ArticlePloS one2015
Ligands Binding to Cell Surface Ganglioside GD2 Cause Src-Dependent Activation of N-Methyl-D-Aspartate Receptor Signaling and Changes in Cellular Morphology.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Immunotherapeutic Strategies Targeting GD2-Expressing Malignancies.Advances in experimental medicine and biology · 2026Review
- The Ying and Yang of Ganglioside Function in Cancer.Cancers · 2023Review
- Multidisciplinary Clinical Care in the Management of Patients Receiving Anti-GD2 Immunotherapy for High-Risk Neuroblastoma.Paediatric drugs · 2023Article
- Outpatient administration of naxitamab in combination with granulocyte-macrophage colony-stimulating factor in patients with refractory and/or relapsed high-risk neuroblastoma: Management of adverse events.Cancer reports (Hoboken, N.J.) · 2023Review
- Biology of GD2 ganglioside: implications for cancer immunotherapy.Frontiers in pharmacology · 2023Review
- The cancer glycocode as a family of diagnostic biomarkers, exemplified by tumor-associated gangliosides.Frontiers in oncology · 2023Review
- Review
- Gangliosides and Neuroblastomas.International journal of molecular sciences · 2020Review
- Disialoganglioside GD2 Expression in Solid Tumors and Role as a Target for Cancer Therapy.Frontiers in oncology · 2020Review
- Aiming for the Sweet Spot: Glyco-Immune Checkpoints and γδ T Cells in Targeted Immunotherapy.Frontiers in immunology · 2020Review
- Transmission pathways and mediators as the basis for clinical pharmacology of pain.Expert review of clinical pharmacology · 2016Article
- Combination Therapy with Pregabalin and Morphine Relieves Dinutuximab-Induced Pain in a 3-Year-Old Girl: A Case Report.Palliative medicine reportsArticle
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Ganglioside GD2 is a plasma membrane glycosphinogolipid. In healthy adults it is expressed at low levels, but it is over-expressed in many cancers. For cancer therapy, GD2 is targeted with anti-GD2 monoclonal antibodies (mAbs), and one adverse side effect is severe visceral pain. Pain is not neuropathic, cannot be blocked with morphine, and stops on discontinuation of mAb therapy. Here, we provide evidence that ligand binding to cell surface GD2 induces rapid and transient activation of Src-family kinases, followed by Src-dependent phosphorylation of NMDA-receptor NR2B subunits selectively, activation of Ca++ fluxes, production of cAMP, and changes in cellular morphology. These GD2-ligand activated signals differ in kinetics and in pharmacology from activation of the same signals in the same cells by BDNF, the growth factor agonist of the TrkB receptor, suggesting biological specificity. Hence, cell surface GD2 regulates pathways that can be associated with neoplasia and with morphine-intractable pain; and this can explain why expression of GD2 correlates with these two pathologies.
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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.