Gabbay R A, Siconolfi-Baez L, Lebovitz H E
Department of Medicine, State University of New York Health Science Center, Brooklyn 11203.
Endocrinology. 1990 Sep;127(3):1194-8. doi: 10.1210/endo-127-3-1194.
The effects of 4 weeks of streptozotocin-induced diabetes in the rat on sciatic nerve homogenate protein kinase activities were studied. There was a 47 +/- 7% inhibition of Ca+2-dependent protein kinase activity in nerves from the diabetic rats compared to that in their paired normal controls. This Ca+2-dependent activity did not require the addition of phospholipid and was only minimally affected by Sephadex G-50 gel filtration, suggesting that endogenous phospholipid activation was not responsible for this activity. The addition of phospholipid in the presence of Ca+2 revealed an additional activity in these homogenates which probably represents the Ca+2-phospholipid-dependent protein kinase (protein kinase-C). The diabetic state did not appear to alter that activity. The Ca+2-dependent protein kinase was sensitive to agents known to inhibit calmodulin-dependent protein kinase or protein kinase-C. The IC50 values of the inhibitors for the Ca+2-dependent protein kinase, however, differed from those reported for the other two kinases.
研究了链脲佐菌素诱导大鼠糖尿病4周对坐骨神经匀浆蛋白激酶活性的影响。与配对的正常对照相比,糖尿病大鼠神经中Ca+2依赖性蛋白激酶活性受到47±7%的抑制。这种Ca+2依赖性活性不需要添加磷脂,并且仅受到Sephadex G-50凝胶过滤的轻微影响,这表明内源性磷脂激活与该活性无关。在Ca+2存在的情况下添加磷脂揭示了这些匀浆中的一种额外活性,这可能代表Ca+2-磷脂依赖性蛋白激酶(蛋白激酶C)。糖尿病状态似乎并未改变该活性。Ca+2依赖性蛋白激酶对已知抑制钙调蛋白依赖性蛋白激酶或蛋白激酶C的试剂敏感。然而,抑制剂对Ca+2依赖性蛋白激酶的IC50值与报道的其他两种激酶的IC50值不同。