首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Defective lymphocyte chemotaxis in β-arrestin2- and GRK6-deficient mice
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Defective lymphocyte chemotaxis in β-arrestin2- and GRK6-deficient mice

机译:β-arrestin2和GRK6缺陷小鼠的淋巴细胞趋化性缺陷

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摘要

Lymphocyte chemotaxis is a complex process by which cells move within tissues and across barriers such as vascular endothelium and is usually stimulated by chemokines such as stromal cell-derived factor-1 (CXCL12) acting via G protein-coupled receptors. Because members of this receptor family are regulated ("desensitized") by G protein-coupled receptor kinase (GRK)-mediated receptor phos- phorylation and β-arrestin binding, we examined signaling and chemotactic responses in splenocytes derived from knockout mice deficient in various β-arrestins and GRKs, with the expectation that these responses might be enhanced.
机译:淋巴细胞趋化性是一个复杂的过程,细胞通过该过程在组织内移动并穿过诸如血管内皮之类的屏障,通常受到趋化因子(例如基质细胞衍生因子1(CXCL12))的刺激,这些趋化因子通过G蛋白偶联受体发挥作用。由于该受体家族的成员受G蛋白偶联受体激酶(GRK)介导的受体磷酸化和β-arrestin结合的调控(“脱敏”),因此我们检查了源自各种缺陷型基因敲除小鼠的脾细胞中的信号传导和趋化反应。 β-arrestins和GRKs,期望可以增强这些反应。

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