Uehara Y, Fukazawa H, Murakami Y, Mizuno S
Department of Antibiotics, National Institute of Health, Tokyo, Japan.
Biochem Biophys Res Commun. 1989 Sep 15;163(2):803-9. doi: 10.1016/0006-291x(89)92293-6.
Herbimycin A, an antibiotic which reverses Rous sarcoma virus transformation, inhibited irreversibly the auto- and trans-phosphorylation activities of p60v-src in in vitro immune complex kinase assays. The addition of a sulfhydryl compound such as dithiothreitol, 2-mercaptoethanol, glutathione (reduced form) or cysteine abolished the ability of herbimycin A to inactivate p60v-src kinase as well as the ability to reverse transformed cell morphology, whereas the addition of oxidized glutathione, cystine or methionine showed no effect. The sulfhydryl alkylating reagent N-ethylmaleimide also, although less effectively, inactivated p60v-src kinase activity in vitro. These results suggest the likelihood that sulfhydryl groups of p60v-src are involved in the inactivation of v-src tyrosine kinase activity by herbimycin A.
除草菌素A是一种能逆转劳氏肉瘤病毒转化的抗生素，在体外免疫复合物激酶试验中，它不可逆地抑制了p60v-src的自身磷酸化和转磷酸化活性。添加巯基化合物，如二硫苏糖醇、2-巯基乙醇、谷胱甘肽（还原型）或半胱氨酸，可消除除草菌素A使p60v-src激酶失活的能力以及逆转转化细胞形态的能力，而添加氧化型谷胱甘肽、胱氨酸或蛋氨酸则无此作用。巯基烷基化试剂N-乙基马来酰亚胺在体外也能使p60v-src激酶活性失活，尽管效果较差。这些结果表明，p60v-src的巯基可能参与了除草菌素A对v-src酪氨酸激酶活性的失活过程。
