ArticleNature communications2014
The immunoglobulin tail tyrosine motif upgrades memory-type BCRs by incorporating a Grb2-Btk signalling module.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 74 citations in OpenAlex.
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- Dynamic Activation of NADPH Oxidases in Immune Responses Modulates Differentiation, Function, and Lifespan of Plasma Cells.European journal of immunology · 2025Article
- Ion channel TRPV2 is critical in enhancing B cell activation and function.The Journal of experimental medicine · 2024Article
- Targeting the NF-κB pathway as a potential regulator of immune checkpoints in cancer immunotherapy.Cellular and molecular life sciences : CMLS · 2024Review
- N-linked Fc glycosylation is not required for IgG-B-cell receptor function in a GC-derived B-cell line.Nature communications · 2024Article
- B-Cell Receptor Signaling and Beyond: The Role of Igα (CD79a)/Igβ (CD79b) in Normal and Malignant B Cells.International journal of molecular sciences · 2023Review
- Proteome analysis of CD5-positive diffuse large B cell lymphoma FFPE tissue reveals downregulation of DDX3X, DNAJB1, and B cell receptor signaling pathway proteins including BTK and Immunoglobulins.Clinical proteomics · 2023Article
- An Optimized Flow Cytometric Method to Demonstrate the Differentiation Stage-Dependent CaInternational journal of molecular sciences · 2023Article
- Stimulation of the catalytic activity of the tyrosine kinase Btk by the adaptor protein Grb2.eLife · 2023Article
- Aberrant B-Cell Activation in Systemic Lupus Erythematosus.Kidney diseases (Basel, Switzerland) · 2022Review
- IgE-expressing long-lived plasma cells in persistent sensitization.Frontiers in pediatrics · 2022Review
- The Small GTPase RHOA Links SLP65 Activation to PTEN Function in Pre B Cells and Is Essential for the Generation and Survival of Normal and Malignant B Cells.Frontiers in immunology · 2022Article
- Bruton's Tyrosine Kinase Inhibition as an Emerging Therapy in Systemic Autoimmune Disease.Drugs · 2021Review
- Critical requirement for BCR, BAFF, and BAFFR in memory B cell survival.The Journal of experimental medicine · 2021Article
- Article
- The regulators of BCR signaling during B cell activation.Blood science (Baltimore, Md.) · 2019Review
- B cell signaling in context.Nature immunology · 2019Review
- Differential organization of tonic and chronic B cell antigen receptors in the plasma membrane.Nature communications · 2019Article
- Epstein-Barr virus microRNAs regulate B cell receptor signal transduction and lytic reactivation.PLoS pathogens · 2019Article
- Molecular regulation of peripheral B cells and their progeny in immunity.Genes & development · 2019Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The vigorous response of IgG-switched memory B cells to recurring pathogens involves enhanced signalling from their B-cell antigen receptors (BCRs). However, the molecular signal amplification mechanisms of memory-type BCRs remained unclear. Here, we identify the immunoglobulin tail tyrosine (ITT) motif in the cytoplasmic segments of membrane-bound IgGs (mIgGs) as the principle signal amplification device of memory-type BCRs in higher vertebrates and decipher its signalling microanatomy. We show that different families of protein tyrosine kinases act upstream and downstream of the ITT. Spleen tyrosine kinase (Syk) activity is required for ITT phosphorylation followed by recruitment of the adaptor protein Grb2 into the mIgG-BCR signalosome. Grb2 in turn recruits Bruton's tyrosine kinase (Btk) to amplify BCR-induced Ca(2+) mobilization. This molecular interplay of kinases and adaptors increases the antigen sensitivity of memory-type BCRs, which provides a cell-intrinsic trigger mechanism for the rapid reactivation of IgG-switched memory B cells on antigen recall.
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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.