Lahav Judith, Karniel Eli, Bagoly Zsuzsa, Sheptovitsky Vera, Dardik Rima, Inbal Aida
Thrombosis and Hemostasis Unit, Beilinson Hospital, Rabin Medical Center, Petah Tikva, Israel.
Thromb Haemost. 2009 May;101(5):840-4.
Tissue transglutaminase was reported to act as protein disulfide isomerase (PDI). We studied whether plasma transglutaminase - coagulation factor XIII (FXIII) - has PDI activity as well. PDI activity was measured by determining the ability to renature reduced-denatured RNase (rdRNase). We found that FXIII can renature rdRNase, with efficiency comparable to commercial PDI. This PDI activity was inhibited by bacitracin. Like tissue transglutaminase, FXIII-mediated PDI activity is independent of its transglutaminase activity and is located on the A subunit. Surface-associated PDI has been previously shown to catalyse two distinct functions: transnitrosation with subsequent release of intracellular nitric oxide and disulfide bond rearrangement during platelet integrin ligation. Our results imply that FXIII-PDI activity may have a role in platelet function.
据报道，组织转谷氨酰胺酶可作为蛋白质二硫键异构酶（PDI）发挥作用。我们研究了血浆转谷氨酰胺酶 - 凝血因子 XIII（FXIII）是否也具有 PDI 活性。通过测定使还原变性核糖核酸酶（rdRNase）复性的能力来测量 PDI 活性。我们发现 FXIII 可以使 rdRNase 复性，其效率与市售 PDI 相当。这种 PDI 活性被杆菌肽抑制。与组织转谷氨酰胺酶一样，FXIII 介导的 PDI 活性与其转谷氨酰胺酶活性无关，且位于 A 亚基上。先前已表明，表面相关的 PDI 可催化两种不同的功能：转亚硝化作用及随后细胞内一氧化氮的释放，以及血小板整合素连接过程中的二硫键重排。我们的结果表明，FXIII-PDI 活性可能在血小板功能中发挥作用。
