ArticleThe Journal of cell biology2007
Coupling Ca2+ store release to Icrac channel activation in B lymphocytes requires the activity of Lyn and Syk kinases.
Article in The Journal of cell biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- CaBiomolecules · 2023Review
- The soluble isoform of human FcɛRI is an endogenous inhibitor of IgE-mediated mast cell responses.Allergy · 2019Article
- The prion protein constitutively controls neuronal store-operated Ca(2+) entry through Fyn kinase.Frontiers in cellular neuroscience · 2015Article
- Transmembrane adaptor protein PAG/CBP is involved in both positive and negative regulation of mast cell signaling.Molecular and cellular biology · 2014Article
- Different agonists recruit different stromal interaction molecule proteins to support cytoplasmic Ca2+ oscillations and gene expression.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Transcription factor NF-κB regulates expression of pore-forming Ca2+ channel unit, Orai1, and its activator, STIM1, to control Ca2+ entry and affect cellular functions.The Journal of biological chemistry · 2012Article
- Tyrosine phosphorylation of 3BP2 regulates B cell receptor-mediated activation of NFAT.The Journal of biological chemistry · 2009Article
- B-lymphocyte calcium influx.Immunological reviews · 2009Review
- Formation of STIM and Orai complexes: puncta and distal caps.Immunological reviews · 2009Review
- Mechanism and regulatory function of CpG signaling via scavenger receptor B1 in primary B cells.The Journal of biological chemistry · 2009Article
- Role of initial protein phosphorylation events and localized release-activated calcium influx in B cell antigen receptor signaling.Journal of leukocyte biology · 2009Article
- The kinase Syk as an adaptor controlling sustained calcium signalling and B-cell development.The EMBO journal · 2008Article
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Authors and funding
5 authors.
Funding
Abstract
Activation of the B cell receptor complex in B lymphocytes causes Ca(2+) release from intracellular stores, which, in turn, activates ion channels known as Icrac. We investigated the mechanisms that link Ca(2+) store release to channel gating in DT40 B lymphocyte cell lines genetically manipulated to suppress the expression of several tyrosine kinases: Btk, Lyn, Syk, and the Blnk adaptor molecule. The simultaneous but not the independent suppression of Lyn and Syk expression prevents the activation of Icrac without interfering with thapsigargin-sensitive Ca(2+) store release. Icrac activation by Ca(2+) is reversed in mutant cells by the homologous expression of the missing kinases. Pharmacological inhibition of kinase activity by LavendustinA and PP2 cause the same functional deficit as the genetic suppression of enzyme expression. Biochemical assays demonstrate that kinase activity is required as a tonic signal: targets must be phosphorylated to link Ca(2+) store release to Icrac gating. The action of kinases on Icrac activation does not arise from control of the expression level of the stromal interaction molecule 1 and Orai1 proteins.
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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.