• 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

在表达v-src宿主范围和激酶活性、转化缺陷等位基因的大鼠和鸡细胞中，转化和pp60v-src自身磷酸化与SHC-GRB2复合物形成相关。

Transformation and pp60v-src autophosphorylation correlate with SHC-GRB2 complex formation in rat and chicken cells expressing host-range and kinase-active, transformation-defective alleles of v-src.

作者信息

Verderame M F, Guan J L, Woods Ignatoski K M

机构信息

Department of Microbiology and Immunology, Pennsylvania State University College of Medicine, Hershey 17033, USA.

出版信息

Mol Biol Cell. 1995 Aug;6(8):953-66. doi: 10.1091/mbc.6.8.953.

DOI:10.1091/mbc.6.8.953
PMID:7579711
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC301255/
Abstract

The biochemical properties of several pp60v-src substrates believed to participate in src-mediated transformation were examined in cells expressing a kinase-active, transformation-defective v-src allele (v-src-F172 delta/Y416F) and its parental allele, v-src-F172 delta, a host-range--dependent allele that transforms chicken cells to a fusiform morphology, but does not transform rat cells. Because pp60v-src-F172 delta is dependent on autophosphorylation for transforming ability, these alleles provide a unique opportunity to examine the role of pp60v-src autophosphorylation in regulating substrate interactions. Increased pp125FAK tyrosine phosphorylation and high levels of pp60v-src-associated phosphotidylinositol-3' kinase activity were detected specifically in chicken cells exhibiting round, refractile transformation but not in cells transformed to a fusiform morphology. Increased pp125FAK kinase activity, but not increased pp125FAK tyrosine-phosphorylation correlated with pp60v-src autophosphorylation and increased anchorage-independent growth. Thus, pp125FAK and PI3'K may participate in morphological transformation by v-src. Furthermore, association of phosphorylated SHC with the adapter GRB2 correlated with increased anchorage-independent growth (and autophosphorylation) in both rat and chicken cells independent of the morphological phenotype induced. Therefore, host-range dependence for transformation may be regulated through association of SHC with GRB2, thus implicating SHC as a crucial substrate for src-dependent transformation.

摘要

在表达激酶活性、转化缺陷型v-src等位基因（v-src-F172δ/Y416F）及其亲本等位基因v-src-F172δ的细胞中，研究了几种被认为参与src介导转化的pp60v-src底物的生化特性。v-src-F172δ是一种宿主范围依赖性等位基因，可将鸡细胞转化为梭形形态，但不能转化大鼠细胞。由于pp60v-src-F172δ的转化能力依赖于自身磷酸化，这些等位基因为研究pp60v-src自身磷酸化在调节底物相互作用中的作用提供了独特的机会。在呈现圆形、折光性转化的鸡细胞中特异性检测到pp125FAK酪氨酸磷酸化增加和高水平的pp60v-src相关磷脂酰肌醇-3'激酶活性，但在转化为梭形形态的细胞中未检测到。pp125FAK激酶活性增加，但pp125FAK酪氨酸磷酸化增加与pp60v-src自身磷酸化和锚定非依赖性生长增加无关。因此，pp125FAK和PI3'K可能参与v-src介导的形态转化。此外，磷酸化的SHC与衔接子GRB2的结合与大鼠和鸡细胞中锚定非依赖性生长增加（和自身磷酸化）相关，与诱导的形态表型无关。因此，转化的宿主范围依赖性可能通过SHC与GRB2的结合来调节，从而表明SHC是src依赖性转化的关键底物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd0/301255/0f611a575163/mbc00077-0023-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd0/301255/8c196f0ad63c/mbc00077-0016-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd0/301255/1ea8e94a6b49/mbc00077-0016-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd0/301255/49700022039e/mbc00077-0017-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd0/301255/e866f24e63a8/mbc00077-0018-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd0/301255/1277d2b7a941/mbc00077-0019-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd0/301255/570c697342f6/mbc00077-0020-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd0/301255/a92a686408b6/mbc00077-0020-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd0/301255/f2e151d87b80/mbc00077-0021-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd0/301255/0f611a575163/mbc00077-0023-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd0/301255/8c196f0ad63c/mbc00077-0016-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd0/301255/1ea8e94a6b49/mbc00077-0016-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd0/301255/49700022039e/mbc00077-0017-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd0/301255/e866f24e63a8/mbc00077-0018-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd0/301255/1277d2b7a941/mbc00077-0019-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd0/301255/570c697342f6/mbc00077-0020-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd0/301255/a92a686408b6/mbc00077-0020-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd0/301255/f2e151d87b80/mbc00077-0021-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fdd0/301255/0f611a575163/mbc00077-0023-a.jpg

相似文献

1
Transformation and pp60v-src autophosphorylation correlate with SHC-GRB2 complex formation in rat and chicken cells expressing host-range and kinase-active, transformation-defective alleles of v-src.在表达v-src宿主范围和激酶活性、转化缺陷等位基因的大鼠和鸡细胞中，转化和pp60v-src自身磷酸化与SHC-GRB2复合物形成相关。
Mol Biol Cell. 1995 Aug;6(8):953-66. doi: 10.1091/mbc.6.8.953.
2
Multiple Grb2-mediated integrin-stimulated signaling pathways to ERK2/mitogen-activated protein kinase: summation of both c-Src- and focal adhesion kinase-initiated tyrosine phosphorylation events.多条由Grb2介导的整合素刺激的信号通路至ERK2/丝裂原活化蛋白激酶：c-Src和粘着斑激酶启动的酪氨酸磷酸化事件的总和。
Mol Cell Biol. 1998 May;18(5):2571-85. doi: 10.1128/MCB.18.5.2571.
3
Autophosphorylation is required for high kinase activity and efficient transformation ability of proteins encoded by host range alleles of v-src.自身磷酸化是v-src宿主范围等位基因编码蛋白的高激酶活性和有效转化能力所必需的。
J Virol. 1994 Nov;68(11):7267-74. doi: 10.1128/JVI.68.11.7267-7274.1994.
4
v-Src-induced degradation of focal adhesion kinase during morphological transformation of chicken embryo fibroblasts.v-Src诱导鸡胚成纤维细胞形态转化过程中粘着斑激酶的降解
Oncogene. 1995 Jun 1;10(11):2247-52.
5
G protein-coupled receptors mediate two functionally distinct pathways of tyrosine phosphorylation in rat 1a fibroblasts. Shc phosphorylation and receptor endocytosis correlate with activation of Erk kinases.G蛋白偶联受体介导大鼠1a成纤维细胞中两种功能不同的酪氨酸磷酸化途径。Shc磷酸化和受体内吞作用与Erk激酶的激活相关。
J Biol Chem. 1997 Dec 12;272(50):31648-56. doi: 10.1074/jbc.272.50.31648.
6
The Shc adaptor protein is highly phosphorylated at conserved, twin tyrosine residues (Y239/240) that mediate protein-protein interactions.Shc衔接蛋白在保守的双酪氨酸残基（Y239/240）处高度磷酸化，这些残基介导蛋白质-蛋白质相互作用。
Curr Biol. 1996 Nov 1;6(11):1435-44. doi: 10.1016/s0960-9822(96)00748-8.
7
Involvement of proline-rich tyrosine kinase 2 in platelet activation: tyrosine phosphorylation mostly dependent on alphaIIbbeta3 integrin and protein kinase C, translocation to the cytoskeleton and association with Shc through Grb2.富含脯氨酸的酪氨酸激酶2参与血小板活化：酪氨酸磷酸化主要依赖αIIbβ3整合素和蛋白激酶C，转位至细胞骨架并通过Grb2与Shc结合。
Biochem J. 2000 Apr 15;347(Pt 2):561-9. doi: 10.1042/0264-6021:3470561.
8
Intracellular targeting of pp60src expression: localization of v-src to adhesion plaques is sufficient to transform chicken embryo fibroblasts.pp60src 表达的细胞内靶向作用：v-src 定位于黏着斑足以转化鸡胚成纤维细胞。
Oncogene. 1992 Dec;7(12):2417-28.
9
Transformation by polyoma virus middle T-antigen involves the binding and tyrosine phosphorylation of Shc.多瘤病毒中T抗原介导的转化涉及Shc的结合和酪氨酸磷酸化。
Nature. 1994 Jan 6;367(6458):87-90. doi: 10.1038/367087a0.
10
Vascular endothelial growth factor induces activation and subcellular translocation of focal adhesion kinase (p125FAK) in cultured rat cardiac myocytes.血管内皮生长因子可诱导培养的大鼠心肌细胞中粘着斑激酶（p125FAK）的激活和亚细胞易位。
Circ Res. 1999 May 28;84(10):1194-202. doi: 10.1161/01.res.84.10.1194.

引用本文的文献

1
Constitutive phosphorylation of a Rac GAP MgcRacGAP is implicated in v-Src-induced transformation of NIH3T3 cells.一种Rac GAP蛋白MgcRacGAP的组成型磷酸化与v-Src诱导的NIH3T3细胞转化有关。
Cancer Sci. 2009 Sep;100(9):1675-9. doi: 10.1111/j.1349-7006.2009.01235.x. Epub 2009 May 31.
2
pp60v-src transformation of rat cells but not chicken cells strongly correlates with low-affinity phosphopeptide binding by the SH2 domain.pp60v-src对大鼠细胞而非鸡细胞的转化与SH2结构域的低亲和力磷酸肽结合密切相关。
Mol Biol Cell. 1997 May;8(5):843-54. doi: 10.1091/mbc.8.5.843.

本文引用的文献

1
Epidermal growth factor regulates p21ras through the formation of a complex of receptor, Grb2 adapter protein, and Sos nucleotide exchange factor.表皮生长因子通过形成受体、Grb2衔接蛋白和Sos核苷酸交换因子的复合物来调节p21ras。
Cell. 1993 May 7;73(3):611-20. doi: 10.1016/0092-8674(93)90146-h.
2
Guanine-nucleotide-releasing factor hSos1 binds to Grb2 and links receptor tyrosine kinases to Ras signalling.鸟嘌呤核苷酸释放因子hSos1与Grb2结合，并将受体酪氨酸激酶与Ras信号传导联系起来。
Nature. 1993 May 6;363(6424):85-8. doi: 10.1038/363085a0.
3
The SH2 and SH3 domains of mammalian Grb2 couple the EGF receptor to the Ras activator mSos1.
哺乳动物Grb2的SH2和SH3结构域将表皮生长因子（EGF）受体与Ras激活剂mSos1偶联起来。
Nature. 1993 May 6;363(6424):83-5. doi: 10.1038/363083a0.
4
Association of Sos Ras exchange protein with Grb2 is implicated in tyrosine kinase signal transduction and transformation.Sos Ras交换蛋白与Grb2的关联涉及酪氨酸激酶信号转导和细胞转化。
Nature. 1993 May 6;363(6424):45-51. doi: 10.1038/363045a0.
5
A Drosophila SH2-SH3 adaptor protein implicated in coupling the sevenless tyrosine kinase to an activator of Ras guanine nucleotide exchange, Sos.一种果蝇SH2-SH3衔接蛋白，参与将无翅酪氨酸激酶与Ras鸟嘌呤核苷酸交换激活剂Sos偶联。
Cell. 1993 Apr 9;73(1):179-91. doi: 10.1016/0092-8674(93)90170-u.
6
An SH3-SH2-SH3 protein is required for p21Ras1 activation and binds to sevenless and Sos proteins in vitro.一种SH3-SH2-SH3蛋白是p21Ras1激活所必需的，并且在体外与七号less和Sos蛋白结合。
Cell. 1993 Apr 9;73(1):169-77. doi: 10.1016/0092-8674(93)90169-q.
7
Grb2 mediates the EGF-dependent activation of guanine nucleotide exchange on Ras.Grb2介导表皮生长因子（EGF）依赖性的Ras鸟嘌呤核苷酸交换激活。
Nature. 1993 May 6;363(6424):88-92. doi: 10.1038/363088a0.
8
Herbimycin A inhibits the association of p60v-src with the cytoskeletal structure and with phosphatidylinositol 3' kinase.除莠霉素A抑制p60v-src与细胞骨架结构以及磷脂酰肌醇3'激酶的结合。
Oncogene. 1993 Mar;8(3):559-64.
9
Cell spreading on extracellular matrix proteins induces tyrosine phosphorylation of tensin.细胞在细胞外基质蛋白上的铺展可诱导张力蛋白的酪氨酸磷酸化。
J Biol Chem. 1993 Jul 15;268(20):14565-7.
10
Highly conserved amino acids in the SH2 and catalytic domains of v-src are altered in naturally occurring, transformation-defective alleles.在v-src的SH2结构域和催化结构域中高度保守的氨基酸在天然存在的、转化缺陷型等位基因中发生了改变。
Oncogene. 1994 Jan;9(1):175-82.