AIM To investigate the relationship between protein tyrosine phosphorylation and volume-regulated chloride channel currents in A10 vascular cells.
目的探讨蛋白酪氨酸磷酸化在胚胎鼠主动脉平滑肌细胞系a10细胞容积调节性氯通道电流中的调控作用。
CONCLUSION: the chloride channel blockers NPPB or NFA lessen the oxidative injury of C6 cells through modulating the function of membrane and down-regulating the protein expression of CLIC4.
结论：氯通道阻断剂NPPB或NFA能够在一定程度上减轻氧化应激引起的C6细胞损伤，可能与调节细胞膜功能和下调CLIC 4蛋白表达有关。
Conclusions S2-protein from SARS coronavirus inhibits the chloride channel function in A549 cells, and both PKC and P38 are not involved in mediating this modulation.
结论SARS冠状病毒S2蛋白能抑制A549细胞氯通道的功能活动，PKC和P38可能不参与S2蛋白对通道电流的抑制作用。
Conclusions S2-protein from SARS coronavirus inhibits the chloride channel function in A549 cells, and both PKC and P38 are not involved in mediating this modulation.
结论SARS冠状病毒S2蛋白能抑制A549细胞氯通道的功能活动，PKC和P38可能不参与S2蛋白对通道电流的抑制作用。
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