Inhibition of neutrophil superoxide formation by 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), and inhibitor of protein kinase-C.

Inhibition of neutrophil superoxide formation by 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), and inhibitor of protein kinase-C.
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1-(5-异喹啉磺酰基)-2-甲基哌嗪 (H-7) 和蛋白激酶-C 抑制剂抑制中性粒细胞超氧化物形成。

DOI:
10.1016/0006-2952(86)90778-1
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发表时间:
1986
影响因子:
5.8
通讯作者:
S. Minakami
S. Minakami
中科院分区:
医学2区
文献类型:
--
作者:
I. Fujita;K. Takeshige;S. Minakami

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Superoxide formation of human neutrophils stimulated by phorbol 12-myristate 13-acetate (PMA),N-formyl-methionyl-leucyl-phenylalanine, or calcium ionophore A23187 was inhibited by pretreatment of the cells with 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), an inhibitor of protein kinase-C, but was not inhibited byN-(2-guanidinoethyl)-5-isoquinolinesulfonamide which has a less inhibitory effect on the protein kinase-C. H-7 also inhibited superoxide formation of PMA-activated cytoplasts, which lack nuclei and granules. The phosphorylation of proteins induced by PMA in the cytoplasts as well as the intact neutrophils was also inhibited by preincubation with H-7. Among several phosphoproteins affected by H-7, one protein with a molecular weight of 19,000 (pI= 4.9) was inhibited markedly.N-(2-Guanidinoethyl)-5-isoquinolinesulfonamide did not inhibit the phosphorylation of proteins induced by PMA. These findings support the possibility that the protein kinase-C is involved in the activation process of superoxide formation.
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