首页> 外文期刊>Journal of pharmacological sciences. >Extracellular-Added ADP-Ribose Increases Intracellular Free Ca2+ Concentration Through Ca2+ Release From Stores, but Not Through TRPM2-Mediated Ca2+ Entry, in Rat β-Cell Line RIN-5F
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Extracellular-Added ADP-Ribose Increases Intracellular Free Ca2+ Concentration Through Ca2+ Release From Stores, but Not Through TRPM2-Mediated Ca2+ Entry, in Rat β-Cell Line RIN-5F

机译:在大鼠β细胞系RIN-5F中,细胞外添加的ADP核糖通过从商店释放Ca2 +而不是通过TRPM2介导的Ca2 +进入来增加细胞内游离Ca2 +浓度。

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References(13) Cited-By(6) Intracellular ADP-ribose is an activator of TRPM2, which is a Ca2+-permeable channel and mediates H2O2-induced cell death, in the TRPM2-expressing rat β-cell line RIN-5F. We examined the effect of extracellular-added ADP-ribose on intracellular Ca2+ concentration in RIN-5F cells. ADP-ribose induced Ca2+ release from the thapsigargin-sensitive Ca2+ store, but not Ca2+ entry across the plasma membrane. A phospholipase C (PLC) inhibitor and a non-specific IP3 receptor inhibitor blocked its Ca2+ release. H2O2-induced Ca2+ entry through TRPM2 was not affected by extracellular ADP-ribose. These findings suggest that extracellular-added ADP-ribose induces Ca2+ release through the PLC-IP3 pathway and does not act as a TRPM2 activator.
机译:参考文献(13)被引用的By(6)细胞内ADP-核糖是TRPM2的激活剂,TRPM2是Ca2 +可渗透的通道,介导H2O2诱导的大鼠β细胞系RIN-5F的细胞死亡。我们检查了细胞外添加的ADP-核糖对RIN-5F细胞中细胞内Ca2 +浓度的影响。 ADP-核糖诱导从毒胡萝卜素敏感的Ca2 +存储中释放Ca2 +,但不会使Ca2 +跨质膜进入。磷脂酶C(PLC)抑制剂和非特异性IP3受体抑制剂可阻止其Ca2 +释放。 H2O2诱导的Ca2 +通过TRPM2进入不受细胞外ADP-核糖的影响。这些发现表明,细胞外添加的ADP-核糖可通过PLC-IP3途径诱导Ca2 +释放,而不充当TRPM2激活剂。

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