Binding uptake and degradation of antithrombin III X protease complexes by cultured corneal endothelial cells.
Binding uptake and degradation of antithrombin III X protease complexes by cultured corneal endothelial cells.
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培养的角膜内皮细胞对抗凝血酶 III X 蛋白酶复合物的结合吸收和降解。
DOI：
10.1016/0014-4827(84)90447-6
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发表时间：
1984
影响因子：
3.7
通讯作者：
N. Farzame
中科院分区：
文献类型：
--
作者：
N. Savion;N. Farzame
在组织培养中研究了~（125）I-AT Ⅲ·蛋白酶复合物与牛角膜内皮细胞的相互作用，~（125）I-AT Ⅲ不与内皮细胞结合，但与凝血酶或胰蛋白酶的复合物与培养物特异性结合。125 I-AT Ⅲ·蛋白酶复合物的结合不是通过游离的抗凝血酶Ⅲ（AT Ⅲ）或游离的蛋白酶的部分，因为AT Ⅲ和凝血酶都不竞争125 I-AT Ⅲ·凝血酶复合物的结合。只有未标记的AT III ·凝血酶复合物与碘化配体竞争结合。125 I-AT III ·胰蛋白酶复合物以1.4 × 10− 7 M的aKD与角膜内皮细胞表面的高亲和力结合位点结合。在2.5 × 10− 7 M125 I-AT III ·胰蛋白酶复合物浓度下观察到与细胞表面的结合饱和，每个细胞的结合位点数约为4 × 104。细胞表面结合在15 min时达到最大值，然后随时间降低。当在37 °C下孵育时，细胞似乎通过吸附性内吞作用将结合的复合物内化，其速率为0.5-0.8 pmole/1 × 106个细胞/h。125 I-AT III ·蛋白酶复合物的内化过程在2.5 × 10− 7 M浓度下达到饱和。由于125 I标记的物质释放到细胞外介质中，而三氯乙酸（TCA）不能将其沉淀，因此，这可能代表125 I-AT Ⅲ·蛋白酶复合物以约0.5pmole/1 × 106个细胞/h的线性速率降解成小片段。上述AT Ⅲ·蛋白酶复合物结合、内化和随后被角膜内皮细胞降解的过程可能代表了病理条件下形成的细胞外AT Ⅲ·蛋白酶复合物的清除机制。
Interaction of125I-labeled human antithrombin III (125I-AT III) · protease complexes with bovine corneal endothelial cells has been studied in tissue culture.125I-AT III does not bind to endothelial cells, but its complexes with either thrombin or trypsin bind specifically to the cultures. The binding of125I-AT III · protease complexes is not via the moiety of the free antithrombin III (AT III) or the free protease, since neither AT III nor thrombin compete on the binding of125I-AT III · thrombin complexes. Only unlabeled AT III · thrombin complexes compete on the binding of the iodinated ligand.125I-AT III · trypsin complexes bind with aKDof 1.4 × 10−7M to high affinity-binding sites present on the cell surface of corneal endothelial cells. Saturation of binding to the cell surface is observed at a concentration of 2.5 × 10−7M125I-AT III · trypsin complexes and the number of binding sites per cell is about 4 × 104. The cell surface binding reaches a maximum by 15 min and then decreases with time. The cells, when incubated at 37 °C, appear to internalize the bound complexes by adsorptive endocytosis which proceeds at a rate of 0.5-0.8 pmole/1 × 106cells/h. The internalization process of125I-AT III · protease complexes is saturated at a concentration of 2.5 × 10−7M. Since the cells release125I-labeled material into the extracellular media which cannot be precipitated by trichloroacetic acid (TCA), it probably represents degradation of125I-AT III · protease complexes into small fragments at a linear rate of about 0.5 pmole/1 × 106cells/h. The described process of AT III · protease complexes binding, internalization and subsequent degradation by corneal endothelial cells may represent a clearing mechanism for extracellular AT III · protease complexes formed under pathological conditions.
抗凝血酶 III 和抗凝血酶 III 复合物的体内代谢。
DOI：
--
发表时间：
1982
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Shifman,MA;Pizzo,SV
通讯作者：
Pizzo,SV
凝血酶与角膜内皮细胞上的特定位点共价结合。
影响因子：
2.9
作者：
Isaacs,JD;Savion,N;Gospodarowicz,D;Fenton2nd,JW;Shuman,MA
通讯作者：
Shuman,MA
凝血酶的内化和降解以及角膜内皮细胞中凝血酶结合位点的上调。
DOI：
--
发表时间：
1981
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Savion,N;Isaacs,JD;Gospodarowicz,D;Shuman,MA
通讯作者：
Shuman,MA