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p60v-src的Src同源2结构域缺失突变体不会使120 - 150 kDa的细胞蛋白磷酸化。

Src homology 2 domain deletion mutants of p60v-src do not phosphorylate cellular proteins of 120-150 kDa.

作者信息

Wendler P A, Boschelli F

机构信息

Department of Biology, Massachusetts Institute of Technology, Cambridge 02139.

出版信息

Oncogene. 1989 Feb;4(2):231-6.

PMID:2494631
Abstract

We have constructed seven deletions in the src homology 2 (SH2) domain of the Rous sarcoma virus src gene and have expressed them and wild-type v-src (wt v-src) in Rat 1 fibroblasts. Transfected cells containing mutant DNAs have reduced focus forming activity when compared to cells containing the wt v-src DNA. In most cases, established cell lines that express these mutants have altered growth properties in soft agar. The src proteins isolated from mutant cell lines have reduced tyrosine kinase activity. We also see differences in the phosphorylation of cellular proteins in vivo. Unlike the wt protein kinase, the SH2 domain mutant kinases do not phosphorylate a set of cellular proteins ranging in size from 120-150 kDa.

摘要

我们在劳氏肉瘤病毒src基因的src同源2(SH2)结构域构建了7个缺失突变体,并在大鼠1型成纤维细胞中表达了这些突变体以及野生型v-src(wt v-src)。与含有wt v-src DNA的细胞相比,含有突变DNA的转染细胞形成集落的活性降低。在大多数情况下,表达这些突变体的已建立细胞系在软琼脂中的生长特性发生了改变。从突变细胞系中分离出的src蛋白酪氨酸激酶活性降低。我们还观察到体内细胞蛋白磷酸化的差异。与wt蛋白激酶不同,SH2结构域突变激酶不会磷酸化一组大小在120 - 150 kDa之间的细胞蛋白。

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