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蛋白激酶C抑制剂可阻断胰岛素和佛波酯刺激的离体大鼠脂肪细胞和BC3H-1肌细胞中的己糖转运。

Protein kinase C inhibitors block insulin and PMA-stimulated hexose transport in isolated rat adipocytes and BC3H-1 myocytes.

作者信息

Standaert M L, Buckley D J, Ishizuka T, Hoffman J M, Cooper D R, Pollet R J, Farese R V

机构信息

Veterans' Administration Hospital, Tampa, FL.

出版信息

Metabolism. 1990 Nov;39(11):1170-9. doi: 10.1016/0026-0495(90)90090-y.

Abstract

Effects of protein kinase C (PKC) inhibitors and "down-regulation" on insulin and PMA-stimulated 2-deoxyglucose transport were determined in isolated rat adipocytes or BC3H-1 myocytes. In both model systems, H-7, sangivamycin, and staurosporine, inhibitors of the catalytic domain of PKC, each effectively blocked insulin and PMA-stimulated hexose uptake at similar concentrations. In the myocytes, staurosporine completely blocked the insulin effect retained post-chronic phorbol myristate acetate (PMA)-induced "down-regulation." These findings indicate (1) that chronic pretreatment with PMA may not lead to a complete loss of PKC activity in the myocyte, and (2) that PKC is involved in insulin-stimulated hexose transport in both isolated rat adipocytes and BC3H-1 myocytes.

摘要

在分离的大鼠脂肪细胞或BC3H-1肌细胞中,测定了蛋白激酶C(PKC)抑制剂和“下调”对胰岛素及佛波酯(PMA)刺激的2-脱氧葡萄糖转运的影响。在这两种模型系统中,PKC催化结构域的抑制剂H-7、桑吉瓦霉素和星形孢菌素,在相似浓度下均能有效阻断胰岛素和PMA刺激的己糖摄取。在肌细胞中,星形孢菌素完全阻断了慢性佛波醇肉豆蔻酸酯乙酸酯(PMA)诱导的“下调”后所保留的胰岛素效应。这些发现表明:(1)用PMA进行慢性预处理可能不会导致肌细胞中PKC活性完全丧失;(2)PKC参与分离的大鼠脂肪细胞和BC3H-1肌细胞中胰岛素刺激的己糖转运。

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