ArticleJournal of immunology (Baltimore, Md. : 1950)2011
A balance of Bruton's tyrosine kinase and SHIP activation regulates B cell receptor cluster formation by controlling actin remodeling.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.
- Bruton's Tyrosine Kinase (BTK) Inhibitors and Autoimmune Diseases: Making Sense of BTK Inhibitor Specificity Profiles and Recent Clinical Trial Successes and Failures.Frontiers in immunology · 2021Pooled it
- A single-molecule reporter of membrane-proximal actin detects rapid remodeling upon B cell receptor clustering.bioRxiv : the preprint server for biology · 2026Article
- MDA5 regulates BCR signaling and B-cell function via NF-κB-mediated DNM1.Cellular & molecular immunology · 2026Article
- The cytoskeletal control of B cell receptor and integrin signaling in normal B cells and chronic lymphocytic leukemia.FEBS letters · 2025Review
- HMGB1 couples LEF1 to regulate B cell immunity.JCI insight · 2025Article
- The Evolving Role of Bruton's Tyrosine Kinase Inhibitors in B Cell Lymphomas.International journal of molecular sciences · 2024Review
- SH2 domain-containing inositol 5-phosphatases support the survival of Burkitt lymphoma cells by promoting energy metabolism.Haematologica · 2024Article
- ZAP-70 augments tonic B-cell receptor and CCR7 signaling in IGHV-unmutated chronic lymphocytic leukemia.Blood advances · 2024Article
- Bruton's tyrosine kinase-bearing B cells and microglia in neuromyelitis optica spectrum disorder.Journal of neuroinflammation · 2023Article
- Article
- WAVE2 Regulates Actin-Dependent Processes Induced by the B Cell Antigen Receptor and Integrins.Cells · 2023Article
- Dimensional effect of graphene nanostructures on cytoskeleton-coupled anti-tumor metastasis.Smart medicine · 2023Article
- SHIP1 Controls Internal Platelet Contraction and αInternational journal of molecular sciences · 2023Article
- The inositol 5-phosphatase INPP5B regulates B cell receptor clustering and signaling.The Journal of cell biology · 2022Article
- Bidirectional feedback between BCR signaling and actin cytoskeletal dynamics.The FEBS journal · 2022Review
- Non-Muscle Myosin II Is Essential for the Negative Regulation of B-Cell Receptor Signaling and B-Cell Activation.Frontiers in immunology · 2022Article
- FCRL1 Regulates B Cell Receptor-Induced ERK Activation through GRB2.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- The Wdr1-LIMK-Cofilin Axis Controls B Cell Antigen Receptor-Induced Actin Remodeling and Signaling at the Immune Synapse.Frontiers in cell and developmental biology · 2021Article
- WASp Is Crucial for the Unique Architecture of the Immunological Synapse in Germinal Center B-Cells.Frontiers in cell and developmental biology · 2021Article
- CX3CR1 positively regulates BCR signaling coupled with cell metabolism via negatively controlling actin remodeling.Cellular and molecular life sciences : CMLS · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
The activation of the BCR, which initiates B cell activation, is triggered by Ag-induced self-aggregation and clustering of receptors at the cell surface. Although Ag-induced actin reorganization is known to be involved in BCR clustering in response to membrane-associated Ag, the underlying mechanism that links actin reorganization to BCR activation remains unknown. In this study, we show that both the stimulatory Bruton's tyrosine kinase (Btk) and the inhibitory SHIP-1 are required for efficient BCR self-aggregation. In Btk-deficient B cells, the magnitude of BCR aggregation into clusters and B cell spreading in response to an Ag-tethered lipid bilayer is drastically reduced, compared with BCR aggregation observed in wild-type B cells. In SHIP-1(-/-) B cells, although surface BCRs aggregate into microclusters, the centripetal movement and growth of BCR clusters are inhibited, and B cell spreading is increased. The persistent BCR microclusters in SHIP-1(-/-) B cells exhibit higher levels of signaling than merged BCR clusters. In contrast to the inhibition of actin remodeling in Btk-deficient B cells, actin polymerization, F-actin accumulation, and Wiskott-Aldrich symptom protein phosphorylation are enhanced in SHIP-1(-/-) B cells in a Btk-dependent manner. Thus, a balance between positive and negative signaling regulates the spatiotemporal organization of the BCR at the cell surface by controlling actin remodeling, which potentially regulates the signal transduction of the BCR. This study suggests a novel feedback loop between BCR signaling and the actin cytoskeleton.
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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.