ArticleProceedings of the National Academy of Sciences of the United States of America2000
The B cell-restricted adaptor BASH is required for normal development and antigen receptor-mediated activation of B cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 135 citations in OpenAlex.
- BLNK negatively regulates innate antifungal immunity through inhibiting c-Cbl-mediated macrophage migration.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- C/EBPβ induces B-cell acute lymphoblastic leukemia and cooperates with BLNK mutations.Cancer science · 2021Article
- Germline deletion of CIN85 in humans with X chromosome-linked antibody deficiency.The Journal of experimental medicine · 2018Article
- PI3K induces B-cell development and regulates B cell identity.Scientific reports · 2018Article
- Principles for the regulation of multiple developmental pathways by a versatile transcriptional factor, BLIMP1.Nucleic acids research · 2017Article
- Novel Innate Immune Genes Regulating the Macrophage Response to Gram Positive Bacteria.Genetics · 2016Article
- Autonomous membrane IgE signaling prevents IgE-memory formation.Nature immunology · 2016Article
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- The B-cell antigen receptor signals through a preformed transducer module of SLP65 and CIN85.The EMBO journal · 2011Article
- The adaptor protein Shc plays a key role during early B cell development.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Pre-B cell receptor-mediated cell cycle arrest in Philadelphia chromosome-positive acute lymphoblastic leukemia requires IKAROS function.The Journal of experimental medicine · 2009Article
- SLP-65 phosphorylation dynamics reveals a functional basis for signal integration by receptor-proximal adaptor proteins.Molecular & cellular proteomics : MCP · 2009Article
- Receptor crosstalk: reprogramming B cell receptor signalling to an alternate pathway results in expression and secretion of the autoimmunity-associated cytokine, osteopontin.Journal of internal medicine · 2009Review
- BLNK binds active H-Ras to promote B cell receptor-mediated capping and ERK activation.The Journal of biological chemistry · 2009Article
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- The SRC family kinase LYN redirects B cell receptor signaling in human SLP65-deficient B cell lymphoma cells.Oncogene · 2006Article
- Dual role of the adaptor protein SLP-65: organizer of signal transduction and tumor suppressor of pre-B cell leukemia.Immunologic research · 2006Review
- Deficiency of BLNK hampers PLC-gamma2 phosphorylation and Ca2+ influx induced by the pre-B-cell receptor in human pre-B cells.Immunology · 2004Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
B cell antigen receptor signals development, activation, proliferation, or apoptosis of B cells depending on their condition, and its proper signaling is critical for activation and homeostasis of the immune system. The B cell-restricted adaptor protein BASH (also termed BLNK/SLP-65) is rapidly phosphorylated by the tyrosine kinase Syk after BCR ligation and binds to various signaling proteins. BASH structurally resembles SLP-76, which is essential for T cell development and T cell receptor signaling. To evaluate the role for BASH in B cell development and function in vivo, we disrupted BASH alleles in embryonic stem cells by means of homologous recombination and used these cells to complement lymphocyte-incompetent blastocysts from RAG2-deficient mice. In the resultant chimeric mice, T cell development was apparently normal, but B cell development was impaired, and a normally rare population of large preB cells expressing preB cell receptor dominated in the bone marrow in place of small preB cells, although they were mostly noncycling. In addition, the mature B cell populations in the periphery and the bone marrow profoundly decreased in size, as did B-1 cells in the peritoneal cavity, and serum Ig was severely reduced. The BASH-deficient B cells scarcely proliferated or up-regulated B7-2 in response to BCR ligation and poorly proliferated upon CD40 ligation or lipopolysaccharide stimulation. This phenotype indicates that BASH is critical for preB cell receptor signaling inducing proliferation of large preB cells and the following differentiation, for peripheral B cell maturation, and for BCR signaling inducing activation/proliferation of B cells.
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