Effect of a dominant inhibitory Ha-ras mutation on mitogenic signal transduction in NIH 3T3 cells.
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Identification of a mammalian gene structurally and functionally related to the CDC25 gene of Saccharomyces cerevisiaeA Ras-GTPase-activating protein SH3-domain-binding proteinProtein binding and signaling properties of RIN1 suggest a unique effector functionTwo human cDNAs, including a homolog of Arabidopsis FUS6 (COP11), suppress G-protein- and mitogen-activated protein kinase-mediated signal transduction in yeast and mammalian cellsShc and Enigma are both required for mitogenic signaling by Ret/ptc2.Activation of extracellular signal-regulated kinase, ERK2, by p21ras oncoproteinTyrosine phosphorylation sites at amino acids 239 and 240 of Shc are involved in epidermal growth factor-induced mitogenic signaling that is distinct from Ras/mitogen-activated protein kinase activationBinding of NCK to SOS and activation of ras-dependent gene expressionThe Ras GTPase-activating protein (GAP) is an SH3 domain-binding protein and substrate for the Src-related tyrosine kinase, HckRapV12 antagonizes Ras-dependent activation of ERK1 and ERK2 by LPA and EGF in Rat-1 fibroblastsVav: a potential link between tyrosine kinases and ras-like GTPases in hematopoietic cell signaling.GTPase-activating protein SH2-SH3 domains induce gene expression in a Ras-dependent fashion.Myosin light chain kinase functions downstream of Ras/ERK to promote migration of urokinase-type plasminogen activator-stimulated cells in an integrin-selective manner.Regulation of tetradecanoyl phorbol acetate-induced responses in NIH 3T3 cells by GAP, the GTPase-activating protein associated with p21c-ras.Interferons block protein kinase C-dependent but not-independent activation of Raf-1 and mitogen-activated protein kinases and mitogenesis in NIH 3T3 cells.Epidermal growth factor receptor induced apoptosis: potentiation by inhibition of Ras signaling.Regulation of exit from quiescence by p27 and cyclin D1-CDK4.Modulation of molecular mechanisms involved in protein synthesis machinery as a new tool for the control of cell proliferation.The Ras/Raf signaling pathway is required for progression of mouse embryos through the two-cell stage.Complex formation between RAS and RAF and other protein kinasesExpression of proto-oncogenes in mouse eggs and preimplantation embryos.Cross-talk between different enhancer elements during mitogenic induction of the human stromelysin-1 gene.K-ras is an essential gene in the mouse with partial functional overlap with N-ras.A requirement for extracellular signal-regulated kinase (ERK) function in the activation of AP-1 by Ha-Ras, phorbol 12-myristate 13-acetate, and serum.Approaches to gene therapy of complex multigenic diseases: cancer as a model and implications for cardiovascular disease and diabetes.Molecular signal integration. Interplay between serine, threonine, and tyrosine phosphorylationRas mediates Src but not epidermal growth factor-receptor tyrosine kinase signaling pathways in GH4 neuroendocrine cells.Polyomavirus middle-sized tumor antigen modulates c-Jun phosphorylation and transcriptional activity.Ras activation of genes: Mob-1 as a model.A transformation in the mechanism by which the urokinase receptor signals provides a selection advantage for estrogen receptor-expressing breast cancer cells in the absence of estrogenMitogen-activated protein kinase-mediated Fas apoptotic signaling pathwayInterference with endogenous ras function inhibits cellular responses to wounding.The chemotactic response to PDGF-BB: evidence of a role for Ras.Signal transduction by nerve growth factor and fibroblast growth factor in PC12 cells requires a sequence of src and ras actions.Inhibition of myogenesis by the H-ras oncogene: implication of a role for protein kinase C.Involvement of the protein tyrosine phosphatase SHP-1 in Ras-mediated activation of the mitogen-activated protein kinase pathway.Ras-dependent and -independent pathways target the mitogen-activated protein kinase network in macrophages.A new function for a phosphotyrosine phosphatase: linking GRB2-Sos to a receptor tyrosine kinase.Two types of RAS mutants that dominantly interfere with activators of RAS.The Saccharomyces cerevisiae SDC25 C-domain gene product overcomes the dominant inhibitory activity of Ha-Ras Asn-17.
P2860
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P2860
Effect of a dominant inhibitory Ha-ras mutation on mitogenic signal transduction in NIH 3T3 cells.
description
1990 nî lūn-bûn
@nan
1990年の論文
@ja
1990年論文
@yue
1990年論文
@zh-hant
1990年論文
@zh-hk
1990年論文
@zh-mo
1990年論文
@zh-tw
1990年论文
@wuu
1990年论文
@zh
1990年论文
@zh-cn
name
Effect of a dominant inhibitor ...... transduction in NIH 3T3 cells.
@ast
Effect of a dominant inhibitor ...... transduction in NIH 3T3 cells.
@en
type
label
Effect of a dominant inhibitor ...... transduction in NIH 3T3 cells.
@ast
Effect of a dominant inhibitor ...... transduction in NIH 3T3 cells.
@en
prefLabel
Effect of a dominant inhibitor ...... transduction in NIH 3T3 cells.
@ast
Effect of a dominant inhibitor ...... transduction in NIH 3T3 cells.
@en
P2093
P2860
P356
P1476
Effect of a dominant inhibitor ...... transduction in NIH 3T3 cells.
@en
P2093
P2860
P304
P356
10.1128/MCB.10.10.5314
P407
P577
1990-10-01T00:00:00Z