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[PMID]:28381191
[Au] Autor:Wu TF; Li YC; Ma SR; Bing-Liu; Zhang WF; Sun ZJ
[Ad] Endereço:1 The State Key Laboratory Breeding Base of Basic Science of Stomatology & Key Laboratory of Oral Biomedicine Ministry of Education, Wuhan University, Wuhan, People's Republic of China.
[Ti] Título:Expression and associations of TRAF1, BMI-1, ALDH1, and Lin28B in oral squamous cell carcinoma.
[So] Source:Tumour Biol;39(4):1010428317695930, 2017 Apr.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tumor necrosis factor receptor-associated factor 1, an adaptor protein of tumor necrosis factor 2, is involved in classical nuclear factor (NF)-κB activation and lymphocyte recruitment. However, less is known about the expression and association of tumor necrosis factor receptor-associated factor 1 with cancer stem cell markers in oral squamous cell carcinoma. This study aimed to investigate the expression of tumor necrosis factor receptor-associated factor 1 and stem cell characteristic markers (lin28 homolog B, B cell-specific Moloney murine leukemia virus integration site 1, and aldehyde dehydrogenase 1) in oral squamous cell carcinoma and analyze their relations. Paraffin-embedded tissues of 78 oral squamous cell carcinomas, 39 normal oral mucosa, and 12 oral dysplasia tissues were employed in tissue microarrays, and the expression of tumor necrosis factor receptor-associated factor 1, B cell-specific Moloney murine leukemia virus integration site 1, aldehyde dehydrogenase 1, and lin28 homolog B was measured by immunohistostaining and digital pathological analysis. The expression of tumor necrosis factor receptor-associated factor 1 was higher in the oral squamous cell carcinoma group as compared with the expression in the oral mucosa (p < 0.01) and oral dysplasia (p < 0.001) groups. In addition, the expression of tumor necrosis factor receptor-associated factor 1 was associated with those of B cell-specific Moloney murine leukemia virus integration site 1, aldehyde dehydrogenase 1, and lin28 homolog B (p = 0.032, r = 0.109; p < 0.0001, r = 0.64; and p < 0.001, r = 0.16) in oral squamous cell carcinoma. The patient survival rate was lower in the highly expressed tumor necrosis factor receptor-associated factor 1 group, although the difference was not significant. The clustering analysis showed that tumor necrosis factor receptor-associated factor 1 was most related to aldehyde dehydrogenase 1. These findings suggest that tumor necrosis factor receptor-associated factor 1 has potential direct/indirect regulations with the cancer stem cell markers in oral squamous cell carcinoma, which may help in further analysis of the cancer stem cell characteristics.
[Mh] Termos MeSH primário: Carcinoma de Células Escamosas/química
Isoenzimas/análise
Neoplasias Bucais/química
Células-Tronco Neoplásicas/química
Complexo Repressor Polycomb 1/análise
Proteínas de Ligação a RNA/análise
Retinal Desidrogenase/análise
Fator 1 Associado a Receptor de TNF/análise
[Mh] Termos MeSH secundário: Biomarcadores
Carcinoma de Células Escamosas/mortalidade
Carcinoma de Células Escamosas/patologia
Seres Humanos
Neoplasias Bucais/mortalidade
Neoplasias Bucais/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (BMI1 protein, human); 0 (Biomarkers); 0 (Isoenzymes); 0 (LIN28B protein, human); 0 (RNA-Binding Proteins); 0 (TNF Receptor-Associated Factor 1); EC 1.2.1.- (aldehyde dehydrogenase 1); EC 1.2.1.36 (Retinal Dehydrogenase); EC 2.3.2.27 (Polycomb Repressive Complex 1)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170418
[Lr] Data última revisão:
170418
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170407
[St] Status:MEDLINE
[do] DOI:10.1177/1010428317695930


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[PMID]:28155233
[Au] Autor:Kim CM; Jeong JH; Son YJ; Choi JH; Kim S; Park HH
[Ad] Endereço:Department of Chemistry and Biochemistry, Graduate School of Biochemistry, Yeungnam University, Gyeongsan, South Korea.
[Ti] Título:Molecular basis for TANK recognition by TRAF1 revealed by the crystal structure of TRAF1/TANK complex.
[So] Source:FEBS Lett;591(5):810-821, 2017 Mar.
[Is] ISSN:1873-3468
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tumor necrosis factor receptor-associated factor 1 (TRAF1) is a multifunctional adaptor protein involved in important processes of cellular signaling, including innate immunity and apoptosis. TRAF family member-associated NF-kappaB activator (TANK) has been identified as a competitive intracellular inhibitor of TRAF2 function. Although TRAF recognition by various receptors has been studied extensively in the field of TRAF-mediated biology, molecular and functional details of TANK recognition and interaction with TRAF1 have not been studied. In this study, we report the crystal structure of the TRAF1/TANK peptide complex. Quantitative interaction experiments showed that TANK peptide interacts with both TRAF1 and TRAF2 with similar affinity in a micromolar range. Our structural study also reveals that TANK binds TRAF1 using a minor minimal consensus motif for TRAF binding, Px(Q/E)xT. DATABASE: Coordinate and structural factor were deposited in the Protein Data Bank under PDB ID code 5H10.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/química
Fator 1 Associado a Receptor de TNF/química
Fator 2 Associado a Receptor de TNF/química
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Sequência de Aminoácidos
Sítios de Ligação
Cristalografia por Raios X
Escherichia coli/genética
Escherichia coli/metabolismo
Expressão Gênica
Seres Humanos
Cinética
Modelos Moleculares
Ligação Proteica
Domínios e Motivos de Interação entre Proteínas
Estrutura Secundária de Proteína
Proteínas Recombinantes/química
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Alinhamento de Sequência
Fator 1 Associado a Receptor de TNF/genética
Fator 1 Associado a Receptor de TNF/metabolismo
Fator 2 Associado a Receptor de TNF/genética
Fator 2 Associado a Receptor de TNF/metabolismo
[Pt] Tipo de publicação:LETTER
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (PSMD2 protein, human); 0 (Recombinant Proteins); 0 (TANK protein, human); 0 (TNF Receptor-Associated Factor 1); 0 (TNF Receptor-Associated Factor 2)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170515
[Lr] Data última revisão:
170515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170204
[St] Status:MEDLINE
[do] DOI:10.1002/1873-3468.12584


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[PMID]:28131816
[Au] Autor:Yamamoto H; Ryu J; Min E; Oi N; Bai R; Zykova TA; Yu DH; Moriyama K; Bode AM; Dong Z
[Ad] Endereço:The Hormel Institute, University of Minnesota, Austin, Minnesota, USA.
[Ti] Título:TRAF1 Is Critical for DMBA/Solar UVR-Induced Skin Carcinogenesis.
[So] Source:J Invest Dermatol;137(6):1322-1332, 2017 Jun.
[Is] ISSN:1523-1747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TRAF1 is a member of the TRAF protein family, which regulates the canonical and noncanonical NF-κB signaling cascades. Although aberrant TRAF1 expression in tumors has been reported, the role of TRAF1 remains elusive. Here, we report that TRAF1 is required for solar UV-induced skin carcinogenesis. Immunohistochemical analysis showed that TRAF1 expression is up-regulated in human actinic keratosis and squamous cell carcinoma. In vivo studies indicated that TRAF1 expression levels in mouse skin are induced by short-term solar UV irradiation, and a long-term skin carcinogenesis study showed that deletion of TRAF1 in mice results in a significant inhibition of skin tumor formation. Moreover, we show that TRAF1 is required for solar UV-induced extracellular signal-regulated kinase-5 (ERK5) phosphorylation and the expression of AP-1 family members (c-Fos/c-Jun). Mechanistic studies showed that TRAF1 expression enhances the ubiquitination of ERK5 on lysine 184, which is necessary for its kinase activity and AP-1 activation. Overall, our results suggest that TRAF1 mediates ERK5 activity by regulating the upstream effectors of ERK5 and also by modulating its ubiquitination status. Targeting TRAF1 function might lead to strategies for preventing and treating skin cancer.
[Mh] Termos MeSH primário: Carcinogênese/efeitos da radiação
Regulação da Expressão Gênica
Queratinócitos/efeitos da radiação
Fator 1 Associado a Receptor de TNF/genética
Raios Ultravioleta/efeitos adversos
[Mh] Termos MeSH secundário: 9,10-Dimetil-1,2-benzantraceno/farmacologia
Análise de Variância
Animais
Carcinogênese/efeitos dos fármacos
Carcinoma de Células Escamosas/genética
Carcinoma de Células Escamosas/patologia
Modelos Animais de Doenças
Epiderme/citologia
Epiderme/patologia
Cromatografia Gasosa-Espectrometria de Massas/métodos
Queratinócitos/citologia
Queratinócitos/patologia
Ceratose Actínica/etiologia
Ceratose Actínica/patologia
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Proteína Quinase 7 Ativada por Mitógeno/metabolismo
Proteína Quinase 7 Ativada por Mitógeno/efeitos da radiação
Distribuição Aleatória
Transdução de Sinais
Neoplasias Cutâneas/etiologia
Neoplasias Cutâneas/fisiopatologia
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (TNF Receptor-Associated Factor 1); 57-97-6 (9,10-Dimethyl-1,2-benzanthracene); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 7)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170913
[Lr] Data última revisão:
170913
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170130
[St] Status:MEDLINE


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[PMID]:28000518
[Au] Autor:Wang KS; Li J; Wang Z; Mi C; Ma J; Piao LX; Xu GH; Li X; Jin X
[Ad] Endereço:a Key Laboratory of Natural Resources of Changbai Mountain & Functional Molecules, Ministry of Education, Molecular Cancer Research Center, College of Pharmacy , Yanbian University , Yanji, Jilin Province , China.
[Ti] Título:Artemisinin inhibits inflammatory response via regulating NF-κB and MAPK signaling pathways.
[So] Source:Immunopharmacol Immunotoxicol;39(1):28-36, 2017 Feb.
[Is] ISSN:1532-2513
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Artemisinin, isolated from the Chinese plant Artemisia annua, has been used for many years to treat different forms of malarial parasites. In this study, we explored the anti-inflammatory activity of artemisinin and the underlying mechanism of this action. We demonstrated that the anti-inflammatory effects of artemisinin in TPA-induced skin inflammation in mice. Then the artemisinin significantly inhibited the expression of NF-κB reporter gene induced by TNF-α in a dose-dependent manner. Artemisinin also inhibited TNF-α induced phosphorylation and degradation of IκBα, p65 nuclear translocation. Artemisinin also has an impact on upstream signaling of IKK through the inhibition of expression of adaptor proteins, TNF receptor-associated factor 2 (TRAF2) and receptor interacting protein 1 (RIP1). Furthermore, pretreatment of cells with artemisinin prevented the TNF-α-induced expression of NF-κB target genes, such as anti-apoptosis (c-IAP1, Bcl-2, and FLIP), proliferation (COX-2, cyclinD1), invasion (MMP-9), angiogenesis (VEGF), and major inflammatory cytokines (TNF-α, iNOS, and MCP1). We also proved that artemisinin potentiated TNF-α-induced apoptosis. Moreover, artemisinin significantly impaired the ROS production and phosphorylation of p38 and ERK, but did not affect the phosphorylation of JNK. Taken together, artemisinin may be a potentially useful therapeutic agent for inflammatory-related diseases.
[Mh] Termos MeSH primário: Artemisininas/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
NF-kappa B/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Relação Dose-Resposta a Droga
Regulação da Expressão Gênica/efeitos dos fármacos
Regulação da Expressão Gênica/imunologia
Seres Humanos
Inflamação/induzido quimicamente
Inflamação/tratamento farmacológico
Inflamação/imunologia
Sistema de Sinalização das MAP Quinases/imunologia
Camundongos
Complexo de Proteínas Formadoras de Poros Nucleares/imunologia
Proteínas de Ligação a RNA/imunologia
Fator 1 Associado a Receptor de TNF/imunologia
Fator 2 Associado a Receptor de TNF/imunologia
Fator de Necrose Tumoral alfa/efeitos adversos
Fator de Necrose Tumoral alfa/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AGFG1 protein, human); 0 (Artemisinins); 0 (NF-kappa B); 0 (Nuclear Pore Complex Proteins); 0 (RNA-Binding Proteins); 0 (TNF Receptor-Associated Factor 1); 0 (TNF Receptor-Associated Factor 2); 0 (Tumor Necrosis Factor-alpha); 9RMU91N5K2 (artemisinine)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170321
[Lr] Data última revisão:
170321
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161222
[St] Status:MEDLINE
[do] DOI:10.1080/08923973.2016.1267744


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[PMID]:27893701
[Au] Autor:Abdul-Sater AA; Edilova MI; Clouthier DL; Mbanwi A; Kremmer E; Watts TH
[Ad] Endereço:Department of Immunology, University of Toronto, Toronto, Ontario, Canada.
[Ti] Título:The signaling adaptor TRAF1 negatively regulates Toll-like receptor signaling and this underlies its role in rheumatic disease.
[So] Source:Nat Immunol;18(1):26-35, 2017 Jan.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TRAF1 is a signaling adaptor known for its role in tumor necrosis factor receptor-induced cell survival. Here we show that monocytes from healthy human subjects with a rheumatoid arthritis-associated single-nucleotide polymorphism (SNP) in the TRAF1 gene express less TRAF1 protein but greater amounts of inflammatory cytokines in response to lipopolysaccharide (LPS). The TRAF1 MATH domain binds directly to three components of the linear ubiquitination (LUBAC) complex, SHARPIN, HOIP and HOIL-1, to interfere with the recruitment and linear ubiquitination of NEMO. This results in decreased NF-κB activation and cytokine production, independently of tumor necrosis factor. Consistent with this, Traf1 mice show increased susceptibility to LPS-induced septic shock. These findings reveal an unexpected role for TRAF1 in negatively regulating Toll-like receptor signaling, providing a mechanistic explanation for the increased inflammation seen with a disease-associated TRAF1 SNP.
[Mh] Termos MeSH primário: Artrite Reumatoide/genética
Leucócitos Mononucleares/imunologia
Monócitos/imunologia
Transdução de Sinais
Fator 1 Associado a Receptor de TNF/metabolismo
[Mh] Termos MeSH secundário: Animais
Citocinas/metabolismo
Predisposição Genética para Doença
Células HEK293
Seres Humanos
Mediadores da Inflamação/metabolismo
Lipopolissacarídeos/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Polimorfismo de Nucleotídeo Único
RNA Interferente Pequeno/genética
Transdução de Sinais/genética
Fator 1 Associado a Receptor de TNF/genética
Receptores Toll-Like/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Inflammation Mediators); 0 (Lipopolysaccharides); 0 (RNA, Small Interfering); 0 (TNF Receptor-Associated Factor 1); 0 (Toll-Like Receptors)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161129
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3618


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[PMID]:28082808
[Au] Autor:Wan XK; Yuan SL; Wang YC; Tao HX; Jiang W; Guan ZY; Cao C; Liu CJ
[Ad] Endereço:Xiu-Kun Wan, Sheng-Ling Yuan, Yan-Chun Wang, Hao-Xia Tao, Wei Jiang, Zhang-Yan Guan, Cheng Cao, Chun-Jie Liu, State Key Laboratory of Pathogen and Biosecurity, Beijing Institute of Biotechnology, Beijing 100071, China.
[Ti] Título: inhibits the cleavage of TRAF1 a CagA-dependent mechanism.
[So] Source:World J Gastroenterol;22(48):10566-10574, 2016 Dec 28.
[Is] ISSN:2219-2840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIM: To study the impact on cleavage of tumor necrosis factor receptor-associated factor 1 (TRAF1) regulated by ( ). METHODS: Cleavage of TRAF1 was detected by western blotting in the human gastric cancer cell line AGS following treatment with an apoptosis inducer. Cleavage of TRAF1 mediated by caspase was examined using specific caspase inhibitors. The effect of the COOH-terminal TRAF1 fragment on gastric cell apoptosis during infection was measured using flow cytometry. The impact of infection on TRAF1 cleavage was detected in the presence of apoptosis inducer. The roles of virulence factors that may regulate TRAF1 cleavage were analyzed using isogenic and null mutants. RESULTS: TRAF1 was found to be cleaved in AGS cells treated with the apoptosis inducer, and caspase-8 was the major caspase involved in the cleavage of TRAF1. The COOH-terminal TRAF1 fragment significantly induced cell apoptosis ( < 0.05) as well as promoted -induced cell apoptosis ( < 0.05). infection was found to significantly inhibit the cleavage of TRAF1 and to inhibit the activation of caspase-8 in the presence of the apoptosis inducer at specific infection times and different cell/bacteria ratios. We also found that the effects of and null mutants on the inhibition of TRAF1 cleavage and activation of caspase-8 were significantly attenuated, compared with wild-type , in the presence of the apoptosis inducer, showing that the virulence factor CagA was mainly involved in the inhibition of TRAF1 cleavage. CONCLUSION: infection significantly inhibits the cleavage of TRAF1 a CagA-dependent mechanism, which would increase the relative amounts of full-length TRAF1 and exert an antiapoptotic effect on -infected cells.
[Mh] Termos MeSH primário: Antígenos de Bactérias/metabolismo
Apoptose
Proteínas de Bactérias/metabolismo
Caspase 8/metabolismo
Helicobacter pylori/patogenicidade
Fator 1 Associado a Receptor de TNF/metabolismo
Fatores de Virulência/metabolismo
[Mh] Termos MeSH secundário: Antígenos de Bactérias/genética
Apoptose/efeitos dos fármacos
Proteínas de Bactérias/genética
Linhagem Celular Tumoral
Técnicas de Cocultura
Cicloeximida/farmacologia
Células Epiteliais/enzimologia
Infecções por Helicobacter/complicações
Infecções por Helicobacter/microbiologia
Helicobacter pylori/genética
Helicobacter pylori/metabolismo
Seres Humanos
Mutação
Estômago
Neoplasias Gástricas/microbiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, Bacterial); 0 (Bacterial Proteins); 0 (TNF Receptor-Associated Factor 1); 0 (VacA protein, Helicobacter pylori); 0 (Virulence Factors); 0 (cagA protein, Helicobacter pylori); 98600C0908 (Cycloheximide); EC 3.4.22.- (CASP8 protein, human); EC 3.4.22.- (Caspase 8)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170114
[St] Status:MEDLINE
[do] DOI:10.3748/wjg.v22.i48.10566


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[PMID]:27827325
[Au] Autor:Heßler N; Geisel MH; Coassin S; Erbel R; Heilmann S; Hennig F; Hoffmann B; Jöckel KH; Moebus S; Moskau-Hartmann S; Nürnberg G; Nürnberg P; Vens M; Klockgether T; Kronenberg F; Scherag A; Ziegler A
[Ad] Endereço:From the Institute of Medical Biometry and Statistics (IMBS), University of Lübeck, University Medical Center Schleswig-Holstein, Campus Lübeck, Germany (N.H., M.V., A.Z.); Clinical Epidemiology, Integrated Research and Treatment Center, Center for Sepsis Control and Care (CSCC), Jena University Hos
[Ti] Título:Linkage and Association Analysis Identifies TRAF1 Influencing Common Carotid Intima-Media Thickness.
[So] Source:Stroke;47(12):2904-2909, 2016 Dec.
[Is] ISSN:1524-4628
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Carotid intima-media thickness is a marker for subclinical atherosclerosis that predicts subsequent clinical cardiovascular events. The aim of this study was to identify chromosomal loci with linkage or association to common carotid intima-media thickness. METHODS: Nuclear families were recruited using the single parental proband sib-pair design. Genotype data were available for 546 individuals from 132 nuclear families of the Bonn IMT Family Study using the Affymetrix GeneChip Human Mapping 250K Sty chip. Multipoint logarithm of the odds (LOD) scores were determined with the quantitative trait locus statistic implemented in multipoint engine for rapid likelihood. Linkage analysis and family-based association tests were conducted. Data from 2471 German participants from the HNR (Heinz Nixdorf Recall) Study were used for subsequent replication. RESULTS: Two new genomic regions with suggestive linkage (LOD>2) were identified on chromosome 4 (LOD=2.26) and on chromosome 17 (LOD=2.01). Previously reported linkage findings were replicated on chromosomes 13 and 14. Fifteen single nucleotide polymorhisms, located on chromosomes 4, 6, and 9, revealed P<10 in the family-based association analyses. One of these signals was replicated in HNR (rs2416804, 1-sided P=1.60×10 , located in the gene TRAF1). CONCLUSIONS: This study presents the first genome-wide linkage and association study of common carotid intima-media thickness in the German population. Alleles of rs2416804 in TRAF1 were identified as being linked and associated with carotid intima-media thickness. Further studies are needed to evaluate the contribution of this locus to the development of atherosclerosis.
[Mh] Termos MeSH primário: Aterosclerose/genética
Espessura Intima-Media Carotídea
Fator 1 Associado a Receptor de TNF/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Feminino
Ligação Genética
Estudo de Associação Genômica Ampla
Alemanha
Seres Humanos
Masculino
Meia-Idade
Núcleo Familiar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (TNF Receptor-Associated Factor 1)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170609
[Lr] Data última revisão:
170609
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161110
[St] Status:MEDLINE


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[PMID]:27592369
[Au] Autor:Cheng T; Sun X; Wu J; Wang M; Eisenberg RA; Chen Z
[Ad] Endereço:Department of Rheumatology, The First Affiliated Hospital of Soochow University, Su Zhou, China. Electronic address: chengtao0526@126.com.
[Ti] Título:Increased serum levels of tumor necrosis factor receptor-associated factor 1 (TRAF1) correlate with disease activity and autoantibodies in rheumatoid arthritis.
[So] Source:Clin Chim Acta;462:103-106, 2016 Nov 01.
[Is] ISSN:1873-3492
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In 2007 a genome wide association analyses revealed an additional risk-associated genetic region in rheumatoid arthritis (RA), the tumor necrosis factor receptor-associated factor 1-complement 5 (TRAF1-C5) containing locus on chromosome 9, comprehensive evaluation of the TRAF1 in RA patients remains necessary. METHODS: Serum was obtained from 79 RA patients and from 38 healthy individuals. Concentrations of TRAF1 were measured by enzyme-linked immune sorbent assay (ELISA). RESULTS: We found that the serum concentration of TRAF1 in RA patients was 35.9±51.2pg/ml, the serum concentration of TRAF1 in healthy controls was 12.5±8.6pg/ml. The difference between these 2 groups was significant (p=0.003). Patients with high disease activity had significantly higher TRAF1 concentration in comparison to patients with low and moderate disease activity (p<0.05). We also found that the numerical DAS28 had a significant positive correlation with TRAF1 concentration (r=0.419, p<0.001). We found that serum GPI and RF concentrations showed a significant positive correlation with TRAF1 concentrations respectively (r=0.767, p<0.001; r=0.365, p=0.001), while CCP concentration showed no significant correlation. CONCLUSIONS: TRAF1 plays a crucial role in the pathogenesis of autoantibodies and may serve as a serologic inflammatory marker of disease activity in RA patients.
[Mh] Termos MeSH primário: Artrite Reumatoide/sangue
Artrite Reumatoide/imunologia
Autoanticorpos/sangue
Fator 1 Associado a Receptor de TNF/sangue
[Mh] Termos MeSH secundário: Artrite Reumatoide/diagnóstico
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (TNF Receptor-Associated Factor 1)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170208
[Lr] Data última revisão:
170208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160905
[St] Status:MEDLINE


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[PMID]:27060717
[Au] Autor:Wan XK; Yuan SL; Tao HX; Diao LP; Wang YC; Cao C; Liu CJ
[Ad] Endereço:State Key Laboratory of Pathogens and Biosecurity, Beijing Institute of Biotechnology, Beijing, China.
[Ti] Título:The Upregulation of TRAF1 Induced by Helicobacter pylori Plays an Antiapoptotic Effect on the Infected Cells.
[So] Source:Helicobacter;21(6):554-564, 2016 Dec.
[Is] ISSN:1523-5378
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Tumor necrosis factor receptor-associated factor 1 (TRAF1) is a member of the TRAF family and is dysregulated in diseases, such as atheroma, lymphoma, and solid tumors, but the role of TRAF1 in gastric cancer remains unknown. This study was aimed to investigate the role of TRAF1 in Helicobacter pylori (H. pylori)-related cell apoptosis and gastric carcinogenesis. MATERIALS AND METHODS: The mRNA and protein expression levels of TRAF1 were measured in a panel of gastric cancer cell lines and in H. pylori -infected mice by quantitative real-time PCR (qPCR) and Western blotting. The transcription factor that mainly affects transcription of TRAF1 during H. pylori infection was identified. The roles of H. pylori virulence factors that regulate TRAF1 expression were analyzed using isogenic cagA-, vacA-, and cagE-null mutants. The effects of TRAF1 on gastric cell viability and apoptosis during H. pylori infection were detected using the standard MTS (cell viability) assay and flow cytometry, respectively. RESULTS: H. pylori infection induced TRAF1 overexpression in both gastric epithelial cells and mice. The expression of TRAF1 in response to H. pylori infection was majorly regulated by the activation of NF-κB and was strongly related to H. pylori virulence factor CagA. The upregulation of TRAF1 inhibited cell apoptosis and increased the viability of infected cells. CONCLUSIONS: H. pylori infection induces the overexpression of TRAF1 in gastric epithelial cells. The upregulation of TRAF1 plays an antiapoptotic role in H. pylori -infected gastric cells and may contribute to the gastric carcinogenesis.
[Mh] Termos MeSH primário: Proteínas Reguladoras de Apoptose/análise
Apoptose
Infecções por Helicobacter/patologia
Fator 1 Associado a Receptor de TNF/análise
[Mh] Termos MeSH secundário: Animais
Proteínas Reguladoras de Apoptose/genética
Linhagem Celular Tumoral
Sobrevivência Celular
Modelos Animais de Doenças
Feminino
Perfilação da Expressão Gênica
Seres Humanos
Camundongos Endogâmicos C57BL
Fator 1 Associado a Receptor de TNF/genética
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apoptosis Regulatory Proteins); 0 (TNF Receptor-Associated Factor 1)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170214
[Lr] Data última revisão:
170214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160410
[St] Status:MEDLINE
[do] DOI:10.1111/hel.12311


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[PMID]:26969755
[Au] Autor:Saxena M; Busca A; Holcik M; Kumar A
[Ad] Endereço:Department of Biochemistry, Microbiology and Immunology, Children's Hospital of Eastern Ontario, University of Ottawa, Ottawa, Ontario K1H 8L1, Canada;
[Ti] Título:Bacterial DNA Protects Monocytic Cells against HIV-Vpr-Induced Mitochondrial Membrane Depolarization.
[So] Source:J Immunol;196(9):3754-67, 2016 05 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Monocytes and macrophages are important HIV reservoirs, as they exhibit marked resistance to apoptosis upon infection. However, the mechanism underlying resistance to apoptosis in these cells is poorly understood. Using HIV-viral protein R-52-96 aa peptide (Vpr), we show that primary monocytes and THP-1 cells treated with Vpr are highly susceptible to mitochondrial depolarization, but develop resistance following stimulation with bacterial DNA or CpG oligodeoxynucleotide. We have shown that Vpr-induced mitochondrial depolarization is mediated by TNFR-associated factor-1 (TRAF-1) and TRAF-2 degradation and subsequent activation of caspase-8, Bid, and Bax. To provide the mechanism governing such resistance to mitochondrial depolarization, our results show that prior stimulation with CpG oligodeoxynucleotide or Escherichia coli DNA prevented: 1) TRAF-1/2 downregulation; 2) activation of caspase-8, Bid, and Bax; and 3) subsequent mitochondrial depolarization and release of apoptosis-inducing factor and cytochrome c Furthermore, this protection was mediated by upregulation of antiapoptotic protein (c-IAP-2) through calmodulin-dependent kinase-II activation. Thus, c-IAP-2 may prevent Vpr-mediated mitochondrial depolarization through stabilizing TRAF-1/2 expression and sequential inhibition of caspase-8, Bid, and Bax.
[Mh] Termos MeSH primário: DNA Bacteriano/imunologia
Proteínas Inibidoras de Apoptose/metabolismo
Macrófagos/imunologia
Monócitos/imunologia
Produtos do Gene vpr do Vírus da Imunodeficiência Humana/metabolismo
[Mh] Termos MeSH secundário: Apoptose
Proteína Agonista de Morte Celular de Domínio Interatuante com BH3/metabolismo
Caspase 8/metabolismo
Linhagem Celular
Escherichia coli/genética
Seres Humanos
Potencial da Membrana Mitocondrial
Fator 1 Associado a Receptor de TNF/metabolismo
Fator 2 Associado a Receptor de TNF/metabolismo
Proteína X Associada a bcl-2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (BAX protein, human); 0 (BH3 Interacting Domain Death Agonist Protein); 0 (BID protein, human); 0 (DNA, Bacterial); 0 (Inhibitor of Apoptosis Proteins); 0 (TNF Receptor-Associated Factor 1); 0 (TNF Receptor-Associated Factor 2); 0 (bcl-2-Associated X Protein); 0 (vpr Gene Products, Human Immunodeficiency Virus); 0 (vpr protein, Human immunodeficiency virus 1); EC 3.4.22.- (Caspase 8)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160313
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1402379



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