首页> 美国卫生研究院文献>Antimicrobial Agents and Chemotherapy >Selective repression of v-abl-encoded protein by N-methylisatin-beta-44-diethylthiosemicarbazone and N-allylisatin-beta-44-diallylthiosemicarbazone.
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Selective repression of v-abl-encoded protein by N-methylisatin-beta-44-diethylthiosemicarbazone and N-allylisatin-beta-44-diallylthiosemicarbazone.

机译:N-甲基异丁香素-β-44-二乙基硫代半乳糖苷和N-烯丙基异丁香素-β-44-二烯丙基硫代半碳素选择性抑制v-abl编码的蛋白。

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摘要

N-Methylisatin-beta-4',4'-diethylthiosemicarbazone (M-IBDET) and N-allylisatin-beta-4',4'-diallylthiosemicarbazone (A-IBDAT) selectively inhibited v-abl protein (P120), an oncogene product associated with tyrosine kinase activity. Concentrations of M-IBDET ranging between 0.17 and 0.64 microM and concentrations of A-IBDAT from 1.45 to 2.9 microM reduced tyrosine kinase activity significantly, whereas 0.64 microM M-IBDET and 2.9 microM A-IBDAT blocked P120 production. Cellular growth rate, protein production, and synthesis of p45 actin and p53 nuclear oncogene were not affected at these conditions. M-IBDET and A-IBDAT selectively suppress the v-abl oncogene as well as Moloney murine leukemia virus production.
机译:N-甲基异丁香素-β-4',4'-二乙基硫代半乳糖苷(M-IBDET)和N-烯丙基异丁香素-β-4',4'-二烯丙基硫代半胱氨酸(A-IBDAT)选择性抑制癌基因产物v-abl蛋白(P120)与酪氨酸激酶活性有关。 M-IBDET的浓度在0.17至0.64 microM之间,A-IBDAT的浓度从1.45至2.9 microM显着降低酪氨酸激酶活性,而0.64 microM M-IBDET和2.9 microM A-IBDAT阻止P120的产生。在这些条件下,细胞生长速率,蛋白质产生以及p45肌动蛋白和p53核癌基因的合成均不受影响。 M-IBDET和A-IBDAT选择性抑制v-abl癌基因以及莫洛尼氏鼠白血病病毒的产生。

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