Overexpressed pp60c-src can induce focus formation without complete transformation of NIH 3T3 cells.
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A phosphotyrosine displacement mechanism for activation of Src by PTPalphaActivation of Src and transformation by an RPTPα splice mutant found in human tumoursMutational analysis of the Src SH3 domain: the same residues of the ligand binding surface are important for intra- and intermolecular interactionsThe hunting of the SrcTwo mechanisms activate PTPalpha during mitosisNecdin, a negative growth regulator, is a novel STAT3 target gene down-regulated in human cancerPhosphotyrosyl peptides block Stat3-mediated DNA binding activity, gene regulation, and cell transformationSH3 domains specifically regulate kinase activity of expressed Src family proteins.Direct interaction of v-Src with the focal adhesion kinase mediated by the Src SH2 domain.Effects of SH2 and SH3 deletions on the functional activities of wild-type and transforming variants of c-Src.Selective binding of activated pp60c-src by an immobilized synthetic phosphopeptide modeled on the carboxyl terminus of pp60c-srcSequence and functional differences between Schmidt-Ruppin D and Schmidt-Ruppin A strains of pp60v-srcTyrosine phosphorylation of three cellular proteins correlates with transformation of rat 1 cells by pp60src.pp60c-src tyrosine kinase, myristylation, and modulatory domains are required for enhanced mitogenic responsiveness to epidermal growth factor seen in cells overexpressing c-srcAugmented mitogenic responsiveness to epidermal growth factor in murine fibroblasts that overexpress pp60c-src.Requirement for Ras/Rac1-mediated p38 and c-Jun N-terminal kinase signaling in Stat3 transcriptional activity induced by the Src oncoprotein.Selective chemical probe inhibitor of Stat3, identified through structure-based virtual screening, induces antitumor activity.Endogenous c-src as a determinant of the tumorigenicity of src oncogenes.A cell-permeable Stat3 SH2 domain mimetic inhibits Stat3 activation and induces antitumor cell effects in vitro.Global phosphoproteomics reveals crosstalk between Bcr-Abl and negative feedback mechanisms controlling Src signaling.pp60(v-src) induction of cyclin D1 requires collaborative interactions between the extracellular signal-regulated kinase, p38, and Jun kinase pathways. A role for cAMP response element-binding protein and activating transcription factor-2 in pp60(v-Role of Stat3 in regulating p53 expression and functionFRNK blocks v-Src-stimulated invasion and experimental metastases without effects on cell motility or growth.Monoclonal 1- and 3-Phosphohistidine Antibodies: New Tools to Study Histidine Phosphorylation.Opposing effects of a ras oncogene on growth factor-stimulated phosphoinositide hydrolysis: desensitization to platelet-derived growth factor and enhanced sensitivity to bradykinin.Oncogene activation of HIV-LTR-driven expression via the NF-kappa B binding sitesRole of the cytoplasmic tyrosines of beta 1A integrins in transformation by v-srcFocus formation: a cell-based assay to determine the oncogenic potential of a gene.A novel small-molecule disrupts Stat3 SH2 domain-phosphotyrosine interactions and Stat3-dependent tumor processesBlood platelets express high levels of the pp60c-src-specific tyrosine kinase activity.Phosphorylation of tyrosine in the carboxyl-terminal tryptic peptide of pp60c-src.Hirsutinolide Series Inhibit Stat3 Activity, Alter GCN1, MAP1B, Hsp105, G6PD, Vimentin, TrxR1, and Importin α-2 Expression, and Induce Antitumor Effects against Human Glioma.Highly specific antibody to Rous sarcoma virus src gene product recognizes nuclear and nucleolar antigens in human cellsPeptide antibodies to the human c-fyn gene product demonstrate pp59c-fyn is capable of complex formation with the middle-T antigen of polyomavirusMalignant transformation but not normal cell growth depends on signal transducer and activator of transcription 3.Immunolocalization of the cellular src protein in interphase and mitotic NIH c-src overexpresser cells.V-src kinase shifts the cadherin-based cell adhesion from the strong to the weak state and beta catenin is not required for the shift.Augmented expression of a myeloid-specific protein tyrosine kinase gene (hck) after macrophage activationRas transformation results in an elevated level of cyclin D1 and acceleration of G1 progression in NIH 3T3 cells.Insulin-like growth factor I receptor signaling in transformation by src oncogenes.
P2860
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P2860
Overexpressed pp60c-src can induce focus formation without complete transformation of NIH 3T3 cells.
description
1985 nî lūn-bûn
@nan
1985年の論文
@ja
1985年論文
@yue
1985年論文
@zh-hant
1985年論文
@zh-hk
1985年論文
@zh-mo
1985年論文
@zh-tw
1985年论文
@wuu
1985年论文
@zh
1985年论文
@zh-cn
name
Overexpressed pp60c-src can in ...... ansformation of NIH 3T3 cells.
@en
type
label
Overexpressed pp60c-src can in ...... ansformation of NIH 3T3 cells.
@en
prefLabel
Overexpressed pp60c-src can in ...... ansformation of NIH 3T3 cells.
@en
P2093
P2860
P356
P1476
Overexpressed pp60c-src can in ...... ansformation of NIH 3T3 cells.
@en
P2093
D Shalloway
P J Johnson
P M Coussens
P2860
P304
P356
10.1128/MCB.5.5.1073
P407
P577
1985-05-01T00:00:00Z