AKT2 is one of the key molecules that involves in the insulin-induced signaling and the development of cancer. In B cells, the function of AKT2 is unclear. In this study, we used AKT2 knockout mice model to study the role of AKT2 in BCR signaling and B cell differentiation. AKT2 promotes the early activation of B cells by enhancing the BCR signaling and actin remodeling. B cells from AKT2 KO mice exhibited defective spreading and BCR clustering upon stimulation in vitro. Disruption of Btk-mediated signaling caused the impaired differentiation of germinal center B cells, and the serum levels of both sepecific IgM and IgG were decreased in the immunized AKT2 KO mice. In addition, the actin remodeling was affected due to the decreased level of the activation of WASP, the actin polymerization regulator, in AKT2 KO mice as well. As a crucial regulator of both BCR signaling and actin remodeling during early activation of B cells, the phosphorylation of CD19 was decreased in the AKT2 absent B cells, while the transcription level was normal. AKT2 involves in the humoral responses, and promotes the BCR signaling and actin remodeling to enhance the activation of B cells via regulating CD19 phosphorylation.

中文翻译：

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AKT2缺乏会损害BCR信号小体的形成。

AKT2是参与胰岛素诱导的信号传导和癌症发展的关键分子之一。在B细胞中，AKT2的功能尚不清楚。在这项研究中，我们使用AKT2基因敲除小鼠模型来研究AKT2在BCR信号传导和B细胞分化中的作用。AKT2通过增强BCR信号传导和肌动蛋白重塑来促进B细胞的早期活化。AKT2 KO小鼠的B细胞在体外刺激后表现出有缺陷的扩散和BCR簇集。Btk介导的信号的破坏导致生发中心B细胞的分化受损，并且在免疫的AKT2 KO小鼠中血清特异性IgM和IgG均降低。另外，肌动蛋白重塑也由于AKT2 KO小鼠中肌动蛋白聚合调节因子WASP的活化水平降低而受到影响。作为BCR早期激活过程中BCR信号转导和肌动蛋白重塑的关键调节剂，在缺少AKT2的B细胞中CD19的磷酸化降低，而转录水平却是正常的。AKT2参与体液反应，并通过调节CD19磷酸化来促进BCR信号传导和肌动蛋白重塑，从而增强B细胞的活化。