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首页> 外文期刊>Molecular and Cellular Biology >Phenotypic change from transformed to normal induced by benzoquinonoid ansamycins accompanies inactivation of p60src in rat kidney cells infected with Rous sarcoma virus.
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Phenotypic change from transformed to normal induced by benzoquinonoid ansamycins accompanies inactivation of p60src in rat kidney cells infected with Rous sarcoma virus.

机译：表型变化由苯醌醌类安沙霉素诱导的转化为正常伴随着被劳斯肉瘤病毒感染的大鼠肾细胞中的p60src失活。

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Three benzenoid ansamycin antibiotics (herbimycin, macbecin, and geldanamycin) were found to reduce the intracellular phosphorylation of p60src at a permissive temperature (33 degrees C) in a rat kidney cell line infected with a temperature-sensitive mutant of Rous sarcoma virus. This effect was accompanied by morphological changes from the transformed to the normal phenotype. The filamentous staining pattern of actin fibers was observed in the cells treated with these antibiotics at 33 degrees C. Removal of the antibiotics allowed the cells to revert to the transformed morphology. Ansamitocin, another benzenoid ansamycin, and naphthalenoid ansamycins such as streptovaricin and rifamycins did not show this effect. Pulse-labeling of the antibiotic-treated cultures with 32Pi showed a marked reduction of 32P radioactivity incorporated into p60src. A parallel experiment with [35S]methionine showed that synthesis of p60src was slightly inhibited. The immune complex prepared by mixing the herbimycin-treated cell extracts with antibody against p60src was inactive in vitro in phosphorylating the complex itself. On the contrary, the immune complex derived from untreated cells was active in vitro even in the presence of the antibiotics. These results suggest that benzoquinonoid ansamycins have no direct effect on src kinase but destroy its intracellular environment, resulting in an irreversible alteration of p60src and loss of catalytic activity.
机译：发现在允许的温度（33摄氏度）下，在感染了对温度敏感的劳斯肉瘤病毒突变的大鼠肾细胞系中，三种苯并安沙霉素抗生素（herbimycin，macbecin和geldanamycin）可降低p60src的细胞内磷酸化。这种作用伴随着从转化表型到正常表型的形态变化。在33℃下用这些抗生素处理的细胞中观察到肌动蛋白纤维的丝状染色模式。去除抗生素使细胞回复到转化的形态。 Ansamitocin，另一种Benzenoid Ansamycin和萘类Ansamycins（如链霉素和利福霉素）均未显示此作用。用32Pi对经抗生素处理的培养物进行脉冲标记显示掺入p60src的32P放射性显着降低。 [35S]蛋氨酸的平行实验表明，p60src的合成受到轻微抑制。通过将除草霉素处理的细胞提取物与针对p60src的抗体混合而制备的免疫复合物在体外使复合物本身磷酸化，从而失活。相反，即使在存在抗生素的情况下，源自未处理细胞的免疫复合物在体外仍具有活性。这些结果表明苯醌醌类安沙霉素对src激酶没有直接作用，但破坏了其细胞内环境，导致p60src的不可逆改变和催化活性的丧失。

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