Larsson O, Barker C J, Sjöholm A, Carlqvist H, Michell R H, Bertorello A, Nilsson T, Honkanen R E, Mayr G W, Zwiller J, Berggren P O
Rolf Luft Center for Diabetes Research, Department of Molecular Medicine, Karolinska Institute, S-171 76 Stockholm, Sweden.
Science. 1997 Oct 17;278(5337):471-4. doi: 10.1126/science.278.5337.471.
Inositol hexakisphosphate (InsP6), the dominant inositol phosphate in insulin-secreting pancreatic beta cells, inhibited the serine-threonine protein phosphatases type 1, type 2A, and type 3 in a concentration-dependent manner. The activity of voltage-gated L-type calcium channels is increased in cells treated with inhibitors of serine-threonine protein phosphatases. Thus, the increased calcium channel activity obtained in the presence of InsP6 might result from the inhibition of phosphatase activity. Glucose elicited a transient increase in InsP6 concentration, which indicates that this inositol polyphosphate may modulate calcium influx over the plasma membrane and serve as a signal in the pancreatic beta cell stimulus-secretion coupling.
肌醇六磷酸（InsP6）是胰岛素分泌性胰腺β细胞中主要的肌醇磷酸，它以浓度依赖性方式抑制1型、2A型和3型丝氨酸 - 苏氨酸蛋白磷酸酶。在用丝氨酸 - 苏氨酸蛋白磷酸酶抑制剂处理的细胞中，电压门控L型钙通道的活性增加。因此，在InsP6存在下获得的钙通道活性增加可能是由于磷酸酶活性受到抑制。葡萄糖引起InsP6浓度的短暂升高，这表明这种肌醇多磷酸可能调节质膜上的钙内流，并作为胰腺β细胞刺激 - 分泌偶联中的一种信号。
