Growth factors modify the epidermal growth factor receptor through multiple pathways.
Growth factors modify the epidermal growth factor receptor through multiple pathways.
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生长因子通过多种途径修饰表皮生长因子受体。
DOI：
10.1002/jcb.240340102
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发表时间：
1987
影响因子：
4
通讯作者：
Rosner,MR
中科院分区：
文献类型：
--
作者：
Friedman,BA;Rosner,MR
以前的研究结果表明，肿瘤促进剂通过激活蛋白激酶C改变表皮生长因子（EGF）受体的性质。二酰基甘油生成因子，如血小板衍生生长因子（PDGF）和p28 sis应该激活蛋白激酶C，并以类似的方式改变EGF受体的特性。为了直接测试蛋白激酶C在来自vsis转化细胞的培养基对EGF受体的作用中的参与，首先用不同浓度的肿瘤促进剂二丁酸佛波酯（PDBu）广泛处理瑞士3T3细胞。结果表明，至少有两种成分对来自v-sisttransformed细胞的培养基对EGF结合的作用起作用：一种赋予蛋白激酶C独立性的不稳定因子和一种似乎依赖于蛋白激酶C的稳定因子。第一种因子的作用不能被转化生长因子-β或EGF在存在或不存在PDGF的情况下模仿。第二种因子的作用类似于PDGF。这些发现表明，EGF受体的异源调节可以通过蛋白激酶C依赖性和非依赖性途径发生。
Previous results have shown that tumor promoters modify the properties of the epidermal growth factor (EGF) receptor through the activation of protein kinase C. Diacylglycerol‐generating factors such as platelet‐derived growth factor (PDGF) and p28sisshould activate protein kinase C and alter EGF receptor properties in a similar manner. To test directly the involvement of protein kinase C in the action of media from v‐sis‐transformed cells on the EGF receptor, Swiss 3T3 cells were first extensively treated with various concentrations of the tumor‐promoter phorbol dibutyrate (PDBu) This treatment reduced levels of active protein kinase C in the cells, making them less responsive to subsequent rechallenge with the tumor promoter. The results demonstrate that there are at least two components to the action of media from v‐sistransformed cells on EGF binding: a labile factor that confers protein kinase C independence and a stable factor that appears to be dependent on protein kinase C. The action of the first factor cannot be mimicked by transforming growth factor‐β or EGF in either the presence or absence of PDGF. The action of the second factor is similar to that of PDGF. These findings indicate that heterologous regulation of the EGF receptor can occur through both protein kinase C‐dependent and ‐independent pathways.