ArticleThe EMBO journal2008
The kinase Syk as an adaptor controlling sustained calcium signalling and B-cell development.
Article in The EMBO journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 83 citations in OpenAlex.
- Repurposing Tyrosine Kinase Inhibitors for Sickle Cell Disease: Focus on Band 3 Phosphorylation.Biomedicines · 2026Review
- New insights into SYK targeting in solid tumors.Trends in pharmacological sciences · 2024Review
- Discovering immunoreceptor coupling and organization motifs.Frontiers in immunology · 2023Article
- Differential Spleen miRNA Expression Profile of Beagle Dogs Infected withAnimals : an open access journal from MDPI · 2022Article
- Role of spleen tyrosine kinase in liver diseases.World journal of gastroenterology · 2020Review
- Continuous signaling of CD79b and CD19 is required for the fitness of Burkitt lymphoma B cells.The EMBO journal · 2018Article
- Unperturbed Immune Function despite Mutation of C-Terminal Tyrosines in Syk Previously Implicated in Signaling and Activity Regulation.Molecular and cellular biology · 2017Article
- The role of ZAP70 kinase in acute lymphoblastic leukemia infiltration into the central nervous system.Haematologica · 2017Article
- Force-dependent calcium signaling and its pathway of human neutrophils on P-selectin in flow.Protein & cell · 2017Article
- Phosphorylation impact on Spleen Tyrosine kinase conformation by Surface Enhanced Raman Spectroscopy.Scientific reports · 2017Article
- TULA-2 Protein Phosphatase Suppresses Activation of Syk through the GPVI Platelet Receptor for Collagen by Dephosphorylating Tyr(P)346, a Regulatory Site of Syk.The Journal of biological chemistry · 2016Article
- Deficient synthesis of class-switched, HIV-neutralizing antibodies to the CD4 binding site and correction by electrophilic gp120 immunogen.AIDS (London, England) · 2014Article
- The autoinhibitory C-terminal SH2 domain of phospholipase C-γ2 stabilizes B cell receptor signalosome assembly.Science signaling · 2014Article
- Depletion of STAT5 blocks TEL-SYK-induced APMF-type leukemia with myelofibrosis and myelodysplasia in mice.Blood cancer journal · 2014Article
- Inducible expression of hyperactive Syk in B cells activates Blimp-1-dependent terminal differentiation.Oncogene · 2014Article
- Global phosphoproteomics of activated B cells using complementary metal ion functionalized soluble nanopolymers.Analytical chemistry · 2014Article
- Spleen tyrosine kinase (Syk)-dependent calcium signals mediate efficient CpG-induced exocytosis of tumor necrosis factor α (TNFα) in innate immune cells.The Journal of biological chemistry · 2013Article
- Signaling of the ITK (interleukin 2-inducible T cell kinase)-SYK (spleen tyrosine kinase) fusion kinase is dependent on adapter SLP-76 and on the adapter function of the kinases SYK and ZAP70.The Journal of biological chemistry · 2013Article
- Internalization of B cell receptors in human EU12 μHC⁺ immature B cells specifically alters downstream signaling events.BioMed research international · 2013Article
- Critical signal transduction pathways in CLL.Advances in experimental medicine and biology · 2013Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Upon B-cell antigen receptor (BCR) activation, the protein tyrosine kinase Syk phosphorylates the adaptor protein SH2 domain-containing leukocyte protein of 65 kDa (SLP-65), thus coupling the BCR to diverse signalling pathways. Here, we report that SLP-65 is not only a downstream target and substrate of Syk but also a direct binding-partner and activator of this kinase. This positive feedback is mediated by the binding of the SH2 domain of SLP-65 to an autophosphorylated tyrosine of Syk. The mutant B cells that cannot form the Syk/SLP-65 complex are defective in BCR-induced extracellular signal-regulated kinase, nuclear factor kappa B and nuclear factor of activated T cells, but not Akt activation, and are blocked in B-cell development. Furthermore, we show that formation of the Syk/SLP-65 complex is required for sustained Ca(2+) responses in activated B cells. We suggest that after activation and internalization of the BCR, Syk remains active as part of a membrane-bound Syk/SLP-65 complex controlling sustained signalling and calcium influx.
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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.