THE PKC-INHIBITOR RO 31-8220 SELECTIVELY SUPPRESSES PMA-INDUCED AND DIACYLGLYCEROL-INDUCED FLUID PINOCYTOSIS AND ACTIN POLYMERIZATION IN PMNS

THE PKC-INHIBITOR RO 31-8220 SELECTIVELY SUPPRESSES PMA-INDUCED AND DIACYLGLYCEROL-INDUCED FLUID PINOCYTOSIS AND ACTIN POLYMERIZATION IN PMNS
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DOI:
10.1006/bbrc.1993.1936
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发表时间:
1993-08-16
影响因子:
3.1
通讯作者:
NIGGLI, V
NIGGLI, V
中科院分区:
生物学4区
文献类型:
--
作者:
KELLER, HU;NIGGLI, V

文献摘要

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蛋白激酶C激活剂佛波酯(PMA,IC_(50)=1.35×10~(-6)−6M)或甘油二酯(OAG,DiC_8)刺激的PMN液体吞饮作用可被抑制95%,而RO31-8220对D2O或fNLPNTL诱导的吞饮作用无影响,但可增强细胞松弛素D诱导的吞饮作用。PMA或甘油二酯诱导的F-肌动蛋白的形成也被选择性地抑制。结果表明,RO31-8220敏感的PKC参与了一类刺激(经典的PKC激活剂)增强胞饮作用和F-肌动蛋白形成的信号转导,而对其他刺激不起作用。
The PKC-inhibitor Ro 31-8220 inhibits stimulated fluid pinocytosis of human PMNs induced by the PKC-activators phorbol myristate acetate (PMA, IC50= 1.35×10−6M) or diacylglycerols (OAG, diC8) by 95%, whereas Ro 31-8220 has no effect on D2O- or fNLPNTL-induced pinocytosis and enhances cytochalasin D-induced pinocytosis. Also formation of F-actin induced by PMA or diacylglycerols is selectively inhibited. The results indicate that a Ro 31-8220-sensitive PKC is involved in signal transduction for enhanced pinocytosis and F-actin formation in response to one class of stimuli (classical activators of PKC) but not to others.