Bam32: a novel mediator of Erk activation in T cells
Bam32: a novel mediator of Erk activation in T cells
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DOI：
10.1093/intimm/dxn039
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发表时间：
2008-07-01
影响因子：
4.4
通讯作者：
Samelson, Lawrence E.
中科院分区：
文献类型：
--
作者：
Sommers, Connie L.;Gurson, Jordan M.;Samelson, Lawrence E.
Bam32（32 kDa的B淋巴细胞衔接分子）是在包括B和T淋巴细胞的一些造血细胞中表达的衔接蛋白。先前显示Bam32缺陷型小鼠在B细胞活化的各个方面具有缺陷，包括B细胞受体（BCR）诱导的Erk活化、BCR诱导的增殖和T非依赖性抗体应答。在这项研究中，我们研究了Bam32在T细胞活化中的作用，使用Bam32缺陷小鼠。通过比较野生型和Bam32缺陷小鼠淋巴结中的CD4（+）T细胞，我们发现Bam32是最佳TCR诱导的Erk活化、细胞因子产生、增殖和肌动蛋白介导的CD4（+）T细胞扩散所必需的。这些结果表明，一种新的途径Erk激活T细胞涉及衔接蛋白Bam32。
Bam32 (B lymphocyte adapter molecule of 32 kDa) is an adapter protein expressed in some hematopoietic cells including B and T lymphocytes. It was previously shown that Bam32-deficient mice have defects in various aspects of B cell activation including B cell receptor (BCR)-induced Erk activation, BCR-induced proliferation and T-independent antibody responses. In this study, we have examined the role of Bam32 in T cell activation using Bam32-deficient mice. By comparing CD4(+) T cells from lymph nodes of wild-type and Bam32-deficient mice, we found that Bam32 was required for optimal TCR-induced Erk activation, cytokine production, proliferation and actin-mediated spreading of CD4(+) T cells. These results indicate a novel pathway to Erk activation in T cells involving the adapter protein Bam32.