ArticleThe Journal of experimental medicine1995
The protein product of the c-cbl protooncogene is phosphorylated after B cell receptor stimulation and binds the SH3 domain of Bruton's tyrosine kinase.
Article in The Journal of experimental medicine, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 128 citations in OpenAlex.
- A PKC-SHP1 signaling axis desensitizes Fcγ receptor signaling by reducing the tyrosine phosphorylation of CBL and regulates FcγR mediated phagocytosis.BMC immunology · 2014Article
- Critical roles of the WASP N-terminal domain and Btk in LPS-induced inflammatory response in macrophages.PloS one · 2012Article
- Conformational snapshots of Tec kinases during signaling.Immunological reviews · 2009Article
- Deregulated Syk inhibits differentiation and induces growth factor-independent proliferation of pre-B cells.The Journal of experimental medicine · 2006Article
- A comprehensive map of the toll-like receptor signaling network.Molecular systems biology · 2006Review
- Beyond the RING: CBL proteins as multivalent adapters.Oncogene · 2001Review
- Stability and peptide binding specificity of Btk SH2 domain: molecular basis for X-linked agammaglobulinemia.Protein science : a publication of the Protein Society · 2000Article
- Signaling network of the Btk family kinases.Oncogene · 2000Article
- Bruton's tyrosine kinase links the B cell receptor to nuclear factor kappaB activation.The Journal of experimental medicine · 2000Article
- Solution structure of the human BTK SH3 domain complexed with a proline-rich peptide from p120cbl.Journal of biomolecular NMR · 2000Article
- Cbl suppresses B cell receptor-mediated phospholipase C (PLC)-gamma2 activation by regulating B cell linker protein-PLC-gamma2 binding.The Journal of experimental medicine · 2000Article
- Article
- Tissue hyperplasia and enhanced T-cell signalling via ZAP-70 in c-Cbl-deficient mice.Molecular and cellular biology · 1998Article
- Involvement of Bruton's tyrosine kinase in FcepsilonRI-dependent mast cell degranulation and cytokine production.The Journal of experimental medicine · 1998Article
- Phosphatidylinositol-3,4,5-trisphosphate (PtdIns-3,4,5-P3)/Tec kinase-dependent calcium signaling pathway: a target for SHIP-mediated inhibitory signals.The EMBO journal · 1998Article
- X-linked agammaglobulinemia: lack of mature B lineage cells caused by mutations in the Btk kinase.Springer seminars in immunopathology · 1998Review
- BTKbase, mutation database for X-linked agammaglobulinemia (XLA).Nucleic acids research · 1998Article
- Phosphorylation of two regulatory tyrosine residues in the activation of Bruton's tyrosine kinase via alternative receptors.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Phosphotyrosine binding domain-dependent upregulation of the platelet-derived growth factor receptor alpha signaling cascade by transforming mutants of Cbl: implications for Cbl's function and oncogenicity.Molecular and cellular biology · 1997Article
- Characterization of Cbl tyrosine phosphorylation and a Cbl-Syk complex in RBL-2H3 cells.The Journal of experimental medicine · 1996Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
X-linked agammaglobulinemia, a B cell immunodeficiency, is caused by mutations in the Bruton's tyrosine kinase (Btk) gene. The absence of a functional Btk protein leads to a failure of B cell differentiation and antibody production. B cell receptor stimulation leads to the phosphorylation of the Btk protein and it is, therefore, likely that Btk is involved in B cell receptor signaling. As a nonreceptor tyrosine kinase, Btk is likely to interact with several proteins within the context of a signal transduction pathway. To understand such interactions, we have generated glutathione S-transferase fusion proteins corresponding to different domains of the human Btk protein. We have identified a 120-kD protein present in human B cells as being bound by the SH3 domain of Btk and which, after B cell receptor stimulation, is one of the major substrates of tyrosine phosphorylation. We have shown that this 120-kD protein is the protein product of c-cbl, a protooncogene, which is known to be phosphorylated in response to T cell receptor stimulation and to interact with several other tyrosine kinases. Association of the SH3 domain of Btk with p120cbl provides evidence for an analogous role for p120cbl in B cell signaling pathways. The p120cbl protein is the first identified ligand of the Btk SH3 domain.
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