Opposing effects of a ras oncogene on growth factor-stimulated phosphoinositide hydrolysis: desensitization to platelet-derived growth factor and enhanced sensitivity to bradykinin.
about
Muscarinic acetylcholine receptor subtypes as agonist-dependent oncogenesPhosphorylation of the RAS2 gene product by protein kinase A inhibits the activation of yeast adenylyl cyclase.Malignant transformation by ras and other oncogenes produces common alterations in inositol phospholipid signaling pathwaysNIH-3T3 cells transformed by the EJ-ras oncogene exhibit reduced platelet-derived growth factor-mediated Ca2+ mobilization.p21ras-induced responsiveness of phosphatidylinositol turnover to bradykinin is a receptor number effect.Effects of ras-encoded proteins and platelet-derived growth factor on inositol phospholipid turnover in NRK cellsAntibody to phosphatidylinositol 4,5-bisphosphate inhibits oncogene-induced mitogenesis.Platelet-derived growth factor stimulates formation of active p21ras.GTP complex in Swiss mouse 3T3 cells.Accumulation of p21ras.GTP in response to stimulation with epidermal growth factor and oncogene products with tyrosine kinase activityDecreased susceptibility of a 70-kDa protein to cathepsin L after phosphorylation by protein kinase C.Effect of protein kinase P on phosphorylations catalyzed by the epidermal growth factorDeregulation of hamster fibroblast proliferation by mutated ras oncogenes is not mediated by constitutive activation of phosphoinositide-specific phospholipase C.Repression of platelet-derived growth factor beta-receptor expression by mitogenic growth factors and transforming oncogenes in murine 3T3 fibroblasts.Specific changes of Ras GTPase-activating protein (GAP) and a GAP-associated p62 protein during calcium-induced keratinocyte differentiationAlterations of G-protein coupling function in phosphoinositide signaling pathways of cells transformed by ras and other membrane-associated and cytoplasmic oncogenes.Antisense-fos RNA causes partial reversion of the transformed phenotypes induced by the c-Ha-ras oncogene.P21 v-ras inhibits induction of c-myc and c-fos expression by platelet-derived growth factor.The biochemistry of ras p21.An overview of tumor biology.Receptor-phosphoinositidase C coupling. Multiple G-proteins?Loss of responsiveness of an AP1-related factor, PEBP1, to 12-O-tetradecanoylphorbol-13-acetate after transformation of NIH 3T3 cells by the Ha-ras oncogene.Possible involvement of normal p21 H-ras in the insulin/insulinlike growth factor 1 signal transduction pathway.High-level expression of c-H-ras1 fails to fully transform rat-1 cells.Desensitization of the Ca2+-mobilizing system to serum growth factors by Ha-ras and v-mos.Involvement of a phosphotyrosine protein phosphatase in the suppression of platelet-derived growth factor receptor autophosphorylation in ras-transformed cells.NIH-3T3 cells transformed with a ras oncogene exhibit a protein kinase C-mediated inhibition of agonist-stimulated Ca2+ inflow.Loss of bradykinin receptors and TPA-stimulated Na+ influx in SV40-transformed WI-38 cells.Desensitization of prostaglandin F2 alpha-stimulated inositol phosphate generation in NIH-3T3 fibroblasts transformed by overexpression of normal c-Ha-ras-1, c-Ki-ras-2 and c-N-ras genes.Regulation of bradykinin receptor level by cholera toxin, pertussis toxin and forskolin in cultured human fibroblasts.Transfection of insulin-producing cells with a transforming c-Ha-ras oncogene stimulates phospholipase C activity.Signal transduction in EJ-H-ras-transformed cells: de novo synthesis of diacylglycerol and subversion of agonist-stimulated inositol lipid metabolism.Scrape-loaded p21ras down-regulates agonist-stimulated inositol phosphate production by a mechanism involving protein kinase C.Differential sensitivity to pertussis toxin of 3T3 cells transformed with different oncogenes.Effects of bradykinin on cell volume and intracellular pH in NIH 3T3 fibroblasts expressing the ras oncogene.Interference of Ha-ras with inositol trisphosphate-mediated Ca(2+)-release.Upregulation of tissue kallikrein, kinin B1 receptor, and kinin B2 receptor in mast and giant cells infiltrating oesophageal squamous cell carcinoma.
P2860
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P2860
Opposing effects of a ras oncogene on growth factor-stimulated phosphoinositide hydrolysis: desensitization to platelet-derived growth factor and enhanced sensitivity to bradykinin.
description
1987 nî lūn-bûn
@nan
1987 թուականի Մայիսին հրատարակուած գիտական յօդուած
@hyw
1987 թվականի մայիսին հրատարակված գիտական հոդված
@hy
1987年の論文
@ja
1987年論文
@yue
1987年論文
@zh-hant
1987年論文
@zh-hk
1987年論文
@zh-mo
1987年論文
@zh-tw
1987年论文
@wuu
name
Opposing effects of a ras onco ...... ced sensitivity to bradykinin.
@ast
Opposing effects of a ras onco ...... ced sensitivity to bradykinin.
@en
Opposing effects of a ras onco ...... ced sensitivity to bradykinin.
@nl
type
label
Opposing effects of a ras onco ...... ced sensitivity to bradykinin.
@ast
Opposing effects of a ras onco ...... ced sensitivity to bradykinin.
@en
Opposing effects of a ras onco ...... ced sensitivity to bradykinin.
@nl
prefLabel
Opposing effects of a ras onco ...... ced sensitivity to bradykinin.
@ast
Opposing effects of a ras onco ...... ced sensitivity to bradykinin.
@en
Opposing effects of a ras onco ...... ced sensitivity to bradykinin.
@nl
P2093
P2860
P356
P1476
Opposing effects of a ras onco ...... ced sensitivity to bradykinin.
@en
P2093
P2860
P304
P356
10.1073/PNAS.84.9.2648
P407
P577
1987-05-01T00:00:00Z