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原文連結
論文資訊
- 類型：已發表論文
- 日期：2013
摘要
Activation of the antigen receptors on the surface of B cells in response to their cognate ligands is tightly controlled by feedback mechanisms. Apart from ligand induced signaling, B cell receptors (BCRs) emanate ligand independent tonic signaling crucial for B cell survival and development. In the absence of a ligand, BCR tonic signaling is controlled by the basal activity of the Src family 蛋白質 tyrosine kinase Lyn and the 蛋白質 tyrosine phosphatase SHP. The binding of an antigen to the BCR causes receptor clustering or aggregation which is one of the earliest events in B cell activation. Lyn binds to aggregated receptors and phosphorylates them. In turn phosphorylation enhances the stability of receptor clusters against dissociation into monomers as well as the binding of Lyn to the recept
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