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Positioning of integrin β1, caveolin-1 and focal adhesion kinase on the adhered membrane of spreading cells

机译:整合素β1,caveolin-1和粘着斑激酶在铺展细胞粘附膜上的定位

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摘要

We have investigated the relationship between the spreading of anchorage-dependent cells and the surface-density distribution of plasma membrane adhesion proteins. The surface positioning and density of integrin β1, caveolin-1 (cav-1), the phosphorylated caveolin-1 (p-cav-1) and the focal adhesion kinase (FAK) located on the adhering cell membrane (ACM) of HUVEC cells was studied. Imaging with TIRF microscopy was used, which enabled us to observe a few-nanometers-thin section of the cell above the plasma membrane in combination with image-based analyses. Integrin β1 and cav-1 have spatial interdependenceon the ACM. Cells treatedwith substances that act on cell spreading caused changes inthe size of the ACM area, as well as a redistribution of several proteins under investigation. Changes to the ACM area correlated positively with those to the surface density of the cav-1. The high integrin β1 and the low cav-1 surface density, and vice versa, following the treatments show that the presence of one of them not only spatially excludes, but also reduces, the occurrence of the other protein on the ACM, which indicates a regulative mechanism between integrin β1 and cav-1.
机译:我们已经研究了锚固依赖性细胞的扩散与质膜粘附蛋白的表面密度分布之间的关系。 HUVEC细胞粘附细胞膜(ACM)上整合素β1,caveolin-1(cav-1),磷酸化caveolin-1(p-cav-1)和黏着斑激酶(FAK)的表面定位和密度被研究了。使用TIRF显微镜成像,结合基于图像的分析,使我们能够观察到质膜上方几纳米厚的细胞切片。整联蛋白β1和cav-1与ACM具有空间依赖性。用作用于细胞扩散的物质处理过的细胞引起了ACM区域大小的变化,以及正在研究的几种蛋白质的重新分布。 ACM面积的变化与cav-1的表面密度呈正相关。处理后,高整合素β1和低cav-1表面密度,反之亦然,表明其中之一的存在不仅在空间上排斥,而且减少了ACM上另一种蛋白质的出现,这表明整合素β1和cav-1之间的调控机制。

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