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[PMID]:25117082
[Au] Autor:Dolgova EV; Alyamkina EA; Efremov YR; Nikolin VP; Popova NA; Tyrinova TV; Kozel AV; Minkevich AM; Andrushkevich OM; Zavyalov EL; Romaschenko AV; Bayborodin SI; Taranov OS; Omigov VV; Shevela EY; Stupak VV; Mishinov SV; Rogachev VA; Proskurina AS; Mayorov VI; Shurdov MA; Ostanin AA; Chernykh ER; Bogachev SS
[Ad] Endereço:Institute of Cytology and Genetics; Siberian Branch of the Russian Academy of Sciences; Novosibirsk, Russia.
[Ti] Título:Identification of cancer stem cells and a strategy for their elimination.
[So] Source:Cancer Biol Ther;15(10):1378-94, 2014 Oct.
[Is] ISSN:1555-8576
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It has been established previously that up to 40% of mouse CD34(+) hematopoietic stem cells are capable of internalizing exogenous dsDNA fragments both in vivo and ex vivo. Importantly, when mice are treated with a combination of cyclophosphamide and dsDNA, the repair of interstrand crosslinks in hematopoietic progenitors is attenuated, and their pluripotency is altered. Here we show for the first time that among various actively proliferating mammalian cell populations there are subpopulations capable of internalizing dsDNA fragments. In the context of cancer, such dsDNA-internalizing cell subpopulations display cancer stem cell-like phenotype. Furthermore, using Krebs-2 ascites cells as a model, we found that upon combined treatment with cyclophosphamide and dsDNA, engrafted material loses its tumor-initiating properties which we attribute to the elimination of tumor-initiating stem cell subpopulation or loss of its tumorigenic potential.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Células-Tronco Neoplásicas/patologia
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Ascite/metabolismo
Ascite/patologia
Neoplasias Encefálicas/metabolismo
Neoplasias Encefálicas/patologia
Carcinoma Krebs 2/metabolismo
Carcinoma Krebs 2/patologia
Proliferação Celular/efeitos dos fármacos
Ciclofosfamida/farmacologia
DNA/metabolismo
DNA/farmacologia
Endocitose
Glioblastoma/metabolismo
Glioblastoma/patologia
Xenoenxertos
Camundongos Endogâmicos CBA
Camundongos Endogâmicos NOD
Camundongos SCID
Células-Tronco Neoplásicas/efeitos dos fármacos
Reparo de DNA por Recombinação/genética
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 8N3DW7272P (Cyclophosphamide); 9007-49-2 (DNA)
[Em] Mês de entrada:1504
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140814
[St] Status:MEDLINE
[do] DOI:10.4161/cbt.29854


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[PMID]:23521072
[Au] Autor:Godovikova TS; Lisitskiy VA; Antonova NM; Popova TV; Zakharova OD; Chubarov AS; Koptyug IV; Sagdeev RZ; Kaptein R; Akulov AE; Kaledin VI; Nikolin VP; Baiborodin SI; Koroleva LS; Silnikov VN
[Ad] Endereço:Institute of Chemical Biology and Fundamental Medicine, SB RAS, 630090 Novosibirsk, Russia. godov@niboch.nsc.ru
[Ti] Título:Ligand-directed acid-sensitive amidophosphate 5-trifluoromethyl-2'-deoxyuridine conjugate as a potential theranostic agent.
[So] Source:Bioconjug Chem;24(5):780-95, 2013 May 15.
[Is] ISSN:1520-4812
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Herein, we report a novel strategy to engineer an acid-sensitive anticancer theranostic agent using a vector-drug ensemble. The ensemble was synthesized by directly conjugating the linoleic acid (LA)-modified branched polyethyleneimine with a chemotherapeutic drug trifluorothymidine. Linoleic acid residues were grafted onto 25 kDa polyethyleneimine (PEI) by treating PEI with linoleic acid chloroanhydride. 5-Trifluoromethyl-2'-deoxyuridine (trifluorothymidine, TFT) was introduced into LA-PEI conjugate by phosphorylating the conjugate with amidophosphate of trifluorothymidine 5'-monophosphate (pTFT), which had been activated by its conversion into the N,N-dimethylaminopyridine derivative. The extent of mononucleotide analog incorporation in the polymer was regulated by the ratio of pTFT to the polymer during the synthesis. Samples containing 20-70 TFT residues per PEI molecule were obtained. The cytotoxicity of PEI-LA-pTFT conjugates decreased with increasing nucleotide content, as examined using the MTT method. Due to the presence of fluorine atoms, TFT-based conjugates could be detected directly in the animals by (19)F magnetic resonance imaging. In addition, the presence of the amidophosphate group in PEI-LA-pTFT conjugates allowed their detection by in vivo(31)P NMR spectroscopy. Indeed, the (31)P NMR signal of a phosphoramide (δ ~ 12 ppm) was observed in the mouse muscle tissue treated with PEI-LA-pTFT conjugate along with the signals from endogenous phosphorus-containing compounds. At the same time, the use of PEI-LA-pTFT conjugate for chemotherapeutic drug delivery is limited due to the low release of pTFT from the carrier. To enhance the release of the drug from the conjugate in the endosomes, PEI-LA polymer was coupled with urocanic acid (UA), which bears imidazole ring and thus can form an acid-labile P-N bond with pTFT. The PEI-LA-UA-pTFT conjugate containing 30 residues of UA and 40 residues of pTFT was tested against the murine Krebs-II ascites carcinoma, grown as an ascetic tumor. The intraperitoneal injection of the conjugates resulted in prolongation of the animals' life and to the complete disappearance of the tumor after three injections.
[Mh] Termos MeSH primário: Antineoplásicos/química
Antineoplásicos/uso terapêutico
Ácido Linoleico/química
Polietilenoimina/análogos & derivados
Trifluridina/química
Trifluridina/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/administração & dosagem
Antineoplásicos/farmacocinética
Carcinoma Krebs 2/tratamento farmacológico
Linhagem Celular Tumoral
Portadores de Fármacos/química
Seres Humanos
Ligantes
Camundongos
Camundongos Endogâmicos C57BL
Trifluridina/administração & dosagem
Trifluridina/farmacocinética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Drug Carriers); 0 (Ligands); 9002-98-6 (Polyethyleneimine); 9KJL21T0QJ (Linoleic Acid); RMW9V5RW38 (Trifluridine)
[Em] Mês de entrada:1311
[Cu] Atualização por classe:130515
[Lr] Data última revisão:
130515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130326
[St] Status:MEDLINE
[do] DOI:10.1021/bc3006072


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[PMID]:19782024
[Au] Autor:Omer AD; Janas MM; Novina CD
[Ad] Endereço:Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.
[Ti] Título:The chicken or the egg: microRNA-mediated regulation of mRNA translation or mRNA stability.
[So] Source:Mol Cell;35(6):739-40, 2009 Sep 24.
[Is] ISSN:1097-4164
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this issue of Molecular Cell, Fabian et al. (2009) demonstrate that in cell-free extracts from mouse Krebs-2 ascites, microRNA-mediated translational repression precedes target mRNA deadenylation, and identify GW182, PABP, and deadenylase subunits CAF1 and CCR4 as factors required for deadenylation.
[Mh] Termos MeSH primário: Inativação Gênica
MicroRNAs/metabolismo
Proteínas de Ligação a Poli(A)/metabolismo
Proteínas/metabolismo
Processamento Pós-Transcricional do RNA
RNA Mensageiro/metabolismo
Complexo de Inativação Induzido por RNA/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteínas Argonauta
Ascite/genética
Ascite/metabolismo
Autoantígenos/metabolismo
Sítios de Ligação
Carcinoma Krebs 2/genética
Carcinoma Krebs 2/metabolismo
Fator de Iniciação 2 em Eucariotos/metabolismo
Fator de Iniciação 4G em Eucariotos/metabolismo
Seres Humanos
Cinética
Camundongos
Proteínas de Ligação a Poli(A)/genética
Biossíntese de Proteínas
Estrutura Terciária de Proteína
Proteínas/genética
Estabilidade de RNA
Complexo de Inativação Induzido por RNA/genética
Receptores CCR4/metabolismo
[Pt] Tipo de publicação:COMMENT; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Argonaute Proteins); 0 (Autoantigens); 0 (Ccr4 protein, mouse); 0 (Cnot7 protein, mouse); 0 (EIF2C2 protein, mouse); 0 (Eukaryotic Initiation Factor-2); 0 (Eukaryotic Initiation Factor-4G); 0 (MicroRNAs); 0 (Poly(A)-Binding Proteins); 0 (Proteins); 0 (RNA, Messenger); 0 (RNA-Induced Silencing Complex); 0 (Receptors, CCR4); 0 (mirnlet7 microRNA, mouse)
[Em] Mês de entrada:0910
[Cu] Atualização por classe:111117
[Lr] Data última revisão:
111117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090929
[St] Status:MEDLINE
[do] DOI:10.1016/j.molcel.2009.09.003


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[PMID]:19716330
[Au] Autor:Fabian MR; Mathonnet G; Sundermeier T; Mathys H; Zipprich JT; Svitkin YV; Rivas F; Jinek M; Wohlschlegel J; Doudna JA; Chen CY; Shyu AB; Yates JR; Hannon GJ; Filipowicz W; Duchaine TF; Sonenberg N
[Ad] Endereço:Department of Biochemistry, McGill University, Montreal, QC H3G 1Y6, Canada.
[Ti] Título:Mammalian miRNA RISC recruits CAF1 and PABP to affect PABP-dependent deadenylation.
[So] Source:Mol Cell;35(6):868-80, 2009 Sep 24.
[Is] ISSN:1097-4164
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:MicroRNAs (miRNAs) inhibit mRNA expression in general by base pairing to the 3'UTR of target mRNAs and consequently inhibiting translation and/or initiating poly(A) tail deadenylation and mRNA destabilization. Here we examine the mechanism and kinetics of miRNA-mediated deadenylation in mouse Krebs-2 ascites extract. We demonstrate that miRNA-mediated mRNA deadenylation occurs subsequent to initial translational inhibition, indicating a two-step mechanism of miRNA action, which serves to consolidate repression. We show that a let-7 miRNA-loaded RNA-induced silencing complex (miRISC) interacts with the poly(A)-binding protein (PABP) and the CAF1 and CCR4 deadenylases. In addition, we demonstrate that miRNA-mediated deadenylation is dependent upon CAF1 activity and PABP, which serves as a bona fide miRNA coactivator. Importantly, we present evidence that GW182, a core component of the miRISC, directly interacts with PABP via its C-terminal region and that this interaction is required for miRNA-mediated deadenylation.
[Mh] Termos MeSH primário: Inativação Gênica
MicroRNAs/metabolismo
Proteínas de Ligação a Poli(A)/metabolismo
Proteínas/metabolismo
Processamento Pós-Transcricional do RNA
RNA Mensageiro/metabolismo
Complexo de Inativação Induzido por RNA/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteínas Argonauta
Ascite/genética
Ascite/metabolismo
Autoantígenos/metabolismo
Sítios de Ligação
Carcinoma Krebs 2/genética
Carcinoma Krebs 2/metabolismo
Sistema Livre de Células
Fator de Iniciação 2 em Eucariotos/metabolismo
Fator de Iniciação 4G em Eucariotos/metabolismo
Células HeLa
Seres Humanos
Cinética
Camundongos
Proteínas de Ligação a Poli(A)/genética
Biossíntese de Proteínas
Estrutura Terciária de Proteína
Proteínas/genética
Estabilidade de RNA
Complexo de Inativação Induzido por RNA/genética
Receptores CCR4/metabolismo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Argonaute Proteins); 0 (Autoantigens); 0 (Ccr4 protein, mouse); 0 (Cnot7 protein, mouse); 0 (EIF2C2 protein, mouse); 0 (Eukaryotic Initiation Factor-2); 0 (Eukaryotic Initiation Factor-4G); 0 (MicroRNAs); 0 (Poly(A)-Binding Proteins); 0 (Proteins); 0 (RNA, Messenger); 0 (RNA-Induced Silencing Complex); 0 (Receptors, CCR4); 0 (mirnlet7 microRNA, mouse)
[Em] Mês de entrada:0910
[Cu] Atualização por classe:161122
[Lr] Data última revisão:
161122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090901
[St] Status:MEDLINE
[do] DOI:10.1016/j.molcel.2009.08.004


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[PMID]:19334534
[Au] Autor:Dmitriev SE; Andreev DE; Ad'ianova ZV; Terenin IM; Shatskii IN
[Ti] Título:[Efficient cap-dependent in vitro and in vivo translation of mammalian mRNAs with long and highly structured 5'-untranslated regions].
[So] Source:Mol Biol (Mosk);43(1):119-25, 2009 Jan-Feb.
[Is] ISSN:0026-8984
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:According to generally accepted scanning model proposed by M. Kozak, the secondary structure of 5'-untranslated regions (5'-UTR) of eukaryotic mRNAs can only cause an inhibitory effect on the translation initiation since it would counteract migration of the 40S ribosomal subunit along the mRNA polynucleotide chain. Thus, the existence of efficiently translatable mRNAs with long and highly structured 5'-UTRs is not compatible with the cap-dependent scanning mechanism. It is expected that such mRNAs should use alternative ways of translation initiation to be efficiently translated, first of all the mechanism of the internal ribosome entry mediated by special RNA structures called IRESes (for Internal Ribosome Entry Sites), which have been proposed to reside within their 5'-UTRs. In this paper, it is shown that this point of view is not correct and most probably based on experiments of mRNA translation in rabbit reticulocyte lysate. This cell free system does not reflect correctly the ratio of translation efficiencies of various mRNAs which is observed in the living cell. Using five different mRNAs of similar design which possess either relatively short leaders of cellular mRNAs (beta-globin and beta-actin mRNAs) or long and highly structured 5'-UTRs (c-myc, LINE-1, Apaf-1 mRNAs), we show that the translation activities of all tested 5'-UTRs are comparable, both in transfected cells and in a whole cytoplasmic extract of cultivated cells. This activity is strongly dependent on the presence of the cap at their 5'-ends.
[Mh] Termos MeSH primário: Regiões 5´ não Traduzidas/fisiologia
Conformação de Ácido Nucleico
Iniciação Traducional da Cadeia Peptídica/fisiologia
Capuzes de RNA/metabolismo
Subunidades Ribossômicas Menores/metabolismo
[Mh] Termos MeSH secundário: Animais
Carcinoma Krebs 2
Sistema Livre de Células
Camundongos
Coelhos
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (5' Untranslated Regions); 0 (RNA Caps)
[Em] Mês de entrada:0904
[Cu] Atualização por classe:090401
[Lr] Data última revisão:
090401
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090402
[St] Status:MEDLINE


  6 / 432 MEDLINE  
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[PMID]:17913619
[Au] Autor:Svitkin YV; Sonenberg N
[Ad] Endereço:Department of Biochemistry, McGill University, Montreal, Quebec, Canada.
[Ti] Título:A highly efficient and robust in vitro translation system for expression of picornavirus and hepatitis C virus RNA genomes.
[So] Source:Methods Enzymol;429:53-82, 2007.
[Is] ISSN:0076-6879
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A Krebs-2 cell-free extract that efficiently translates encephalomyocarditis virus (EMCV) RNA and extensively processes the viral polyprotein is also capable of supporting complete infectious EMCV replication. The system displays high RNA synthesis activity and de novo synthesis of virus up to titers of 2 x 10(7) to 6 x 10(7) plaque-forming units (pfu)/ml. The preparation of Krebs-2 cell extract and methods of analysis of EMCV-specific processes in vitro are described. We also demonstrate that the Krebs-2 cell-free system translates the entire open reading frame of the hepatitis C virus (HCV) RNA and properly processes the viral polyprotein when supplemented with canine microsomal membranes. In addition to processing, other posttranslational modifications of HCV proteins take place in vitro, such as the N-terminal glycosylation of the E1 and the E2 precursor (E2-p7) and phosphorylation of NS5A. The HCV RNA-programmed Krebs-2 cell-free extract should prove very useful as a novel screen for drugs that inhibit NS3-mediated processing. The use of this system should help fill the gap in understanding the regulation of synthesis and maturation of HCV proteins. With further optimization of cell-free conditions, the entire reconstitution of infectious HCV synthesis in vitro might become feasible.
[Mh] Termos MeSH primário: Vírus da Encefalomiocardite/metabolismo
Genoma Viral/fisiologia
Hepacivirus/metabolismo
Biossíntese de Proteínas/fisiologia
RNA Viral/fisiologia
Replicação Viral/fisiologia
[Mh] Termos MeSH secundário: Animais
Carcinoma Krebs 2/metabolismo
Sistema Livre de Células
Feminino
Glicosilação
Camundongos
Proteínas do Envelope Viral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA, Viral); 0 (Viral Envelope Proteins)
[Em] Mês de entrada:0712
[Cu] Atualização por classe:071004
[Lr] Data última revisão:
071004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:071005
[St] Status:MEDLINE


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[PMID]:17656684
[Au] Autor:Mathonnet G; Fabian MR; Svitkin YV; Parsyan A; Huck L; Murata T; Biffo S; Merrick WC; Darzynkiewicz E; Pillai RS; Filipowicz W; Duchaine TF; Sonenberg N
[Ad] Endereço:Department of Biochemistry and McGill Cancer Center, McGill University, Montreal, Quebec, Canada, H3G 1Y6.
[Ti] Título:MicroRNA inhibition of translation initiation in vitro by targeting the cap-binding complex eIF4F.
[So] Source:Science;317(5845):1764-7, 2007 Sep 21.
[Is] ISSN:1095-9203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:MicroRNAs (miRNAs) play an important role in gene regulatory networks in animals. Yet, the mechanistic details of their function in translation inhibition or messenger RNA (mRNA) destabilization remain controversial. To directly examine the earliest events in this process, we have developed an in vitro translation system using mouse Krebs-2 ascites cell-free extract that exhibits an authentic miRNA response. We show here that translation initiation, specifically the 5' cap recognition process, is repressed by endogenous let-7 miRNAs within the first 15 minutes of mRNA exposure to the extract when no destabilization of the transcript is observed. Our results indicate that inhibition of translation initiation is the earliest molecular event effected by miRNAs. Other mechanisms, such as mRNA degradation, may subsequently consolidate mRNA silencing.
[Mh] Termos MeSH primário: Fator de Iniciação 4F em Eucariotos/fisiologia
Regulação da Expressão Gênica/fisiologia
MicroRNAs/fisiologia
Biossíntese de Proteínas/fisiologia
Capuzes de RNA/fisiologia
[Mh] Termos MeSH secundário: Animais
Carcinoma Krebs 2
Extratos Celulares
Vírus da Encefalomiocardite/genética
Luciferases de Renilla/genética
Camundongos
Ribossomos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cell Extracts); 0 (Eukaryotic Initiation Factor-4F); 0 (MicroRNAs); 0 (RNA Caps); EC 1.13.12.5 (Luciferases, Renilla)
[Em] Mês de entrada:0709
[Cu] Atualização por classe:070921
[Lr] Data última revisão:
070921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070728
[St] Status:MEDLINE


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[PMID]:16771140
[Au] Autor:Astakhova TM; Sharova NP
[Ti] Título:[Exclusion of immune proteasomes from mouse ascitic carcinoma Krebs-II cells].
[So] Source:Izv Akad Nauk Ser Biol;(3):275-83, 2006 May-Jun.
[Is] ISSN:1026-3470
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Pools of 26S and 20S proteasomes were studied in the spleen, liver, lung, and ascitic carcinoma Krebs-II of mouse. Western blotting demonstrated that the pool of 26S proteasomes in ascitic carcinoma Krebs-II was twice that in control lung cells and did not significantly differ by total 26S proteasome quantities from the spleen and liver. At the same time, the level of immune subunit LMP7 was 12 times lower in it compared to lung proteasomes and 4-5 times lower compared to spleen and liver proteasomes. Immune subunit LMP2 was undetectable by this technique in the ascitic carcinoma in contrast to the lung, spleen, and liver. All immune subunits in the studied organs and ascitic carcinoma Krebs-II are components of 26S but not 20S proteasomes.
[Mh] Termos MeSH primário: Carcinoma Krebs 2/imunologia
Cisteína Endopeptidases/imunologia
Complexo de Endopeptidases do Proteassoma/imunologia
[Mh] Termos MeSH secundário: Animais
Western Blotting
Camundongos
Especificidade de Órgãos/imunologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; ENGLISH ABSTRACT; JOURNAL ARTICLE
[Nm] Nome de substância:
144416-78-4 (LMP-2 protein); EC 3.4.22.- (Cysteine Endopeptidases); EC 3.4.25.1 (Proteasome Endopeptidase Complex); EC 3.4.99.- (ATP dependent 26S protease)
[Em] Mês de entrada:0607
[Cu] Atualização por classe:161020
[Lr] Data última revisão:
161020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:060615
[St] Status:MEDLINE


  9 / 432 MEDLINE  
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[PMID]:12743313
[Au] Autor:Svitkin YV; Sonenberg N
[Ad] Endereço:Department of Biochemistry and McGill Cancer Center, McGill University, Montreal, Quebec, Canada H3G 1Y6. yuri.svitkine@mcgill.ca
[Ti] Título:Cell-free synthesis of encephalomyocarditis virus.
[So] Source:J Virol;77(11):6551-5, 2003 Jun.
[Is] ISSN:0022-538X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We developed a system for complete replication of encephalomyocarditis virus (EMCV) in a test tube by using an in vitro translation extract from Krebs-2 cells. Efficient virus synthesis occurred in a narrow range of Mg(2+) and EMCV RNA concentrations. Excess input RNA impaired RNA replication and virus production but not translation. This suggests the existence of a negative-feedback mechanism for regulation of RNA replication by the viral plus-strand RNA or proteins.
[Mh] Termos MeSH primário: Sistema Livre de Células
Vírus da Encefalomiocardite/metabolismo
Biossíntese de Proteínas
RNA Viral/biossíntese
Replicação Viral
[Mh] Termos MeSH secundário: Animais
Carcinoma Krebs 2/metabolismo
Carcinoma Krebs 2/virologia
Vírus da Encefalomiocardite/genética
Proteínas Virais/metabolismo
Virologia/métodos
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA, Viral); 0 (Viral Proteins)
[Em] Mês de entrada:0306
[Cu] Atualização por classe:140611
[Lr] Data última revisão:
140611
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:030514
[St] Status:MEDLINE


  10 / 432 MEDLINE  
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[PMID]:10445150
[Au] Autor:Mastikhin IV; Teslenko VS; Gorchakov VN; Nikolin VP; Kolosova NG
[Ti] Título:[Registration of cavitation processes in biological objects after acoustic shock wave using NMR-tomography and histological analysis].
[Ti] Título:Registratsiia kavitatsionnykh protsessov v biologicheskikh on''ektakh pri udarno-volnovom vozdeistvii metodami IaMR-tomografii i gistologicheskogo analiza..
[So] Source:Biull Eksp Biol Med;127(6):713-6, 1999 Jun.
[Is] ISSN:0365-9615
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Mh] Termos MeSH primário: Acústica
Carcinoma Krebs 2/patologia
[Mh] Termos MeSH secundário: Animais
Carcinoma Krebs 2/terapia
Feminino
Imagem por Ressonância Magnética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:9909
[Cu] Atualização por classe:081008
[Lr] Data última revisão:
081008
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:990813
[St] Status:MEDLINE



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