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[PMID]:23908351
[Au] Autor:Petti LM; Talbert-Slagle K; Hochstrasser ML; DiMaio D
[Ad] Endereço:From the Department of Genetics, Department of Molecular Biophysics and Biochemistry, Department of Therapeutic Radiology.
[Ti] Título:A single amino acid substitution converts a transmembrane protein activator of the platelet-derived growth factor ß receptor into an inhibitor.
[So] Source:J Biol Chem;288(38):27273-86, 2013 Sep 20.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Receptors for PDGF play an important role in cell proliferation and migration and have been implicated in certain cancers. The 44-amino acid E5 protein of bovine papillomavirus binds to and activates the PDGFß receptor (PDGFßR), resulting in oncogenic transformation of cultured fibroblasts. Previously, we isolated an artificial 36-amino acid transmembrane protein, pTM36-4, which transforms cells because of its ability to activate the PDGFßR despite limited sequence similarity to E5. Here, we demonstrated complex formation between the PDGFßR and three pTM36-4 mutants: T21E, T21Q, and T21N. T21Q retained wild type transforming activity and activated the PDGFßR in a ligand-independent manner as a consequence of binding to the transmembrane domain of the PDGFßR, but T21E and T21N were severely defective. In fact, T21N substantially inhibited E5-induced PDGFßR activation and transformation in both mouse and human fibroblasts. T21N did not prevent E5 from binding to the receptor, and genetic evidence suggested that T21N and E5 bind to nonidentical sites in the transmembrane domain of the receptor. T21N also inhibited transformation and PDGFßR activation induced by v-Sis, a viral homologue of PDGF-BB, as well as PDGF-induced mitogenesis and signaling by preventing phosphorylation of the PDGFßR at particular tyrosine residues. These results demonstrated that T21N acts as a novel inhibitor of the PDGFßR and validated a new strategy for designing highly specific short transmembrane protein inhibitors of growth factor receptors and possibly other transmembrane proteins.
[Mh] Termos MeSH primário: Ativadores de Enzimas/metabolismo
Fibroblastos/metabolismo
Mutação de Sentido Incorreto
Proteínas Oncogênicas v-sis/metabolismo
Inibidores de Proteínas Quinases/metabolismo
Receptor beta de Fator de Crescimento Derivado de Plaquetas
[Mh] Termos MeSH secundário: Substituição de Aminoácidos
Animais
Papillomavirus Bovino 1/genética
Papillomavirus Bovino 1/metabolismo
Bovinos
Linhagem Celular
Transformação Celular Viral/genética
Fibroblastos/patologia
Seres Humanos
Masculino
Camundongos
Proteínas Oncogênicas v-sis/genética
Proteínas Oncogênicas Virais/genética
Proteínas Oncogênicas Virais/metabolismo
Fosforilação/genética
Receptor beta de Fator de Crescimento Derivado de Plaquetas/agonistas
Receptor beta de Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores
Receptor beta de Fator de Crescimento Derivado de Plaquetas/genética
Receptor beta de Fator de Crescimento Derivado de Plaquetas/metabolismo
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Enzyme Activators); 0 (Oncogene Proteins v-sis); 0 (Oncogene Proteins, Viral); 0 (Protein Kinase Inhibitors); 0 (oncogene protein E5, Bovine papillomavirus type 1); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor beta)
[Em] Mês de entrada:1311
[Cu] Atualização por classe:161202
[Lr] Data última revisão:
161202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130803
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M113.470054


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[PMID]:22512244
[Au] Autor:Heldin CH
[Ad] Endereço:Ludwig Institute for Cancer Research, Uppsala University, Uppsala, Sweden.
[Ti] Título:Autocrine PDGF stimulation in malignancies.
[So] Source:Ups J Med Sci;117(2):83-91, 2012 May.
[Is] ISSN:2000-1967
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Platelet-derived growth factor (PDGF) isoforms are important mitogens for different types of mesenchymal cells, which have important functions during the embryonal development and in the adult during wound healing and tissue homeostasis. In tumors, PDGF isoforms are often over-expressed and contribute to the growth of both normal and malignant cells. This review focuses on tumors expressing PDGF isoforms together with their tyrosine kinase receptors, thus resulting in autocrine stimulation of growth and survival. Patients with such tumors could benefit from treatment with inhibitors of either PDGF or PDGF receptors.
[Mh] Termos MeSH primário: Neoplasias/fisiopatologia
Fator de Crescimento Derivado de Plaquetas/fisiologia
Isoformas de Proteínas/fisiologia
[Mh] Termos MeSH secundário: Antineoplásicos/farmacologia
Antineoplásicos/uso terapêutico
Seres Humanos
Mutação
Neoplasias/tratamento farmacológico
Proteínas Oncogênicas v-sis/química
Fator de Crescimento Derivado de Plaquetas/antagonistas & inibidores
Fator de Crescimento Derivado de Plaquetas/química
Receptores do Fator de Crescimento Derivado de Plaquetas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Oncogene Proteins v-sis); 0 (Platelet-Derived Growth Factor); 0 (Protein Isoforms); EC 2.7.10.1 (Receptors, Platelet-Derived Growth Factor)
[Em] Mês de entrada:1208
[Cu] Atualização por classe:150225
[Lr] Data última revisão:
150225
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120420
[St] Status:MEDLINE
[do] DOI:10.3109/03009734.2012.658119


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[PMID]:17481961
[Au] Autor:Wu JC; Cheung CM; Wong VW; Sung JJ
[Ad] Endereço:Institute of Digestive Disease, The Chinese University of Hong Kong, Shatin, Hong Kong. justinwu@cuhk.edu.hk
[Ti] Título:Distinct clinical characteristics between patients with nonerosive reflux disease and those with reflux esophagitis.
[So] Source:Clin Gastroenterol Hepatol;5(6):690-5, 2007 Jun.
[Is] ISSN:1542-7714
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND & AIMS: It has been postulated that nonerosive reflux disease (NERD) and erosive reflux disease (ERD) are 2 distinct entities of gastroesophageal reflux disease. The aim of this study was to compare the clinical characteristics between patients with NERD and those with ERD. METHODS: We prospectively recruited consecutive patients presenting with weekly attacks of heartburn or acid regurgitation. Exclusion criteria included gastric surgery, recent use of nonsteroidal anti-inflammatory drug or proton pump inhibitor, and peptic ulcer disease. Concomitant functional dyspepsia, irritable bowel syndrome, and psychological disorders were documented. Endoscopy, esophageal manometry, acid perfusion test, and 24-hour ambulatory pH monitoring were performed. Risk factors of NERD were determined by multivariate analysis. RESULTS: Two hundred fourteen patients (NERD, 113; ERD, 111) were studied. NERD patients were characterized by higher prevalence of Helicobacter pylori (36.3% vs 18%, P = .005), functional dyspepsia (64.6% vs 42.3%, P = .003), irritable bowel syndrome (44.2% vs 15.3%, P < .001), psychological disorders (9% vs 0.9%, P = .04), and positive acid perfusion test (40.7% vs 19.8%, P = .004). ERD patients had more hiatal hernias (35.1% vs 17.1%, P = .009), higher esophageal acid exposure (total time esophageal pH <4, 4.2% +/- 2.1% vs 5.9% +/- 2.3%; P = .01), and esophageal dysmotility (P < .05). With multivariate analysis, H pylori (odds ratio, 1.8; 95% confidence interval [CI], 1.1-3.2), irritable bowel syndrome (odds ratio, 2.8; 95% CI, 1.6-5.3), and positive acid perfusion test (odds ratio, 1.9; 95% CI, 1.4-2.8) were independent risk factors for NERD. CONCLUSIONS: Patients with NERD and ERD have distinct differences in clinical characteristics. NERD is characterized by higher prevalence of functional gastrointestinal disorders and esophageal acid hypersensitivity.
[Mh] Termos MeSH primário: Esofagite Péptica/diagnóstico
Refluxo Gastroesofágico/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Índice de Massa Corporal
Esofagite Péptica/epidemiologia
Esofagoscopia
Feminino
Refluxo Gastroesofágico/epidemiologia
Seres Humanos
Concentração de Íons de Hidrogênio
Síndrome do Intestino Irritável/epidemiologia
Masculino
Manometria
Meia-Idade
Análise Multivariada
Proteínas Oncogênicas v-sis
Estudos Prospectivos
Fatores de Risco
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Oncogene Proteins v-sis)
[Em] Mês de entrada:0711
[Cu] Atualização por classe:070604
[Lr] Data última revisão:
070604
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070508
[St] Status:MEDLINE


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[PMID]:15850576
[Au] Autor:Li J; Gran B; Zhang GX; Rostami A; Kamoun M
[Ad] Endereço:Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, 3400 Spruce Street, Philadelphia, PA 19104, USA.
[Ti] Título:IL-27 subunits and its receptor (WSX-1) mRNAs are markedly up-regulated in inflammatory cells in the CNS during experimental autoimmune encephalomyelitis.
[So] Source:J Neurol Sci;232(1-2):3-9, 2005 May 15.
[Is] ISSN:0022-510X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:IL-27 (EBI3p28) is a recently discovered heterodimeric cytokine, which is functionally related to IL-23p40p19 and IL-12p40p35. IL-27 acts in synergy with IL-12 early during Th1 development from naive T cells. IL-27 functions through the WSX-1 and the gpl30 receptor subunits, which shares homology with the IL-12Rbeta2 subunit. We have previously reported that IL-23 is up-regulated in CD11b+ microglia/macrophages in the CNS during the early phase of experimental autoimmune encephalomyelitis (EAE), and thus may contribute to the early induction of EAE. In the present study, we examined the expression of IL-27 and its receptor in the CNS, spleen, and lymph nodes at different stages of EAE actively induced with myelin oligodendrocyte glycoprotein peptide(35-55). Our findings show that IL-27 EBI3 and p28 mRNA were up-regulated to a maximum level at the peak of disease in APC from the CNS and lymph nodes, but not in the spleen. Moreover, IL-27 receptor (WSX-1) expression was greatly up-regulated during the early stage of EAE in both the CNS and lymph nodes. Taken together, our data show that subunits of IL-27 and its receptor (WSX-1) mRNAs are markedly up-regulated in inflammatory cells in the CNS at the peak of disease. Thus, IL-27 produced by infiltrating cells in the CNS may regulate in a paracrine manner the Th1 response in EAE.
[Mh] Termos MeSH primário: Sistema Nervoso Central/metabolismo
Encefalomielite Autoimune Experimental/metabolismo
Inflamação/metabolismo
Interleucinas/biossíntese
RNA Mensageiro/biossíntese
Receptores de Citocinas/biossíntese
[Mh] Termos MeSH secundário: Animais
Antígeno CD11b/metabolismo
Linfócitos T CD4-Positivos/metabolismo
Cinética
Macrófagos/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Microglia/metabolismo
Proteínas Oncogênicas v-sis/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Células Th1
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD11b Antigen); 0 (Il27 protein, mouse); 0 (Il27ra protein, mouse); 0 (Interleukins); 0 (Oncogene Proteins v-sis); 0 (RNA, Messenger); 0 (Receptors, Cytokine)
[Em] Mês de entrada:0507
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:050427
[St] Status:MEDLINE


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[PMID]:14515146
[Au] Autor:Funa K; Uramoto H
[Ad] Endereço:Institute of Anatomy and Cell Biology, Göteborg University, Box 420, SE-405 30 Gothenburg, Sweden. keiko.funa@anatcell.gu.se
[Ti] Título:Regulatory mechanisms for the expression and activity of platelet-derived growth factor receptor.
[So] Source:Acta Biochim Pol;50(3):647-58, 2003.
[Is] ISSN:0001-527X
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:PDGF is one of the most potent serum mitogens, and the signalling mechanism by way of its receptor tyrosine-kinase has been extensively studied since its first purification in 1979. The identification of homology between the simian sarcoma virus oncogene, v-sis, and the B-chain of PDGF, as well as the frequent over-expression of both the ligands and receptors in various tumours and stroma led to the proposal of the PDGF-mediated autocrine and paracrine hypothesis. Consistent with the important roles of PDGF in the growth and survival of cells, the expression and activity of PDGF receptors are tightly controlled by both positive and negative feedback mechanisms at different levels. The deregulation of the control system can result in serious pathological conditions such as chronic inflammation and tumours. Understanding the molecular mechanisms for the regulatory system and the signalling pathway of PDGF is essential in order to find effective therapies in the diseases where PDGF is involved.
[Mh] Termos MeSH primário: Transformação Celular Neoplásica/metabolismo
Proteínas Oncogênicas v-sis/genética
Fator de Crescimento Derivado de Plaquetas/metabolismo
Receptores do Fator de Crescimento Derivado de Plaquetas/metabolismo
[Mh] Termos MeSH secundário: Animais
Divisão Celular/fisiologia
Sobrevivência Celular/fisiologia
Dimerização
Seres Humanos
Fosforilação
Fator de Crescimento Derivado de Plaquetas/genética
Receptores do Fator de Crescimento Derivado de Plaquetas/genética
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Oncogene Proteins v-sis); 0 (Platelet-Derived Growth Factor); EC 2.7.10.1 (Receptors, Platelet-Derived Growth Factor)
[Em] Mês de entrada:0408
[Cu] Atualização por classe:091119
[Lr] Data última revisão:
091119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:030930
[St] Status:MEDLINE


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[PMID]:12912978
[Au] Autor:Huang SS; Tang FM; Huang YH; Liu IH; Hsu SC; Chen ST; Huang JS
[Ad] Endereço:Departments of Biochemistry and Molecular Biology, St. Louis University School of Medicine, St. Louis, Missouri 63104, USA. huangjs@slu.edu
[Ti] Título:Cloning, expression, characterization, and role in autocrine cell growth of cell surface retention sequence binding protein-1.
[So] Source:J Biol Chem;278(44):43855-69, 2003 Oct 31.
[Is] ISSN:0021-9258
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cell surface retention sequence binding protein-1 (CRSBP-1) is a cell surface binding protein for the cell surface retention sequence (CRS) motif of the v-sis gene product (platelet-derived growth factor-BB). It has been shown to be responsible for cell surface retention of the v-sis gene product in v-sis-transformed cells (fibroblasts) and has been hypothesized to play a role in autocrine growth and transformation of these cells. Here we demonstrate that the CRSBP-1 cDNA cloned from bovine liver libraries encodes a 322-residue type I membrane protein containing a 23-residue signal peptide, a 215-residue cell surface domain, a 21-residue transmembrane domain, and a 63-residue cytoplasmic domain. CRSBP-1 expressed in transfected cells is an approximately 120-kDa disulfide-linked homodimeric glycoprotein and exhibits dual ligand (CRS-containing growth regulators (v-sis gene product and insulin-like growth factor binding protein-3, IGFBP-3) and hyaluronic acid) binding activity. CRSBP-1 overexpression (by stable transfection of cells with CRSBP-1 cDNA) enhances autocrine loop signaling, cell growth, and tumorigenicity (in mice) of v-sis-transformed cells. CRSBP-1 expression also enhances autocrine cell growth mediated by IGFBP-3 in human lung carcinoma cells (H1299 cells), which express very little, if any, endogenous CRSBP-1 and exhibits a mitogenic response to exogenous IGFBP-3, stably transfected with IGFBP-3 cDNA. However, CRSBP-1 overexpression does not affect growth of normal and transformed cells that do not produce these CRS-containing growth regulators. These results suggest that CRSBP-1 plays a role in autocrine regulation of cell growth mediated by growth regulators containing CRS.
[Mh] Termos MeSH primário: Proteínas de Membrana/biossíntese
Proteínas de Membrana/genética
[Mh] Termos MeSH secundário: Motivos de Aminoácidos
Sequência de Aminoácidos
Animais
Sequência de Bases
Western Blotting
Bovinos
Divisão Celular
Linhagem Celular Transformada
Linhagem Celular Tumoral
Citoplasma/metabolismo
DNA Complementar/metabolismo
Detergentes/farmacologia
Dimerização
Dissulfetos/química
Fibroblastos/metabolismo
Biblioteca Gênica
Glicoproteínas/química
Seres Humanos
Immunoblotting
Proteína 3 de Ligação a Fator de Crescimento Semelhante à Insulina/metabolismo
Fígado/metabolismo
Proteínas de Membrana/fisiologia
Camundongos
Dados de Sequência Molecular
Células NIH 3T3
Octoxinol/farmacologia
Proteínas Oncogênicas v-sis/metabolismo
Peptídeos/química
Ligação Proteica
Sinais Direcionadores de Proteínas
Homologia de Sequência de Aminoácidos
Fatores de Tempo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (Detergents); 0 (Disulfides); 0 (Glycoproteins); 0 (Insulin-Like Growth Factor Binding Protein 3); 0 (Membrane Proteins); 0 (Oncogene Proteins v-sis); 0 (Peptides); 0 (Protein Sorting Signals); 0 (cell-surface retention-binding protein 1); 9002-93-1 (Octoxynol)
[Em] Mês de entrada:0312
[Cu] Atualização por classe:071114
[Lr] Data última revisão:
071114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:030813
[St] Status:MEDLINE


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[PMID]:12014510
[Au] Autor:Levine RA
[Ad] Endereço:Department of Molecular Medicine, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA. ral1@cornell.edu
[Ti] Título:Overexpression of the sis oncogene in a canine osteosarcoma cell line.
[So] Source:Vet Pathol;39(3):411-2, 2002 May.
[Is] ISSN:0300-9858
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Specific oncogenes that contribute to the pathogenesis of canine osteosarcoma (OS) have not been identified. In the process of characterizing four OS cell lines, we have found one cell line, CO8, that overexpresses the sis oncogene, which encodes the platelet-derived growth factor (PDGF)-beta. The expression of an important downstream transcriptional target of the PDGF signaling pathway, c-myc, is also elevated fourfold. Conditioned medium from CO8 alone specifically induces tyrosine phosphorylation and therefore the activation of the PDGF-alpha and PDGF-beta receptors on murine 3T3 cells. All of the canine OS lines tested contain PDGF receptors and therefore are capable of responding to PDGE Given the importance of PDGF in promoting cell proliferation, migration, and cell survival, the activation of the sis oncogene and the resultant growth factor autocrine loop potentially contribute to the pathogenesis of a subset of canine osteosarcomas.
[Mh] Termos MeSH primário: Neoplasias Ósseas/veterinária
Doenças do Cão/patologia
Genes sis
Proteínas Oncogênicas v-sis/biossíntese
Osteossarcoma/veterinária
[Mh] Termos MeSH secundário: Células 3T3
Animais
Northern Blotting/veterinária
Neoplasias Ósseas/genética
Neoplasias Ósseas/metabolismo
Neoplasias Ósseas/patologia
Meios de Cultivo Condicionados
Doenças do Cão/metabolismo
Cães
Regulação Neoplásica da Expressão Gênica
Genes myc/genética
Camundongos
Proteínas Oncogênicas v-sis/genética
Osteossarcoma/genética
Osteossarcoma/metabolismo
Osteossarcoma/patologia
Fosforilação
RNA Neoplásico/química
RNA Neoplásico/genética
Receptores do Fator de Crescimento Derivado de Plaquetas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Culture Media, Conditioned); 0 (Oncogene Proteins v-sis); 0 (RNA, Neoplasm); EC 2.7.10.1 (Receptors, Platelet-Derived Growth Factor)
[Em] Mês de entrada:0211
[Cu] Atualização por classe:170214
[Lr] Data última revisão:
170214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:020517
[St] Status:MEDLINE


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[PMID]:10198059
[Au] Autor:Ahn HY; Hadizadeh KR; Seul C; Yun YP; Vetter H; Sachinidis A
[Ad] Endereço:Department of Pharmacology, College of Medicine, Chungbuk National University, Cheongju 361-763, South Korea.
[Ti] Título:Epigallocathechin-3 gallate selectively inhibits the PDGF-BB-induced intracellular signaling transduction pathway in vascular smooth muscle cells and inhibits transformation of sis-transfected NIH 3T3 fibroblasts and human glioblastoma cells (A172).
[So] Source:Mol Biol Cell;10(4):1093-104, 1999 Apr.
[Is] ISSN:1059-1524
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Enhanced activity of receptor tyrosine kinases such as the PDGF beta-receptor and EGF receptor has been implicated as a contributing factor in the development of malignant and nonmalignant proliferative diseases such as cancer and atherosclerosis. Several epidemiological studies suggest that green tea may prevent the development of cancer and atherosclerosis. One of the major constituents of green tea is the polyphenol epigallocathechin-3 gallate (EGCG). In an attempt to offer a possible explanation for the anti-cancer and anti-atherosclerotic activity of EGCG, we examined the effect of EGCG on the PDGF-BB-, EGF-, angiotensin II-, and FCS-induced activation of the 44 kDa and 42 kDa mitogen-activated protein (MAP) kinase isoforms (p44(mapk)/p42(mapk)) in cultured vascular smooth muscle cells (VSMCs) from rat aorta. VSMCs were treated with EGCG (1-100 microM) for 24 h and stimulated with the above mentioned agonists for different time periods. Stimulation of the p44(mapk)/p42(mapk) was detected by the enhanced Western blotting method using phospho-specific MAP kinase antibodies that recognized the Tyr204-phosphorylated (active) isoforms. Treatment of VSMCs with 10 and 50 microM EGCG resulted in an 80% and a complete inhibition of the PDGF-BB-induced activation of MAP kinase isoforms, respectively. In striking contrast, EGCG (1-100 microM) did not influence MAP kinase activation by EGF, angiotensin II, and FCS. Similarly, the maximal effect of PDGF-BB on the c-fos and egr-1 mRNA expression as well as on intracellular free Ca2+ concentration was completely inhibited in EGCG-treated VSMCs, whereas the effect of EGF was not affected. Quantification of the immunoprecipitated tyrosine-phosphorylated PDGF-Rbeta, phosphatidylinositol 3'-kinase, and phospholipase C-gamma1 by the enhanced Western blotting method revealed that EGCG treatment effectively inhibits tyrosine phosphorylation of these kinases in VSMCs. Furthermore, we show that spheroid formation of human glioblastoma cells (A172) and colony formation of sis-transfected NIH 3T3 cells in semisolid agar are completely inhibited by 20-50 microM EGCG. Our findings demonstrate that EGCG is a selective inhibitor of the tyrosine phosphorylation of PDGF-Rbeta and its downstream signaling pathway. The present findings may partly explain the anti-cancer and anti-atherosclerotic activity of green tea.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Catequina/análogos & derivados
Proteínas Quinases Ativadas por Mitógeno
Músculo Liso Vascular/fisiologia
Fator de Crescimento Derivado de Plaquetas/farmacologia
Proteínas Oncogênicas de Retroviridae/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Células 3T3
Animais
Aorta
Neoplasias Encefálicas
Cálcio/metabolismo
Proteínas Quinases Dependentes de Cálcio-Calmodulina/metabolismo
Catequina/farmacologia
Transformação Celular Neoplásica
Células Cultivadas
Glioblastoma
Seres Humanos
Cinética
Camundongos
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno
Músculo Liso Vascular/citologia
Músculo Liso Vascular/efeitos dos fármacos
Proteínas Oncogênicas v-sis
Fosforilação
Fosfotirosina/metabolismo
Proteínas Proto-Oncogênicas c-sis
Ratos
Ratos Endogâmicos WKY
Proteínas Recombinantes/metabolismo
Proteínas Oncogênicas de Retroviridae/genética
Transdução de Sinais/fisiologia
Chá
Transfecção
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Oncogene Proteins v-sis); 0 (Platelet-Derived Growth Factor); 0 (Proto-Oncogene Proteins c-sis); 0 (Recombinant Proteins); 0 (Retroviridae Proteins, Oncogenic); 0 (Tea); 1B56C968OA (becaplermin); 21820-51-9 (Phosphotyrosine); 8R1V1STN48 (Catechin); BQM438CTEL (epigallocatechin gallate); EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinases); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); SY7Q814VUP (Calcium)
[Em] Mês de entrada:9905
[Cu] Atualização por classe:161124
[Lr] Data última revisão:
161124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:990410
[St] Status:MEDLINE


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[PMID]:10187853
[Au] Autor:Boensch C; Huang SS; Connolly DT; Huang JS
[Ad] Endereço:Department of Biochemistry and Molecular Biology, St. Louis University School of Medicine, St. Louis, Missouri 63104, USA.
[Ti] Título:Cell surface retention sequence binding protein-1 interacts with the v-sis gene product and platelet-derived growth factor beta-type receptor in simian sarcoma virus-transformed cells.
[So] Source:J Biol Chem;274(15):10582-9, 1999 Apr 09.
[Is] ISSN:0021-9258
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cell surface retention sequence (CRS) binding protein-1 (CRSBP-1) is a newly identified membrane glycoprotein which is hypothesized to be responsible for cell surface retention of the oncogene v-sis and c-sis gene products and other secretory proteins containing CRSs. In simian sarcoma virus-transformed NIH 3T3 cells (SSV-NIH 3T3 cells), a fraction of CRSBP-1 was demonstrated at the cell surface and underwent internalization/recycling as revealed by cell surface 125I labeling and its resistance/sensitivity to trypsin digestion. However, the majority of CRSBP-1 was localized in intracellular compartments as evidenced by the resistance of most of the 35S-metabolically labeled CRSBP-1 to trypsin digestion, and by indirect immunofluorescent staining. CRSBP-1 appeared to form complexes with proteolytically processed forms (generated at and/or after the trans-Golgi network) of the v-sis gene product and with a approximately 140-kDa proteolytically cleaved form of the platelet-derived growth factor (PDGF) beta-type receptor, as demonstrated by metabolic labeling and co-immunoprecipitation. CRSBP-1, like the v-sis gene product and PDGF beta-type receptor, underwent rapid turnover which was blocked in the presence of 100 microM suramin. In normal and other transformed NIH 3T3 cells, CRSBP-1 was relatively stable and did not undergo rapid turnover and internalization/recycling at the cell surface. These results suggest that in SSV-NIH 3T3 cells, CRSBP-1 interacts with and forms ternary and binary complexes with the newly synthesized v-sis gene product and PDGF beta-type receptor at the trans-Golgi network and that the stable binary (CRSBP-1.v-sis gene product) complex is transported to the cell surface where it presents the v-sis gene product to unoccupied PDGF beta-type receptors during internalization/recycling.
[Mh] Termos MeSH primário: Transformação Celular Viral
Proteínas de Membrana/metabolismo
Receptores do Fator de Crescimento Derivado de Plaquetas/metabolismo
Proteínas Oncogênicas de Retroviridae/metabolismo
Vírus do Sarcoma do Macaco-Barrigudo/metabolismo
[Mh] Termos MeSH secundário: Células 3T3
Animais
Técnica Indireta de Fluorescência para Anticorpo
Camundongos
Proteínas Oncogênicas v-sis
Coelhos
Receptor beta de Fator de Crescimento Derivado de Plaquetas
Suramina/metabolismo
Propriedades de Superfície
Tripsina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (Oncogene Proteins v-sis); 0 (Retroviridae Proteins, Oncogenic); 0 (cell-surface retention-binding protein 1); 6032D45BEM (Suramin); EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor beta); EC 2.7.10.1 (Receptors, Platelet-Derived Growth Factor); EC 3.4.21.4 (Trypsin)
[Em] Mês de entrada:9905
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM; X
[Da] Data de entrada para processamento:990403
[St] Status:MEDLINE


  10 / 64 MEDLINE  
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[PMID]:9373173
[Au] Autor:Huang SS; Koh HA; Huang JS
[Ad] Endereço:E.A. Doisy Department of Biochemistry and Molecular Biology, St. Louis University School of Medicine, MO 63104, USA.
[Ti] Título:Suramin enters and accumulates in low pH intracellular compartments of v-sis-transformed NIH 3T3 cells.
[So] Source:FEBS Lett;416(3):297-301, 1997 Oct 27.
[Is] ISSN:0014-5793
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Using acridine orange as a reporter compound, we demonstrate that suramin enters and accumulates in low pH intracellular compartments (endosomes, lysosomes, and trans-Golgi complex) of normal and v-sis-transformed NIH 3T3 cells. The concentration of suramin in these acidic compartments is estimated to be > 150 microM, higher than the concentration known to completely inhibit interaction of the platelet-derived growth factor (PDGF) receptor and v-sis gene product. These results support the hypothesis that suramin reverses the transformed phenotype of v-sis-transformed cells by entering the cell via endocytosis and blocking interaction of the v-sis gene product and PDGF receptor in intracellular organelles.
[Mh] Termos MeSH primário: Transformação Celular Neoplásica
Organelas/metabolismo
Proteínas Oncogênicas de Retroviridae/biossíntese
Suramina/metabolismo
[Mh] Termos MeSH secundário: Células 3T3
Laranja Acridina
Animais
Linhagem Celular
Linhagem Celular Transformada
Endossomos/metabolismo
Complexo de Golgi/metabolismo
Concentração de Íons de Hidrogênio
Cinética
Lisossomos/metabolismo
Camundongos
Proteínas Oncogênicas v-sis
Ratos
Receptores do Fator de Crescimento Derivado de Plaquetas/efeitos dos fármacos
Receptores do Fator de Crescimento Derivado de Plaquetas/fisiologia
Suramina/farmacocinética
Suramina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, P.H.S.
[Nm] Nome de substância:
0 (Oncogene Proteins v-sis); 0 (Retroviridae Proteins, Oncogenic); 6032D45BEM (Suramin); EC 2.7.10.1 (Receptors, Platelet-Derived Growth Factor); F30N4O6XVV (Acridine Orange)
[Em] Mês de entrada:9712
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:971231
[St] Status:MEDLINE



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