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首页> 外文期刊>Platelets >Distinct roles of ligand affinity and cytoskeletal anchorage in alphaIIbbeta3 (GP IIb/IIIa)-mediated cell aggregation and adhesion.
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Distinct roles of ligand affinity and cytoskeletal anchorage in alphaIIbbeta3 (GP IIb/IIIa)-mediated cell aggregation and adhesion.

机译:配体亲和力和细胞骨架锚定在alphaIIbbeta3(GP IIb / IIIa)介导的细胞聚集和粘附中的不同作用。

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摘要

Platelet integrin alphaIIbbeta3 (GP IIb/IIla) is functionally modulated by changes in ligand affinity or in cytoskeletal anchorage. CHO cells transfected with wild-type/mutated alphaIIbbeta3 allow the dissection of the relative contributions of the two regulatory mechanisms in alphaIIbbeta3-mediated adhesion and aggregation. Mutations included a truncation of the cytoplasmic domain of the beta-subunit, resulting in a loss of cytoskeletal anchorage of alphaIIbbeta3, and a VGFFK-deletion of the alpha-subunit, resulting in a permanent high affinity state. alphaIIbbeta3-mediated cell aggregation is dependent on the high affinity state but only partially on the cytoskeletal anchorage of alphaIIbbeta3. In contrast, alphaIIbbeta3-mediated cell adhesion is dependent on the cytoskeletal anchorage but only partially on the high affinity state of alphaIIbbeta3. Thus, the functional evaluation of mutated alphaIIbbeta3 implies a differential role of affinity state and cytoskeletal anchorage for alphaIIbbeta3-mediated cell adhesion and aggregation.
机译:血小板整联蛋白αIIbbeta3(GP IIb / IIla)通过配体亲和力或细胞骨架锚定的变化进行功能调节。转染了野生型/突变的alphaIIbbeta3的CHO细胞允许解剖两种调节机制在alphaIIbbeta3介导的粘附和聚集中的相对贡献。突变包括β亚基的胞质结构域的截断,导致alphaIIbbeta3的细胞骨架锚定丢失,以及alpha亚基的VGFFK缺失,导致永久性高亲和力状态。 alphaIIbbeta3介导的细胞聚集取决于高亲和力状态,但仅部分取决于alphaIIbbeta3的细胞骨架锚定。相比之下,alphaIIbbeta3介导的细胞粘附取决于细胞骨架锚定,但仅部分取决于alphaIIbbeta3的高亲和力状态。因此,突变的alphaIIbbeta3的功能评估暗示亲和状态和细胞骨架锚定对alphaIIbbeta3介导的细胞粘附和聚集的不同作用。

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