Sato K, Mitsumoto Y, Mohri T
2nd Division, Hokuriku University School of Pharmacy, Ishikawa, Japan.
Biochem Biophys Res Commun. 1988 Jun 16;153(2):570-5. doi: 10.1016/s0006-291x(88)81133-1.
Stimulation of leucine uptake by addition of concanavalin A, mediated by increase of intracellular free Ca2+ concentration [( Ca2+]), in lymphocytes (Mitsumoto, Y., Sato, K. and Mohri, T. (1988) Biochim. Biophys. Acta 968, 353-358) was abolished by N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) and chlorpromazine, which inhibited membrane hyperpolarization induced by the mitogen. Quinine (0.5-1 mM) completely inhibited the concanavalin A-induced hyperpolarization and extensively inhibited the induced stimulation of leucine uptake. Based on these results, we suggest that the stimulation of leucine uptake by concanavalin A is largely due to activation of the Ca2+-dependent K+ channel which reinforces negative potential of the plasma membrane and is regulated by calmodulin.
通过添加伴刀豆球蛋白A刺激亮氨酸摄取,这是由淋巴细胞内细胞游离钙离子浓度[(Ca2+)]升高介导的(光本洋、佐藤和森,(1988年)《生物化学与生物物理学报》968卷,353 - 358页),被N -(6 - 氨基己基)- 5 - 氯 - 1 - 萘磺酰胺(W - 7)和氯丙嗪消除,它们抑制了有丝分裂原诱导的膜超极化。奎宁(0.5 - 1 mM)完全抑制了伴刀豆球蛋白A诱导的超极化,并广泛抑制了诱导的亮氨酸摄取刺激。基于这些结果,我们认为伴刀豆球蛋白A刺激亮氨酸摄取主要是由于钙依赖性钾通道的激活,该通道增强了质膜的负电位并受钙调蛋白调节。