Transformation of NIH 3T3 cells by HER3 or HER4 receptors requires the presence of HER1 or HER2
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Interactions among genes in the ErbB-Neuregulin signalling network are associated with increased susceptibility to schizophreniaThe HER2 Receptor in Breast Cancer: Pathophysiology, Clinical Use, and New Advances in TherapyA natural ErbB4 isoform that does not activate phosphoinositide 3-kinase mediates proliferation but not survival or chemotaxisCripto enhances the tyrosine phosphorylation of Shc and activates mitogen-activated protein kinase (MAPK) in mammary epithelial cellsActivation of HER4 by heparin-binding EGF-like growth factor stimulates chemotaxis but not proliferationAnalysis of Grb7 recruitment by heregulin-activated erbB receptors reveals a novel target selectivity for erbB3ErbB-1 and ErbB-2 acquire distinct signaling properties dependent upon their dimerization partner.Essential role for Rac in heregulin beta1 mitogenic signaling: a mechanism that involves epidermal growth factor receptor and is independent of ErbB4.Interaction of the PA2G4 (EBP1) protein with ErbB-3 and regulation of this binding by heregulinPI3K mutations in breast cancer: prognostic and therapeutic implicationsThe Wilms' tumor gene product WT1 mediates the down-regulation of the rat epidermal growth factor receptor by nerve growth factor in PC12 cellsThe relationship between human epidermal growth-like factor receptor expression and cellular transformation in NIH3T3 cellsControlled dimerization of ErbB receptors provides evidence for differential signaling by homo- and heterodimersThe ErbB signaling network: receptor heterodimerization in development and cancerA novel putative protein-tyrosine phosphatase contains a BRO1-like domain and suppresses Ha-ras-mediated transformation.Activation of ErbB3-PI3-kinase pathway is correlated with malignant phenotypes of adenocarcinomas.Take your partners, please--signal diversification by the erbB family of receptor tyrosine kinases.Glial-neuronal interactions in the neuroendocrine control of mammalian puberty: facilitatory effects of gonadal steroids.ErbB tyrosine kinases and the two neuregulin families constitute a ligand-receptor network.Activation of the Ras/mitogen-activated protein kinase pathway by kinase-defective epidermal growth factor receptors results in cell survival but not proliferation.ErbB-2, the preferred heterodimerization partner of all ErbB receptors, is a mediator of lateral signaling.Differential endocytic routing of homo- and hetero-dimeric ErbB tyrosine kinases confers signaling superiority to receptor heterodimers.Elevated expression of activated forms of Neu/ErbB-2 and ErbB-3 are involved in the induction of mammary tumors in transgenic mice: implications for human breast cancerThe C-terminus of the kinase-defective neuregulin receptor ErbB-3 confers mitogenic superiority and dictates endocytic routing.Ectopic expression of the ErbB-3 binding protein ebp1 inhibits growth and induces differentiation of human breast cancer cell lines.ErbB2 potentiates breast tumor proliferation through modulation of p27(Kip1)-Cdk2 complex formation: receptor overexpression does not determine growth dependencyDifferential regulation of tumor angiogenesis by distinct ErbB homo- and heterodimersThe role of HER3, the unpretentious member of the HER family, in cancer biology and cancer therapeutics.Extracellular domains drive homo- but not hetero-dimerization of erbB receptorsResiliency and vulnerability in the HER2-HER3 tumorigenic driver.A system for quantifying dynamic protein interactions defines a role for Herceptin in modulating ErbB2 interactions.Modeling the effects of HER/ErbB1-3 coexpression on receptor dimerization and biological responseTime-resolved fluorescence resonance energy transfer (TR-FRET) to analyze the disruption of EGFR/HER2 dimers: a new method to evaluate the efficiency of targeted therapy using monoclonal antibodiesProfiling epidermal growth factor receptor and heregulin receptor 3 heteromerization using receptor tyrosine kinase heteromer investigation technology.Protein kinases in mammary gland development and cancer.Mechanism in the sequential control of cell morphology and S phase entry by epidermal growth factor involves distinct MEK/ERK activations.Developing inhibitors of the epidermal growth factor receptor for cancer treatment.The ErbB4 CYT2 variant protects EGFR from ligand-induced degradation to enhance cancer cell motility.Combining anti-ERBB3 antibodies specific for domain I and domain III enhances the anti-tumor activity over the individual monoclonal antibodiesHeregulin negatively regulates transcription of ErbB2/3 receptors via an AKT-mediated pathway
P2860
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P2860
Transformation of NIH 3T3 cells by HER3 or HER4 receptors requires the presence of HER1 or HER2
description
1996 nî lūn-bûn
@nan
1996 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
1996 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
1996年の論文
@ja
1996年論文
@yue
1996年論文
@zh-hant
1996年論文
@zh-hk
1996年論文
@zh-mo
1996年論文
@zh-tw
1996年论文
@wuu
name
Transformation of NIH 3T3 cell ...... s the presence of HER1 or HER2
@ast
Transformation of NIH 3T3 cell ...... s the presence of HER1 or HER2
@en
Transformation of NIH 3T3 cell ...... s the presence of HER1 or HER2
@nl
type
label
Transformation of NIH 3T3 cell ...... s the presence of HER1 or HER2
@ast
Transformation of NIH 3T3 cell ...... s the presence of HER1 or HER2
@en
Transformation of NIH 3T3 cell ...... s the presence of HER1 or HER2
@nl
prefLabel
Transformation of NIH 3T3 cell ...... s the presence of HER1 or HER2
@ast
Transformation of NIH 3T3 cell ...... s the presence of HER1 or HER2
@en
Transformation of NIH 3T3 cell ...... s the presence of HER1 or HER2
@nl
P2093
P2860
P356
P1476
Transformation of NIH 3T3 cell ...... s the presence of HER1 or HER2
@en
P2093
A Thomason
S K Yoshinaga
P2860
P304
P356
10.1074/JBC.271.7.3884
P407
P577
1996-02-16T00:00:00Z