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Pesquisa : D12.776.624.664.520.750.925 [Categoria DeCS]
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[PMID]:28113043
[Au] Autor:Yao Y; Vasoya D; Kgosana L; Smith LP; Gao Y; Wang X; Watson M; Nair V
[Ad] Endereço:1​Avian Viral Disease Programme & UK-China Centre of Excellence on Avian Disease Research, The Pirbright Institute, Pirbright, Ash Road, Guildford, Surrey GU24 0NF, UK.
[Ti] Título:Activation of gga-miR-155 by reticuloendotheliosis virus T strain and its contribution to transformation.
[So] Source:J Gen Virol;98(4):810-820, 2017 Apr.
[Is] ISSN:1465-2099
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The v-rel oncoprotein encoded by reticuloendotheliosis virus T strain (Rev-T) is a member of the rel/NF-κB family of transcription factors capable of transformation of primary chicken spleen and bone marrow cells. Rapid transformation of avian haematopoietic cells by v-rel occurs through a process of deregulation of multiple protein-encoding genes through its direct effect on their promoters. More recently, upregulation of oncogenic miR-155 and its precursor pre-miR-155 was demonstrated in both Rev-T-infected chicken embryo fibroblast cultures and Rev-T-induced B-cell lymphomas. Through electrophoresis mobility shift assay and reporter analysis on the gga-miR-155 promoter, we showed that the v-rel-induced miR-155 overexpression occurred by the direct binding to one of the putative NF-κB binding sites. Using the v-rel-induced transformation model on chicken embryonic splenocyte cultures, we could demonstrate a dynamic increase in miR-155 levels during the transformation. Transcriptome profiles of lymphoid cells transformed by v-rel showed upregulation of miR-155 accompanied by downregulation of a number of putative miR-155 targets such as Pu.1 and CEBPß. We also showed that v-rel could rescue the suppression of miR-155 expression observed in Marek's disease virus (MDV)-transformed cell lines, where its functional viral homologue MDV-miR-M4 is overexpressed. Demonstration of gene expression changes affecting major molecular pathways, including organismal injury and cancer in avian macrophages transfected with synthetic mature miR-155, underlines its potential direct role in transformation. Our study suggests that v-rel-induced transformation involves a complex set of events mediated by the direct activation of NF-κB targets, together with inhibitory effects on microRNA targets.
[Mh] Termos MeSH primário: Transformação Celular Viral
Interações Hospedeiro-Patógeno
Proteínas Oncogênicas v-rel/metabolismo
RNA Mensageiro/biossíntese
Vírus da Reticuloendoteliose/patogenicidade
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Galinhas
Perfilação da Expressão Gênica
Leucócitos Mononucleares/virologia
Regiões Promotoras Genéticas
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Oncogene Proteins v-rel); 0 (RNA, Messenger)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170124
[St] Status:MEDLINE
[do] DOI:10.1099/jgv.0.000718


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[PMID]:27440135
[Au] Autor:Myrthianou E; Zervou MI; Budu-Aggrey A; Eliopoulos E; Kardassis D; Boumpas DT; Kougkas N; Barton A; Sidiropoulos P; Goulielmos GN
[Ad] Endereço:a Laboratory of Molecular Medicine and Human Genetics, Department of Internal Medicine , School of Medicine, University of Crete , Heraklion , Greece.
[Ti] Título:Investigation of the genetic overlap between rheumatoid arthritis and psoriatic arthritis in a Greek population.
[So] Source:Scand J Rheumatol;46(3):180-186, 2017 May.
[Is] ISSN:1502-7732
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Several rheumatoid arthritis (RA) susceptibility loci have also been found to be associated with psoriatic arthritis (PsA), demonstrating that there is a degree of genetic overlap between various autoimmune diseases. We sought to investigate whether single nucleotide polymorphisms (SNPs) mapping to previously reported RA and/or PsA susceptibility loci, including PLCL2, CCL21, REL, STAT4, CD226, PTPN22, and TYK2, are associated with risk for the two diseases in a genetically homogeneous Greek population. METHOD: This study included 392 RA patients, 126 PsA patients, and 521 healthy age- and sex-matched controls from Greece. Genotyping of the SNPs was performed with Taqman primer/probe sets. Bioinformatic analysis was performed using BlastP, PyMOL, and Maestro and Desmond. RESULTS: A significant association was detected between the GC genotype of rs34536443 (TYK2) in both the PsA and RA cohorts. The C allele of this SNP was associated with PsA only. Evidence for association with PsA was also found for the GG genotype and G allele of the rs10181656 SNP of STAT4. The TC genotype of the rs763361 SNP of CD226 was associated with PsA only. CONCLUSIONS: Genetic overlap between PsA and RA was detected for the rs34536443 SNP of the TYK2 gene within a Greek population. An association of STAT4 (rs10181656) with PsA was confirmed whereas CD226 (rs763361) was associated with PsA but not with RA, in contrast to previous reports. The different findings of this study compared to previous ones highlights the importance of comparative studies that include various ethnic or racial populations.
[Mh] Termos MeSH primário: Artrite Psoriásica/genética
Artrite Reumatoide/genética
Grupo com Ancestrais do Continente Europeu/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Alelos
Antígenos de Diferenciação de Linfócitos T/genética
Estudos de Casos e Controles
Quimiocina CCL21/genética
Estudos de Coortes
Feminino
Predisposição Genética para Doença
Genótipo
Técnicas de Genotipagem
Grécia
Seres Humanos
Peptídeos e Proteínas de Sinalização Intracelular/genética
Masculino
Meia-Idade
Modelos Moleculares
Proteínas Oncogênicas v-rel/genética
Polimorfismo de Nucleotídeo Único
Proteína Tirosina Fosfatase não Receptora Tipo 22/genética
Fator de Transcrição STAT4/genética
TYK2 Quinase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Differentiation, T-Lymphocyte); 0 (CCL21 protein, human); 0 (CD226 antigen); 0 (Chemokine CCL21); 0 (Intracellular Signaling Peptides and Proteins); 0 (Oncogene Proteins v-rel); 0 (PLCL2 protein, human); 0 (STAT4 Transcription Factor); 0 (STAT4 protein, human); EC 2.7.10.2 (TYK2 Kinase); EC 2.7.10.2 (TYK2 protein, human); EC 3.1.3.48 (PTPN22 protein, human); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 22)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160722
[St] Status:MEDLINE
[do] DOI:10.1080/03009742.2016.1199734


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[PMID]:27779701
[Au] Autor:Lai X; Guo Y; Guo Z; Liu R; Wang X; Wang F
[Ad] Endereço:Department of Urology Surgery, Dongying People's Hospital, Dongying, Shandong, P.R. China.
[Ti] Título:Downregulation of microRNA­574 in cancer stem cells causes recurrence of prostate cancer via targeting REL.
[So] Source:Oncol Rep;36(6):3651-3656, 2016 Dec.
[Is] ISSN:1791-2431
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:miR­574­5p has been reported involved in the pathogenesis of numerous human malignancies such as colorectal and lung cancer. In this study, we aimed to explore the roles of REL and miR­574 in the recurrence of prostate cancer (PCa) and to identify the underlying molecular mechanisms. Our literature search found that miR­574 is regulated in cancer stem cells (CSCs), and next we used the microRNA (miRNA) database (www.mirdb.org) to find REL as a target of miR­574. Luciferase assay was performed to verify the miRNA/target relationship. Oligo-transfection, real­time PCR and western blot analysis were used to support the conclusions. We validated REL to be the direct gene via luciferase reporter assay system, and real­time PCR and western blot analysis were also conducted to study the mRNA and protein expression level of REL between different groups (recurrence and non­recurrence) or cells treated with scramble control, miR­574 mimics, REL siRNA and miR­574 inhibitors, indicating the negative regulatory relationship between miR­574 and REL. We also investigated the relative viability of prostate CSCs when transfected with scramble control, miR­574 mimics, REL siRNA and miR­574 inhibitors to validate miR­574 to be positively interfering with the viability of prostate CSCs. We then investigated the relative apoptosis of prostate CSCs when transfected with scramble control, miR­574 mimics, REL siRNA and miR­574 inhibitors. The results showed miR­574 inhibited apoptosis. In conclusion, miR­574 might be a novel prognostic and therapeutic target in the management of PCa recurrence.
[Mh] Termos MeSH primário: MicroRNAs/fisiologia
Recidiva Local de Neoplasia/metabolismo
Células-Tronco Neoplásicas/metabolismo
Proteínas Oncogênicas v-rel/genética
Neoplasias da Próstata/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Sequência de Bases
Sítios de Ligação
Linhagem Celular Tumoral
Regulação para Baixo
Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Masculino
Recidiva Local de Neoplasia/genética
Proteínas Oncogênicas v-rel/metabolismo
Neoplasias da Próstata/genética
Neoplasias da Próstata/patologia
Interferência de RNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (MIRN574 microRNA, human); 0 (MicroRNAs); 0 (Oncogene Proteins v-rel)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170317
[Lr] Data última revisão:
170317
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.3892/or.2016.5196


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[PMID]:26971222
[Au] Autor:Li K; Yang W; Li Z; Jia W; Li J; Zhang P; Xiao T
[Ad] Endereço:College of Life Science, Northwest A&F University, Yangling, Shaanxi 712100, China. Electronic address: likeyou2675@nwsuaf.edu.cn.
[Ti] Título:Bitter apricot essential oil induces apoptosis of human HaCaT keratinocytes.
[So] Source:Int Immunopharmacol;34:189-98, 2016 May.
[Is] ISSN:1878-1705
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Psoriasis is a chronic skin disease that affects approximately 2% of the world's population. Conventional therapeutic approaches are not effective or necessarily safe for treating symptoms due to the serious side effects and resistance to currently prescribed drugs. Traditionally, in oriental medicine, apricot seed (Semen Armeniacae amarum) is used to treat skin diseases. However, the underlying mechanism of action has not been systematically elucidated. In the present study, the anti-proliferative effect of bitter apricot essential oil (BAEO) on cultured HaCaT cells was evaluated and the mechanism of action investigated. BAEO was isolated by hydrodistillation, and gas chromatography-mass spectrometry (GC-MS) analysis identified benzaldehyde (75.35%), benzoic acid (6.21%) and mandelonitrile (5.38%). HaCaT cell growth, measured by sulforhodamine B assay (SRB), was inhibited by BAEO with an IC50 value of 142.45 µg/ml. Apoptosis of HaCaT cells treated with BAEO was detected by cell cycle, flow cytometry, and western blot analyses. These measurements revealed G0/G1 cell cycle arrest, elevated numbers of early and late stage apoptotic cells, and caspases-3/8/9 and PARP activation. Z-VAD-FMK, a broad-spectrum caspase inhibitor, attenuated BAEO-induced apoptosis. Also, increased Bax and decreased Bcl-2 levels suggest that BAEO-induced apoptosis is mediated through both death receptor and mitochondrial pathways. Moreover, reduced Rel/NF-κB levels suggest that BAEO-mediated apoptosis is also associated with inhibition of the NF-κB pathway. These data suggest that BAEO is a naturally occurring material that functions as a potent pro-apoptotic factor for human keratinocytes. Thus, it is a promising candidate to treat psoriasis.
[Mh] Termos MeSH primário: Queratinócitos/efeitos dos fármacos
Mitocôndrias/efeitos dos fármacos
Óleos Voláteis/farmacologia
Prunus armeniaca/imunologia
Psoríase/tratamento farmacológico
[Mh] Termos MeSH secundário: Clorometilcetonas de Aminoácidos/farmacologia
Apoptose/efeitos dos fármacos
Caspases/metabolismo
Linhagem Celular
Seres Humanos
Queratinócitos/fisiologia
NF-kappa B/metabolismo
Proteínas Oncogênicas v-rel/metabolismo
Proteínas Proto-Oncogênicas c-bcl-2/genética
Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Receptores de Morte Celular/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amino Acid Chloromethyl Ketones); 0 (NF-kappa B); 0 (Oils, Volatile); 0 (Oncogene Proteins v-rel); 0 (Proto-Oncogene Proteins c-bcl-2); 0 (Receptors, Death Domain); 0 (benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone); EC 3.4.22.- (Caspases)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161231
[Lr] Data última revisão:
161231
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160314
[St] Status:MEDLINE


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[PMID]:26804211
[Au] Autor:Annemann M; Plaza-Sirvent C; Schuster M; Katsoulis-Dimitriou K; Kliche S; Schraven B; Schmitz I
[Ad] Endereço:Institute of Molecular and Clinical Immunology, Otto-von-Guericke University, Leipziger Straße 44, 39120 Magdeburg, Germany.
[Ti] Título:Atypical IκB proteins in immune cell differentiation and function.
[So] Source:Immunol Lett;171:26-35, 2016 Mar.
[Is] ISSN:1879-0542
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:The NF-κB/Rel signalling pathway plays a crucial role in numerous biological processes, including innate and adaptive immunity. NF-κB is a family of transcription factors, whose activity is regulated by the inhibitors of NF-κB (IκB). The IκB proteins comprise two distinct groups, the classical (cytoplasmic) and the atypical (nuclear) IκB proteins. Although the cytoplasmic regulation of NF-κB is well characterised, its nuclear regulation mechanisms remain marginally elucidated. However, work from recent years indicated that nuclear IκBs contribute significantly to the modulation of NF-κB-mediated transcription in the immune system. Here, we discuss the role of the atypical IκB proteins Bcl-3, IκBζ, IκBNS, IκBη and IκBL for the regulation of gene expression and effector functions in immune cells.
[Mh] Termos MeSH primário: Quinase I-kappa B/imunologia
Macrófagos/imunologia
NF-kappa B/metabolismo
Proteínas Nucleares/imunologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Seres Humanos
Imunidade
Imunomodulação
NF-kappa B/imunologia
Proteínas Oncogênicas v-rel/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (NF-kappa B); 0 (Nuclear Proteins); 0 (Oncogene Proteins v-rel); EC 2.7.11.10 (I-kappa B Kinase)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160126
[St] Status:MEDLINE


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[PMID]:26277107
[Au] Autor:Humphries J; Harter B
[Ad] Endereço:Lawrence University, Appleton, WI 54911, USA. Electronic address: judith.humphries@lawrence.edu.
[Ti] Título:Identification of nuclear factor kappaB (NF-κB) binding motifs in Biomphalaria glabrata.
[So] Source:Dev Comp Immunol;53(2):366-70, 2015 Dec.
[Is] ISSN:1879-0089
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Biomphalaria glabrata acts as the intermediate host to the parasite, Schistosoma mansoni, and for this reason, the immune system of B. glabrata has been researched extensively. Several studies have demonstrated that the transcriptome profile of B. glabrata changes following exposure to a variety of pathogens, yet very little is known regarding the regulation of gene expression in this species. Nuclear factor kappaB (NF-κB) homologues have recently been identified in B. glabrata but few functional studies have been carried out on this family of transcription factors. The aims of this study therefore were to identify NF-κB binding sites (κB motifs) in B. glabrata and examine them via functional assays. Two different κB motifs were predicted. Furthermore, the Rel homology domain (RHD) of a B. glabrata NF-κB was able to bind these κB motifs in EMSAs, as well as a vertebrate κB motif.
[Mh] Termos MeSH primário: Biomphalaria/imunologia
NF-kappa B/metabolismo
Proteínas Oncogênicas v-rel/metabolismo
Schistosoma mansoni/fisiologia
Esquistossomose mansoni/fisiopatologia
[Mh] Termos MeSH secundário: Motivos de Aminoácidos/genética
Animais
Sítios de Ligação/genética
Ensaio de Desvio de Mobilidade Eletroforética
Interações Hospedeiro-Parasita
Seres Humanos
Imunidade Inata
Estágios do Ciclo de Vida
NF-kappa B/genética
Ligação Proteica
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (NF-kappa B); 0 (Oncogene Proteins v-rel)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:150929
[Lr] Data última revisão:
150929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150817
[St] Status:MEDLINE


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[PMID]:25766281
[Au] Autor:Cardinaud M; Dheilly NM; Huchette S; Moraga D; Paillard C
[Ad] Endereço:UMR 6539-LEMAR (Laboratoire des Sciences de l'Environnement Marin), IUEM (Institut Universitaire Européen de la Mer), Université de Bretagne Occidentale (UBO), CNRS, IRD, Ifremer, Technopôle Brest Iroise, 29280 Plouzané, France. Electronic address: marion.cardinaud@gmail.com.
[Ti] Título:The early stages of the immune response of the European abalone Haliotis tuberculata to a Vibrio harveyi infection.
[So] Source:Dev Comp Immunol;51(2):287-97, 2015 Aug.
[Is] ISSN:1879-0089
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vibrio harveyi is a marine bacterial pathogen responsible for episodic abalone mortalities in France, Japan and Australia. In the European abalone, V. harveyi invades the circulatory system in a few hours after exposure and is lethal after 2 days of infection. In this study, we investigated the responses of European abalone immune cells over the first 24 h of infection. Results revealed an initial induction of immune gene expression including Rel/NF-kB, Mpeg and Clathrin. It is rapidly followed by a significant immuno-suppression characterized by reduced cellular hemocyte parameters, immune response gene expressions and enzymatic activities. Interestingly, Ferritin was overexpressed after 24 h of infection suggesting that abalone attempt to counter V. harveyi infection using soluble effectors. Immune function alteration was positively correlated with V. harveyi concentration. This study provides the evidence that V. harveyi has a hemolytic activity and an immuno-suppressive effect in the European abalone.
[Mh] Termos MeSH primário: Ferritinas/metabolismo
Gastrópodes/imunologia
Hemócitos/imunologia
Vibrioses/imunologia
Vibrio/imunologia
[Mh] Termos MeSH secundário: Animais
Clatrina/genética
Clatrina/metabolismo
Europa (Continente)
Ferritinas/genética
Regulação da Expressão Gênica
Hemócitos/microbiologia
Hemólise
Imunidade
Imunomodulação
NF-kappa B/genética
NF-kappa B/metabolismo
Proteínas Oncogênicas v-rel/genética
Proteínas Oncogênicas v-rel/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Clathrin); 0 (NF-kappa B); 0 (Oncogene Proteins v-rel); 9007-73-2 (Ferritins)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:150524
[Lr] Data última revisão:
150524
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150314
[St] Status:MEDLINE


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[PMID]:23454593
[Au] Autor:Hwang SY; Hwang JS; Kim SY; Han IO
[Ad] Endereço:Department of Physiology and Biophysics, Inha University, College of Medicine, Incheon, Republic of Korea.
[Ti] Título:Glucosamine inhibits lipopolysaccharide-stimulated inducible nitric oxide synthase induction by inhibiting expression of NF-kappaB/Rel proteins at the mRNA and protein levels.
[So] Source:Nitric Oxide;31:1-8, 2013 May 31.
[Is] ISSN:1089-8611
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Expression of inducible nitric oxide synthase (iNOS) protein by lipopolysaccharide (LPS) in BV2 microglia cells increased in a biphasic manner. Glucosamine (GlcN) selectively suppressed the late- but not early-stage iNOS response to LPS. Prolonged induction of iNOS expression by LPS was inhibited by cycloheximide, suggesting that de novo protein synthesis was required. Late-phase activation of nuclear factor-kappaB (NF-κB) activity required for sustained iNOS induction. Nuclear translocation and DNA binding of NF-κB, and Rel proteins expressions were inhibited by GlcN at later time points but not upon immediate early-stage activation by LPS. We show that GlcN selectively inhibits sustained iNOS induction by inhibiting Rel protein expression at both the mRNA and protein levels; such expression is required for prolonged iNOS induction by LPS. Our results provide mechanistic evidence that GlcN regulates inflammation, represented by iNOS. The implication of these results is that GlcN may be a potent transcriptional regulator of iNOS and other genes involved in the general inflammation process.
[Mh] Termos MeSH primário: Glucosamina/farmacologia
Lipopolissacarídeos/antagonistas & inibidores
NF-kappa B/antagonistas & inibidores
Óxido Nítrico Sintase Tipo II/biossíntese
Proteínas Oncogênicas v-rel/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Western Blotting
Linhagem Celular
Indução Enzimática/efeitos dos fármacos
Lipopolissacarídeos/farmacologia
Camundongos
Proteínas Quinases Ativadas por Mitógeno/antagonistas & inibidores
Proteínas Quinases Ativadas por Mitógeno/metabolismo
NF-kappa B/biossíntese
NF-kappa B/genética
Óxido Nítrico Sintase Tipo II/metabolismo
Proteínas Oncogênicas v-rel/biossíntese
Proteínas Oncogênicas v-rel/genética
RNA Mensageiro/antagonistas & inibidores
RNA Mensageiro/genética
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Lipopolysaccharides); 0 (NF-kappa B); 0 (Oncogene Proteins v-rel); 0 (RNA, Messenger); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, mouse); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); N08U5BOQ1K (Glucosamine)
[Em] Mês de entrada:1311
[Cu] Atualização por classe:161020
[Lr] Data última revisão:
161020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130305
[St] Status:MEDLINE


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[PMID]:22408080
[Au] Autor:Courtine E; Cagnard N; Mazzolini J; Antona M; Pène F; Fitting C; Jacques S; Rousseau C; Niedergang F; Gerondakis S; Chiche JD; Ouaaz F; Mira JP
[Ad] Endereço:CNRS, UMR 8104, INSERM, U1016, Institut Cochin, Paris, France.
[Ti] Título:Combined loss of cRel/p50 subunits of NF-κB leads to impaired innate host response in sepsis.
[So] Source:Innate Immun;18(5):753-63, 2012 Oct.
[Is] ISSN:1753-4267
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:NF-κB, which comprises homo- and hetero-dimers of the five members of the Rel family, plays a crucial role in immunity to infection. The cRel and p50 subunits have been implicated in the development and function of the immune cells, but their in vivo importance remains poorly explored in sepsis. We aimed to study the impact of the combined loss of these two subunits on the innate response to infection in a cecal ligation and puncture model of sepsis. We have explored the possible defects in host defense, including pathogen clearance, bacterial phagocytosis and cytokine plasma release. We also performed gene profiling of cRel(-/-)p50(-/-) and wild-type LPS-stimulated peritoneal macrophages. Deficiency of cRel and p50 led to enhanced mortality to sepsis that was associated with defective macrophages phagocytosis, decreased bacterial clearance and moderate cytokine response. Transcription profile analysis revealed a common inflammatory response but a significant down-regulated transcription of genes encoding for pathogen recognition receptors and antimicrobial molecules, supporting the in vivo findings in mice. In conclusion, the cRel and p50 subunits of NF-κB play an important combined role in the innate response and are crucial for survival and pathogen clearance in polymicrobial sepsis.
[Mh] Termos MeSH primário: Macrófagos/imunologia
Subunidade p50 de NF-kappa B/metabolismo
NF-kappa B/metabolismo
Proteínas Oncogênicas v-rel/metabolismo
Sepse/imunologia
[Mh] Termos MeSH secundário: Animais
Ceco
Células Cultivadas
Feminino
Perfilação da Expressão Gênica
Seres Humanos
Imunidade Inata/genética
Ligadura
Lipopolissacarídeos/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Modelos Animais
Proteínas Mutantes/genética
NF-kappa B/genética
Subunidade p50 de NF-kappa B/genética
Proteínas Oncogênicas v-rel/genética
Punções
Sepse/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Lipopolysaccharides); 0 (Mutant Proteins); 0 (NF-kappa B); 0 (NF-kappa B p50 Subunit); 0 (Oncogene Proteins v-rel)
[Em] Mês de entrada:1303
[Cu] Atualização por classe:120928
[Lr] Data última revisão:
120928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120313
[St] Status:MEDLINE


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[PMID]:21470298
[Au] Autor:Dahl JL; Lau Bonilla D
[Ad] Endereço:Department of Biology, University of Minnesota Duluth, Duluth, MN, USA. jldahl@d.umn.edu
[Ti] Título:The wag31 gene of Mycobacterium tuberculosis is positively regulated by the stringent response.
[So] Source:FEMS Microbiol Lett;319(2):153-9, 2011 Jun.
[Is] ISSN:1574-6968
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The stringent response of Mycobacterium tuberculosis is coordinated by Rel and is required for full virulence in animal models. A serological-based approach identified Wag31(Mtb) as a protein that is upregulated in M. tuberculosis in a rel-dependent manner. This positive regulation was confirmed by analysis of M. tuberculosis mRNA expression. Mycobacterium smegmatis was used to confirm that the expression of wag31(Mtb) from its native promoter is positively regulated by the stringent response. Furthermore, elevated wag31(Mtb) expression in M. smegmatis drastically alters the cell-surface hydrophobic properties.
[Mh] Termos MeSH primário: Proteínas de Bactérias/genética
Mycobacterium tuberculosis/genética
Regulação para Cima
[Mh] Termos MeSH secundário: Proteínas de Bactérias/metabolismo
Regulação Bacteriana da Expressão Gênica
Mycobacterium tuberculosis/metabolismo
Proteínas Oncogênicas v-rel/genética
Proteínas Oncogênicas v-rel/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Oncogene Proteins v-rel)
[Em] Mês de entrada:1108
[Cu] Atualização por classe:110518
[Lr] Data última revisão:
110518
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110408
[St] Status:MEDLINE
[do] DOI:10.1111/j.1574-6968.2011.02278.x



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