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首页> 外文期刊>Cellular immunology >CARD19, the protein formerly known as BinCARD, is a mitochondrial protein that does not regulate Bcl10-dependent NF-kappa B activation after TCR engagement
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CARD19, the protein formerly known as BinCARD, is a mitochondrial protein that does not regulate Bcl10-dependent NF-kappa B activation after TCR engagement

机译：CARD19，以前称为Bincard的蛋白质是一种线粒体蛋白质，其在TCR接合后不调节BCL10依赖性NF-Kappa B的活化

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After T cell receptor (TCR) engagement, the CARD11-Bcl10-Malt1 (CBM) complex oligomerizes to transduce NF-kappa B activating signals. Bcl10 is then degraded to limit NF-kappa B activation. The cDNA AK057716 (BinCARD-1) was reported to encode a novel CARD protein that interacts with Bcl10 and modestly inhibits NF-kappa B activation. In a later study, a second isoform, BinCARD-2, was identified. Here, we report that the cDNA AK057716 (BinCARD-1) is an incompletely spliced derivative of the gene product of C9orf89, whereas CARD19 (BinCARD-2) re-presents the properly spliced isoform, with conservation across diverse species. Immunoblotting revealed expression of CARD19 in T cells, but no evidence of BinCARD-1 expression, and microscopy demonstrated that endogenous CARD19 localizes to mitochondria. Although we confirmed that both BinCARD-1 and CARD19 can inhibit NF-kappa B activation and promote Bcl10 degradation when transiently overexpressed in HEK293T cells, loss of endogenous CARD19 expression had little effect on Bcl10-dependent NF-kappa B activation, activation of Malt1 protease function, or Bcl10 degradation after TCR engagement in primary murine CD8 T cells. Together, these data indicate that the only detectable translated product of C9orf89 is the mitochondrial protein CARD19, which does not play a discernible role in TCR-dependent, Bcl10-mediated signal transduction to Malt1 or NF-kappa B.
机译：在T细胞受体（TCR）结合后，CARD11-Bcl10-Malt1（CBM）复合物寡聚以转导NF-κB激活信号。然后，Bcl10被降解以限制NF-κB的激活。据报道，cDNA AK057716（BinCARD-1）编码一种与Bcl10相互作用并适度抑制NF-κB激活的新型CARD蛋白。在后来的一项研究中，第二种异构体BinCARD-2被鉴定出来。在这里，我们报告说，cDNA AK057716（BinCARD-1）是C9orf89基因产物的不完全剪接衍生物，而CARD19（BinCARD-2）重新呈现了正确剪接的异构体，在不同物种中具有保守性。免疫印迹显示CARD19在T细胞中表达，但没有证据表明BinCARD-1表达，显微镜显示内源性CARD19定位于线粒体。虽然我们证实BinCARD-1和CARD19在HEK293T细胞中瞬时过度表达时可抑制NF-κB激活并促进Bcl10降解，但内源性CARD19表达的缺失对Bcl10依赖性NF-κB激活、Malt1蛋白酶功能的激活或TCR参与原代小鼠CD8 T细胞后的Bcl10降解几乎没有影响。总之，这些数据表明C9orf89唯一可检测的翻译产物是线粒体蛋白CARD19，它在TCR依赖的Bcl10介导的Malt1或NF-κB信号转导中不起明显作用。

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