P60(V-SRC) CAUSES TYROSINE PHOSPHORYLATION AND INACTIVATION OF THE N-CADHERIN CATENIN CELL-ADHESION SYSTEM
P60(V-SRC) CAUSES TYROSINE PHOSPHORYLATION AND INACTIVATION OF THE N-CADHERIN CATENIN CELL-ADHESION SYSTEM
复制标题
DOI：
10.1002/j.1460-2075.1993.tb05658.x
复制
发表时间：
1993-01-01
期刊：
影响因子：
11.4
通讯作者：
NAGAI, Y
中科院分区：
文献类型：
--
作者：
HAMAGUCHI, M;MATSUYOSHI, N;NAGAI, Y
Rous肉瘤病毒转化鸡胚胎成纤维细胞可强烈抑制N-钙粘附素介导的细胞-细胞黏附，但不抑制其表达。这种抑制与N-钙粘蛋白和连环素的酪氨酸磷酸化有关，这两种与钙粘附素相关的蛋白质被认为是调节钙粘附素功能的蛋白。用RSV的非肉豆蔻化和温度敏感突变体以及有效的酪氨酸激酶抑制剂Herbimycin A进行的实验表明，对细胞黏附的抑制和连环蛋白的酪氨酸磷酸化都是高度转化特异性的。
Transformation of chick embryonic fibroblasts with Rous sarcoma virus strongly suppresses N-cadherin-mediated cell-cell adhesion, without inhibiting its expression. This suppression is correlated with tyrosine phosphorylation of N-cadherin and catenins, the cadherin-associated proteins, which are known to regulate cadherin function. Experiments with non-myristylation and temperature-sensitive mutants of RSV and with herbimycin A, a potent inhibitor of tyrosine kinases, suggest that both the suppression of cell adhesion and tyrosine phosphorylation of catenins are highly transformation-specific.