• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

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。

相似文献

1
Src homology 2 domain deletion mutants of p60v-src do not phosphorylate cellular proteins of 120-150 kDa.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。
Oncogene. 1989 Feb;4(2):231-6.
2
Most of the substrates of oncogenic viral tyrosine protein kinases can be phosphorylated by cellular tyrosine protein kinases in normal cells.致癌病毒酪氨酸蛋白激酶的大多数底物在正常细胞中可被细胞酪氨酸蛋白激酶磷酸化。
Oncogene Res. 1988 Sep;3(2):105-15.
3
Localization of major potential substrates of p60v-src kinase in the plasma membrane matrix fraction.p60v-src激酶主要潜在底物在质膜基质组分中的定位。
Oncogene Res. 1989;4(1):29-37.
4
From c-src to v-src, or the case of the missing C terminus.从c-src到v-src,或者C端缺失的情况。
Cancer Surv. 1986;5(2):159-72.
5
Reduced phosphotyrosine binding by the v-Src SH2 domain is compatible with wild-type transformation.v-Src SH2结构域降低的磷酸酪氨酸结合能力与野生型转化兼容。
Oncogene. 1996 Feb 15;12(4):727-34.
6
Structural and functional motifs of the Rous sarcoma virus src protein.劳氏肉瘤病毒src蛋白的结构和功能基序
Gene Amplif Anal. 1986;4:1-19.
7
Deletional analysis of the N-terminal half of the lyn gene.对lyn基因N端一半区域的缺失分析。
Kobe J Med Sci. 1990 Dec;36(5-6):137-51.
8
Augmentation of metalloproteinase (gelatinase) activity secreted from Rous sarcoma virus-infected cells correlates with transforming activity of src.
Oncogene. 1995 Mar 16;10(6):1037-43.
9
Correlation of V-src gene amplification with the tumorigenic phenotype in a Syrian hamster embryo cell line.叙利亚仓鼠胚胎细胞系中V-src基因扩增与致瘤表型的相关性
Cancer Res. 1987 Sep 1;47(17):4663-6.
10
Suppression of v-Src transformation in primary rat embryo fibroblasts.原代大鼠胚胎成纤维细胞中v-Src转化的抑制
Oncogene. 1995 Jul 20;11(2):231-8.

引用本文的文献

1
A cell-based screen for inhibitors of protein folding and degradation.基于细胞的蛋白质折叠和降解抑制剂筛选。
Cell Stress Chaperones. 2010 Nov;15(6):913-27. doi: 10.1007/s12192-010-0200-3. Epub 2010 Aug 19.
2
CDC37 is required for p60v-src activity in yeast.CDC37是酵母中p60v-src活性所必需的。
Mol Biol Cell. 1996 Sep;7(9):1405-17. doi: 10.1091/mbc.7.9.1405.
3
The Ydj1 molecular chaperone facilitates formation of active p60v-src in yeast.Ydj1分子伴侣促进酵母中活性p60v-src的形成。
Mol Biol Cell. 1996 Jan;7(1):91-100. doi: 10.1091/mbc.7.1.91.
4
Expression of p60v-src in Saccharomyces cerevisiae results in elevation of p34CDC28 kinase activity and release of the dependence of DNA replication on mitosis.酿酒酵母中p60v-src的表达导致p34CDC28激酶活性升高,并解除DNA复制对有丝分裂的依赖性。
Mol Cell Biol. 1993 Aug;13(8):5112-21. doi: 10.1128/mcb.13.8.5112-5121.1993.
5
The common src homology region 2 domain of cytoplasmic signaling proteins is a positive effector of v-fps tyrosine kinase function.细胞质信号蛋白常见的src同源区域2结构域是v-fps酪氨酸激酶功能的正效应物。
Mol Cell Biol. 1989 Oct;9(10):4131-40. doi: 10.1128/mcb.9.10.4131-4140.1989.
6
A glycoprotein in the plasma membrane matrix as a major potential substrate of p60v-src.一种存在于质膜基质中的糖蛋白,是p60v-src的主要潜在底物。
Mol Cell Biol. 1990 Feb;10(2):830-6. doi: 10.1128/mcb.10.2.830-836.1990.
7
Activation of the proto-oncogene p60c-src by point mutations in the SH2 domain.通过SH2结构域中的点突变激活原癌基因p60c-src。
Mol Cell Biol. 1990 Jun;10(6):2855-62. doi: 10.1128/mcb.10.6.2855-2862.1990.
8
Identification and characterization of a novel cytoskeleton-associated pp60src substrate.一种新型细胞骨架相关pp60src底物的鉴定与表征
Mol Cell Biol. 1991 Oct;11(10):5113-24. doi: 10.1128/mcb.11.10.5113-5124.1991.
9
Regulation of the oncogenic activity of the cellular src protein requires the correct spacing between the kinase domain and the C-terminal phosphorylated tyrosine (Tyr-527).细胞src蛋白致癌活性的调控需要激酶结构域与C末端磷酸化酪氨酸(Tyr-527)之间有正确的间距。
Mol Cell Biol. 1991 Dec;11(12):5832-8. doi: 10.1128/mcb.11.12.5832-5838.1991.
10
The SH2 and SH3 domains of pp60src direct stable association with tyrosine phosphorylated proteins p130 and p110.pp60src的SH2和SH3结构域介导与酪氨酸磷酸化蛋白p130和p110的稳定结合。
EMBO J. 1991 Jul;10(7):1689-98. doi: 10.1002/j.1460-2075.1991.tb07693.x.