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首页> 外文期刊>Molecular and Cellular Biology >Cbp Deficiency Alters Csk Localization in Lipid Rafts but Does Not Affect T-Cell Development
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Cbp Deficiency Alters Csk Localization in Lipid Rafts but Does Not Affect T-Cell Development

机译：Cbp缺乏症改变脂质筏中的Csk定位，但不影响T细胞发育

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The ubiquitously expressed transmembrane adaptor Csk-binding protein (Cbp) recruits Csk to lipid rafts, where the latter exerts its negative regulatory effect on the Src family of protein tyrosine kinases. We have inactivated Cbp in the mouse germ line. In contrast to Csk gene inactivation, which leads to embryonic lethality and impaired T-cell development, Cbp-deficient mice were viable and exhibited normal T-cell development but with an increased thymocyte population. In the absence of Cbp, the amount of Csk that localizes to the lipid rafts was greatly reduced. Interestingly, this altered lipid raft localization of Csk did not lead to any detectable biochemical or functional defect in T cells. The T-cell receptor-induced intracellular calcium flux, cell proliferation, and cytokine secretion were not affected by the absence of Cbp. Peripheral T-cell tolerance to superantigen SEB was also largely intact in Cbp-deficient mice. Thus, Cbp is dispensable for T-cell development and activation.
机译：普遍表达的跨膜衔接子Csk结合蛋白（Cbp）将Csk募集到脂质筏上，后者在其对蛋白酪氨酸激酶的Src家族起负调控作用。我们已经灭活了小鼠种系中的Cbp。与导致胚胎致死力和T细胞发育受损的 Csk 基因失活相反，Cbp缺陷小鼠具有生存力，并表现出正常的T细胞发育，但胸腺细胞数量增加。在没有Cbp的情况下，大大减少了定位在脂质筏上的Csk量。有趣的是，这种改变的Csk脂质筏定位​​没有导致T细胞中任何可检测到的生化或功能缺陷。 T细胞受体诱导的细胞内钙通量，细胞增殖和细胞因子分泌不受Cbp的影响。在Cbp缺陷型小鼠中，外周血T细胞对超抗原SEB的耐受性也基本完好。因此，Cbp对于T细胞的发育和激活是必不可少的。

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