Taniguchi M, Uehara Y, Matsuyama M, Takahashi M
Department of Pathology, Nagoya University School of Medicine, Japan.
Biochem Biophys Res Commun. 1993 Aug 31;195(1):208-14. doi: 10.1006/bbrc.1993.2031.
We examined the effect of herbimycin A, a potent inhibitor of tyrosine kinases, on NIH(ret) cells and TPC-1 papillary thyroid carcinoma cells, both of which express the active ret genes. Herbimycin A reversed the morphology of NIH(ret) cells to flat cells with a concomitant reassembly of microfilament bundles. On the other hand, it did not induce a significant change in cell shape of TPC-1 cells. When tyrosine kinase activities of the active ret gene products in herbimycin A-treated NIH(ret) and TPC-1 cells were examined in immunocomplex kinase assays, they drastically decreased in both cells as compared with untreated cells. In addition, herbimycin A strongly inhibited tyrosine phosphorylation of 40 kDa and 31 kDa proteins present in the immunoprecipitates of both cells, suggesting that these proteins could associate with the Ret proteins.
我们研究了酪氨酸激酶的强效抑制剂赫伯霉素A对NIH(ret)细胞和TPC-1甲状腺乳头状癌细胞的影响，这两种细胞均表达活性ret基因。赫伯霉素A使NIH(ret)细胞的形态逆转成扁平细胞，同时微丝束重新组装。另一方面，它并未诱导TPC-1细胞的细胞形态发生显著变化。当通过免疫复合物激酶测定法检测经赫伯霉素A处理的NIH(ret)和TPC-1细胞中活性ret基因产物的酪氨酸激酶活性时，与未处理细胞相比，两种细胞中的酪氨酸激酶活性均大幅降低。此外，赫伯霉素A强烈抑制两种细胞免疫沉淀物中存在的40 kDa和31 kDa蛋白质的酪氨酸磷酸化，表明这些蛋白质可能与Ret蛋白相关。
