目的从红细胞膜蛋白磷酸化改变的角度探讨葡萄糖6磷酸脱氢酶(G6PD)缺乏症溶血的机制。
Objective To explore the hemolytic mechanism of glucose 6 phosphate dehydrogenase (G6PD) deficient erythrocytes in the view of phosphorylation of membrane protein.
观察3t 3 -L1脂肪细胞长期暴露到高浓度葡萄糖对糖的转运活动和胰岛素信号蛋白的表达及磷酸化的影响。
We investigated the cellular effect of high glucose using 3t3-l1 adipocytes on glucose transport activity, the expression of insulin signaling proteins and IRS1 tyrosine phosphorylation.
方法：以磷酸化的PVA 海藻酸钙为载体包埋黑曲霉细胞，与固定化的葡萄糖异构酶协同反应，以蔗糖为原料转化生产低聚果糖。
Methods: Aspergillus niger cells entrapped by modified phosphorylated polyvinyl alcohol(PVA) alginate gel co react with immobilized glucose isomerase to transfer sucrose to FOS.
1的612位丝氨酸被MAPK磷酸化后会下调胰岛素信号，这可能是对高葡萄糖/葡萄糖胺比值的一种反应。
Phosphorylation of IRS-1 at Ser612 by MAPK downregulates insulin signaling and may be part of a response to high glucose/glucosamine levels (11).
而氨基葡萄糖可能会借由抑制MAPK路径的磷酸化来减缓介白素- 8的表现，进而来降低摄护腺癌细胞之增生及转移。
Glucosamine appears to inhibit IL-1b-mediated MAP kinase phosphorylation to reduce IL-8 expression, and therefore to retard prostate cancer cell proliferation and migration.
而氨基葡萄糖可能会借由抑制MAPK路径的磷酸化来减缓介白素- 8的表现，进而来降低摄护腺癌细胞之增生及转移。
Glucosamine appears to inhibit IL-1b-mediated MAP kinase phosphorylation to reduce IL-8 expression, and therefore to retard prostate cancer cell proliferation and migration.
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