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- W1497451313 abstract "Abstract Lymphocytes express both Wiskott-Aldrich syndrome protein (WASP) and N-WASP. WASP deficiency, the cause of WAS, generates more severe defects in T-cells than B cells, suggesting a strong compensatory role of N-WASP in B cells. Using knockout mouse models, this study shows that WASP knockout (WKO) reduces B cell spreading, B cell receptor (BCR) aggregation, tyrosine phosphorylation, Btk phosphorylation and F-actin accumulation at the B cell surface induced by membrane-associated antigen, and WASP/N-WASP double knockout nearly abolished these activities. However, in B cells with N-WASP conditional knockout (cNKO), B cell spreading and F-actin accumulation are enhanced, while the merge of BCR aggregates and attenuation of tyrosine and Btk phosphorylation are inhibited. Additionally, cNKO has a much stronger inhibitory effect on BCR endocytosis than WKO. In contrast to Btk-dependent activation of WASP, N-WASP phosphorylation is upregulated by Btk-deficiency but downregulated by SHIP KO. Furthermore, the phosphorylation of WASP and N-WASP is inversely regulated by each other. These results reveal that the combined function of WASP and N-WASP is required for the optimal activation of the BCR and its signaling attenuation, but these two proteins function distinctively: WASP and N-WASP play dominant roles in the initiation and attenuation of BCR activation respectively. Thus, the integrated action of WASP and N-WASP provide a critical regulatory mechanism for BCR activation." @default.
- W1497451313 created "2016-06-24" @default.
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- W1497451313 date "2012-05-01" @default.
- W1497451313 modified "2023-10-03" @default.
- W1497451313 title "Pivotal roles of both Wiskott-Aldrich syndrome protein (WASP) and N-WASP in the activation and attenuation of the B cell receptor (P1093) (42.1)" @default.
- W1497451313 doi "https://doi.org/10.4049/jimmunol.188.supp.42.1" @default.
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