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  • Title: Inhibition of neutrophil superoxide formation by 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), and inhibitor of protein kinase-C.
    Author: Fujita I, Takeshige K, Minakami S.
    Journal: Biochem Pharmacol; 1986 Dec 15; 35(24):4555-62. PubMed ID: 3024655.
    Abstract:
    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 by N-(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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