Modulation of cell adhesion and motility in the immune system by Myo1f
Modulation of cell adhesion and motility in the immune system by Myo1f
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DOI：
10.1126/science.1131920
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发表时间：
2006-10-06
期刊：
影响因子：
56.9
通讯作者：
Flavell, Richard A.
中科院分区：
文献类型：
--
作者：
Kim, Sangwon V.;Mehal, Wajahat Z.;Flavell, Richard A.
虽然I类肌球蛋白已知发挥广泛的作用，长尾I类肌球蛋白在脊椎动物中的生理功能仍然难以捉摸。我们证明，这些蛋白质之一，Myo1f，主要在哺乳动物免疫系统中表达。来自Myo1f缺陷小鼠的细胞表现出异常增加的粘附性和降低的运动性，这是由于含β 2整联蛋白颗粒的胞吐作用增强所致。此外，与Myo1f共定位的皮质肌动蛋白在Myo1f缺陷细胞中减少。在体内，Myo1f缺陷小鼠对单核细胞增生李斯特菌感染的易感性增加，中性粒细胞反应受损。因此，Myo1f指导免疫细胞运动和先天宿主防御感染。
Although class I myosins are known to play a wide range of roles, the physiological function of long-tailed class I myosins in vertebrates remains elusive. We demonstrated that one of these proteins, Myo1f, is expressed predominantly in the mammalian immune system. Cells from Myo1f-deficient mice exhibited abnormally increased adhesion and reduced motility, resulting from augmented exocytosis of beta 2 integrin - containing granules. Also, the cortical actin that co-localizes with Myo1f was reduced in Myo1f-deficient cells. In vivo, Myo1f-deficient mice showed increased susceptibility to infection by Listeria monocytogenes and an impaired neutrophil response. Thus, Myo1f directs immune cell motility and innate host defense against infection.