gal-3 can localize to intracellular sites, gal-3 is secreted by DLBCL cells and binds back to the cell surface in a carbohydrate-dependent manner. The major counterreceptor for gal-3 on DLBCL cells was identified as the transmembrane tyrosine phosphatase CD45. Removal of cell-surface gal-3 from CD45 with the polyvalent glycan inhibitor GCS-100 rendered DLBCL cells susceptible to chemotherapeutic agents. Binding of gal-3 to CD45 modulated tyrosine phosphatase activity; removal of endogenous cell-surface gal-3 from CD45 with GCS-100 increased phosphatase activity, while addition of exogenous gal-3 reduced phosphatase activity. Moreover, the increased susceptibility of DLBCL cells to chemotherapeutic agents after removal of gal-3 by GCS-100 required CD45 phosphatase activity. Gal-3 binding to a subset of highly glycosylated CD45 glycoforms was regulated by the C2GnT-1 glycosyltransferase, indicating that specific glycosylation of CD45 is important for regulation of gal-3-mediated signaling. These data identify a novel role for cell-surface gal-3 and CD45 in DLBCL survival and suggest novel therapeutic targets to sensitize DLBCL cells to death.
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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.