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Pesquisa : D12.644.360.024.500 [Categoria DeCS]
Referências encontradas : 452 [refinar]
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[PMID]:28380049
[Au] Autor:Rosenberger CM; Podyminogin RL; Diercks AH; Treuting PM; Peschon JJ; Rodriguez D; Gundapuneni M; Weiss MJ; Aderem A
[Ad] Endereço:Center for Infectious Disease Research, Seattle, WA United States of America.
[Ti] Título:miR-144 attenuates the host response to influenza virus by targeting the TRAF6-IRF7 signaling axis.
[So] Source:PLoS Pathog;13(4):e1006305, 2017 Apr.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Antiviral responses must rapidly defend against infection while minimizing inflammatory damage, but the mechanisms that regulate the magnitude of response within an infected cell are not well understood. miRNAs are small non-coding RNAs that suppress protein levels by binding target sequences on their cognate mRNA. Here, we identify miR-144 as a negative regulator of the host antiviral response. Ectopic expression of miR-144 resulted in increased replication of three RNA viruses in primary mouse lung epithelial cells: influenza virus, EMCV, and VSV. We identified the transcriptional network regulated by miR-144 and demonstrate that miR-144 post-transcriptionally suppresses TRAF6 levels. In vivo ablation of miR-144 reduced influenza virus replication in the lung and disease severity. These data suggest that miR-144 reduces the antiviral response by attenuating the TRAF6-IRF7 pathway to alter the cellular antiviral transcriptional landscape.
[Mh] Termos MeSH primário: Influenza Humana/imunologia
MicroRNAs/metabolismo
Orthomyxoviridae/genética
Transdução de Sinais
Fator 6 Associado a Receptor de TNF/genética
Peptídeos e Proteínas Associados a Receptores de Fatores de Necrose Tumoral/genética
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Células Epiteliais/virologia
Perfilação da Expressão Gênica
Genes Reporter
Seres Humanos
Influenza Humana/virologia
Pulmão/virologia
Camundongos
Camundongos Endogâmicos C57BL
MicroRNAs/genética
Orthomyxoviridae/imunologia
Orthomyxoviridae/fisiologia
Processamento Pós-Transcricional do RNA
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Fator 6 Associado a Receptor de TNF/metabolismo
Peptídeos e Proteínas Associados a Receptores de Fatores de Necrose Tumoral/metabolismo
Carga Viral
Replicação Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN144 microRNA, mouse); 0 (MicroRNAs); 0 (RNA, Messenger); 0 (TNF Receptor-Associated Factor 6); 0 (Traf7 protein, mouse); 0 (Tumor Necrosis Factor Receptor-Associated Peptides and Proteins)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170516
[Lr] Data última revisão:
170516
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006305


  2 / 452 MEDLINE  
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[PMID]:28314689
[Au] Autor:Sahm F; Schrimpf D; Stichel D; Jones DTW; Hielscher T; Schefzyk S; Okonechnikov K; Koelsche C; Reuss DE; Capper D; Sturm D; Wirsching HG; Berghoff AS; Baumgarten P; Kratz A; Huang K; Wefers AK; Hovestadt V; Sill M; Ellis HP; Kurian KM; Okuducu AF; Jungk C; Drueschler K; Schick M; Bewerunge-Hudler M; Mawrin C; Seiz-Rosenhagen M; Ketter R; Simon M; Westphal M; Lamszus K; Becker A; Koch A; Schittenhelm J; Rushing EJ; Collins VP; Brehmer S; Chavez L; Platten M; Hänggi D; Unterberg A; Paulus W; Wick W; Pfister SM; Mittelbronn M; Preusser M; Herold-Mende C; Weller M; von Deimling A
[Ad] Endereço:Department of Neuropathology, Institute of Pathology, Ruprecht-Karls-University Heidelberg, Heidelberg, Germany; Clinical Cooperation Unit Neuropathology, German Cancer Research Center (DKFZ), Heidelberg, Germany.
[Ti] Título:DNA methylation-based classification and grading system for meningioma: a multicentre, retrospective analysis.
[So] Source:Lancet Oncol;18(5):682-694, 2017 May.
[Is] ISSN:1474-5488
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The WHO classification of brain tumours describes 15 subtypes of meningioma. Nine of these subtypes are allotted to WHO grade I, and three each to grade II and grade III. Grading is based solely on histology, with an absence of molecular markers. Although the existing classification and grading approach is of prognostic value, it harbours shortcomings such as ill-defined parameters for subtypes and grading criteria prone to arbitrary judgment. In this study, we aimed for a comprehensive characterisation of the entire molecular genetic landscape of meningioma to identify biologically and clinically relevant subgroups. METHODS: In this multicentre, retrospective analysis, we investigated genome-wide DNA methylation patterns of meningiomas from ten European academic neuro-oncology centres to identify distinct methylation classes of meningiomas. The methylation classes were further characterised by DNA copy number analysis, mutational profiling, and RNA sequencing. Methylation classes were analysed for progression-free survival outcomes by the Kaplan-Meier method. The DNA methylation-based and WHO classification schema were compared using the Brier prediction score, analysed in an independent cohort with WHO grading, progression-free survival, and disease-specific survival data available, collected at the Medical University Vienna (Vienna, Austria), assessing methylation patterns with an alternative methylation chip. FINDINGS: We retrospectively collected 497 meningiomas along with 309 samples of other extra-axial skull tumours that might histologically mimic meningioma variants. Unsupervised clustering of DNA methylation data clearly segregated all meningiomas from other skull tumours. We generated genome-wide DNA methylation profiles from all 497 meningioma samples. DNA methylation profiling distinguished six distinct clinically relevant methylation classes associated with typical mutational, cytogenetic, and gene expression patterns. Compared with WHO grading, classification by individual and combined methylation classes more accurately identifies patients at high risk of disease progression in tumours with WHO grade I histology, and patients at lower risk of recurrence among WHO grade II tumours (p=0·0096) from the Brier prediction test). We validated this finding in our independent cohort of 140 patients with meningioma. INTERPRETATION: DNA methylation-based meningioma classification captures clinically more homogenous groups and has a higher power for predicting tumour recurrence and prognosis than the WHO classification. The approach presented here is potentially very useful for stratifying meningioma patients to observation-only or adjuvant treatment groups. We consider methylation-based tumour classification highly relevant for the future diagnosis and treatment of meningioma. FUNDING: German Cancer Aid, Else Kröner-Fresenius Foundation, and DKFZ/Heidelberg Institute of Personalized Oncology/Precision Oncology Program.
[Mh] Termos MeSH primário: Metilação de DNA
Neoplasias Meníngeas/classificação
Neoplasias Meníngeas/genética
Meningioma/classificação
Meningioma/genética
Recidiva Local de Neoplasia/genética
[Mh] Termos MeSH secundário: Variações do Número de Cópias de DNA
Análise Mutacional de DNA
Proteínas de Ligação a DNA/genética
Progressão da Doença
Intervalo Livre de Doença
Feminino
Genoma
Seres Humanos
Fatores de Transcrição Kruppel-Like/genética
Masculino
Neoplasias Meníngeas/patologia
Meningioma/patologia
Gradação de Tumores
Recidiva Local de Neoplasia/patologia
Neurofibromina 2/genética
Proteínas Nucleares/genética
Proteínas Proto-Oncogênicas c-akt/genética
Estudos Retrospectivos
Análise de Sequência de RNA
Receptor Smoothened/genética
Taxa de Sobrevida
Fatores de Transcrição/genética
Transcriptoma
Peptídeos e Proteínas Associados a Receptores de Fatores de Necrose Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (ARID1A protein, human); 0 (ARID1B protein, human); 0 (DNA-Binding Proteins); 0 (GKLF protein); 0 (Kruppel-Like Transcription Factors); 0 (Neurofibromin 2); 0 (Nuclear Proteins); 0 (SMO protein, human); 0 (Smoothened Receptor); 0 (TRAF7 protein, human); 0 (Transcription Factors); 0 (Tumor Necrosis Factor Receptor-Associated Peptides and Proteins); EC 2.7.11.1 (AKT1 protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170810
[Lr] Data última revisão:
170810
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170319
[St] Status:MEDLINE


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[PMID]:28274739
[Au] Autor:Lambert S; Swindell WR; Tsoi LC; Stoll SW; Elder JT
[Ad] Endereço:Department of Dermatology, University of Michigan, Ann Arbor, Michigan, USA.
[Ti] Título:Dual Role of Act1 in Keratinocyte Differentiation and Host Defense: TRAF3IP2 Silencing Alters Keratinocyte Differentiation and Inhibits IL-17 Responses.
[So] Source:J Invest Dermatol;137(7):1501-1511, 2017 Jul.
[Is] ISSN:1523-1747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:TRAF3IP2 is a candidate psoriasis susceptibility gene encoding Act1, an adaptor protein with ubiquitin ligase activity that couples the IL-17 receptor to downstream signaling pathways. We investigated the role of Act1 in keratinocyte responses to IL-17 using a tetracycline inducible short hairpin RNA targeting TRAF3IP2. Tetracycline exposure for 7 days effectively silenced TRAF3IP2 mRNA and Act1 protein, resulting in 761 genes with significant changes in expression (495 down, 266 up; >1.5-fold, P < 0.05). Gene ontology analysis showed that genes affected by TRAF3IP2 silencing are involved in epidermal differentiation, with early differentiation genes (KRT1, KRT10, DSC1, DSG1) being down-regulated and late differentiation genes (SPRR2, SPRR3, LCE3) being up-regulated. AP1 binding sites were enriched upstream of genes up-regulated by TRAF3IP2 silencing. Correspondingly, nuclear expression of FosB and Fra1 was increased in TRAF3IP2-silenced cells. Many genes involved in host defense were induced by IL-17 in a TRAF3IP2-dependent fashion. Inflammatory differentiation conditions (serum addition for 4 days postconfluence) markedly amplified these IL-17 responses and increased basal levels and TRAF3IP2 silencing-dependent up-regulation of multiple late differentiation genes. These findings suggest that TRAF3IP2 may alter both epidermal homeostasis and keratinocyte defense responses to influence psoriasis risk.
[Mh] Termos MeSH primário: Conexina 43/metabolismo
Regulação da Expressão Gênica
Interleucina-17/metabolismo
Queratinócitos/metabolismo
Fragmentos de Peptídeos/metabolismo
Psoríase/genética
RNA/genética
Peptídeos e Proteínas Associados a Receptores de Fatores de Necrose Tumoral/genética
[Mh] Termos MeSH secundário: Diferenciação Celular
Células Cultivadas
Seres Humanos
Queratinócitos/patologia
Reação em Cadeia da Polimerase
Psoríase/metabolismo
Psoríase/patologia
Transdução de Sinais
Peptídeos e Proteínas Associados a Receptores de Fatores de Necrose Tumoral/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACT1 protein); 0 (Connexin 43); 0 (Interleukin-17); 0 (Peptide Fragments); 0 (TRAF3IP2 protein, human); 0 (Tumor Necrosis Factor Receptor-Associated Peptides and Proteins); 63231-63-0 (RNA)
[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:170310
[St] Status:MEDLINE


  4 / 452 MEDLINE  
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[PMID]:28107378
[Au] Autor:Conigliaro P; Ciccacci C; Politi C; Triggianese P; Rufini S; Kroegler B; Perricone C; Latini A; Novelli G; Borgiani P; Perricone R
[Ad] Endereço:Clinic of Rheumatology, Allergology and Clinical Immunology, Department of "Medicina dei Sistemi", University of Rome Tor Vergata, Rome, Italy.
[Ti] Título:Polymorphisms in STAT4, PTPN2, PSORS1C1 and TRAF3IP2 Genes Are Associated with the Response to TNF Inhibitors in Patients with Rheumatoid Arthritis.
[So] Source:PLoS One;12(1):e0169956, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Rheumatoid Arthritis (RA) is a progressive autoimmune disease characterized by chronic joint inflammation and structural damage. Remission or at least low disease activity (LDA) represent potentially desirable goals of RA treatment. Single nucleotide polymorphisms (SNPs) in several genes might be useful for prediction of response to therapy. We aimed at exploring 4 SNPs in candidate genes (STAT4, PTPN2, PSORS1C1 and TRAF3IP2) in order to investigate their potential role in the response to therapy with tumor necrosis factor inhibitors (TNF-i) in RA patients. METHODS: In 171 RA patients we investigated the following SNPs: rs7574865 (STAT4), rs2233945 (PSORS1C1), rs7234029 (PTPN2) and rs33980500 (TRAF3IP2). Remission, LDA, and EULAR response were registered at 6 months and 2 years after initiation of first line TNF-i [Adalimumab (ADA) and Etanercept (ETN)]. RESULTS: STAT4 variant allele was associated with the absence of a good/moderate EULAR response at 2 years of treatment in the whole RA group and in ETN treated patients. The PTPN2 SNP was associated with no good/moderate EULAR response at 6 months in ADA treated patients. Patients carrying PSORS1C1 variant allele did not reach LDA at 6 months in both the whole RA group and ETN treated patients. TRAF3IP2 variant allele was associated with the lack of LDA and remission achievement at 6 months in all RA cohort while an association with no EULAR response at 2 years of treatment occurred only in ETN treated patients. CONCLUSIONS: For the first time, we reported that SNPs in STAT4, PTPN2, PSORS1C1, and TRAF3IP2 are associated with response to TNF-i treatment in RA patients; however, these findings should be validated in a larger population.
[Mh] Termos MeSH primário: Artrite Reumatoide/tratamento farmacológico
Polimorfismo de Nucleotídeo Único
Proteína Tirosina Fosfatase não Receptora Tipo 2/genética
Proteínas/genética
Fator de Transcrição STAT4/genética
Peptídeos e Proteínas Associados a Receptores de Fatores de Necrose Tumoral/genética
Fator de Necrose Tumoral alfa/antagonistas & inibidores
[Mh] Termos MeSH secundário: Adulto
Idoso
Artrite Reumatoide/genética
Feminino
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (PSORS1C1 protein, human); 0 (Proteins); 0 (STAT4 Transcription Factor); 0 (STAT4 protein, human); 0 (TRAF3IP2 protein, human); 0 (Tumor Necrosis Factor Receptor-Associated Peptides and Proteins); 0 (Tumor Necrosis Factor-alpha); EC 3.1.3.48 (PTPN2 protein, human); EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 2)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170810
[Lr] Data última revisão:
170810
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170121
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0169956


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[PMID]:28019650
[Au] Autor:Klein CJ; Wu Y; Jentoft ME; Mer G; Spinner RJ; Dyck PJ; Dyck PJ; Mauermann ML
[Ad] Endereço:Department of Neurology, Mayo Clinic, Rochester, MN.
[Ti] Título:Genomic analysis reveals frequent TRAF7 mutations in intraneural perineuriomas.
[So] Source:Ann Neurol;81(2):316-321, 2017 Feb.
[Is] ISSN:1531-8249
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Intraneural perineuriomas are benign peripheral nerve sheath tumors that cause progressive debilitating focal extremity weakness. The etiology of perineuriomas is largely unknown. We utilized whole exome sequencing, copy number algorithm evaluation, and high-resolution whole genome microarray to investigate for a genetic causal link to intraneural perineuriomas. Ten of 16 (60%) tumor cases had mutations in the WD40 domain of TRAF7, the same location for causal mutations of meningiomas. Two additional perineurioma cases had large chromosomal abnormalities in multiple chromosomes, including chromosome 22q. This study identifies a common cause for intraneural perineuriomas and an unexpected shared pathogenesis with intracranial meningiomas. Ann Neurol 2017;81:316-321.
[Mh] Termos MeSH primário: Neoplasias da Bainha Neural/genética
Peptídeos e Proteínas Associados a Receptores de Fatores de Necrose Tumoral/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Criança
Pré-Escolar
Exoma
Feminino
Genômica
Seres Humanos
Masculino
Meia-Idade
Mutação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (TRAF7 protein, human); 0 (Tumor Necrosis Factor Receptor-Associated Peptides and Proteins)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170630
[Lr] Data última revisão:
170630
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161227
[St] Status:MEDLINE
[do] DOI:10.1002/ana.24854


  6 / 452 MEDLINE  
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[PMID]:27818344
[Au] Autor:Wei J; Zang S; Xu M; Zheng Q; Chen X; Qin Q
[Ad] Endereço:Key Laboratory of Tropical Marine Bio-resources and Ecology, South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzhou, 510301, PR China; Guangdong Provincial Key Laboratory of Applied Marine Biology, South China Sea Institute of Oceanology, Chinese Academy of Sciences, Guangzh
[Ti] Título:TRAF6 is a critical factor in fish immune response to virus infection.
[So] Source:Fish Shellfish Immunol;60:6-12, 2017 Jan.
[Is] ISSN:1095-9947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tumor necrosis factor receptor-associated factor 6 (TRAF6) is one of the key adaptor molecule in Toll-like receptor signal transduction that triggers downstream cascades involved in innate immunity. In our previous study, the molecular characteristics of EtTRAF6 (TRAF6 from Epinephelus tauvina), the tissue distributions, expression patterns after challenging with bacterial and viral pathogens were investigated. Here we identified EtTRAF6 as an important regulator of virus-triggered signaling pathway. Overexpression of EtTRAF6-ORF and truncated forms of EtTRAF6, including EtTRAF6-C (delete the MATH domain), EtTRAF6-N (delete the RING domain) and EtTRAF6-MATH, inhibited IFN-ß activity strongly in grouper spleen (GS) cells. Overexpression of EtTRAF6 repressed virus-induced production of type I IFNs. When EtTRAF6 cotransfected with EcIRF3 or EcIRF7, EtTRAF6 inhibited IRF-induced activation of IFN-ß. Over-expressed EtTRAF6 inhibited the transcription of SGIV genes significantly in GS cells. Although TRAF6 has a role in apoptosis regulation, it is not known if EtTRAF6 has any role in apoptosis regulation. Strikingly, when over-expressed in fathead minnow (FHM) cells, EtTRAF6 protected them from cell death induced by SGIV. Therefore, these results suggest that TRAF6 may play a critical role in their response to SGIV infection, through regulation of a cell death pathway that is common to fish and humans.
[Mh] Termos MeSH primário: Bass
Infecções por Vírus de DNA/veterinária
Doenças dos Peixes/imunologia
Proteínas de Peixes/genética
Proteínas de Peixes/imunologia
Peptídeos e Proteínas Associados a Receptores de Fatores de Necrose Tumoral/genética
Peptídeos e Proteínas Associados a Receptores de Fatores de Necrose Tumoral/imunologia
[Mh] Termos MeSH secundário: Animais
Infecções por Vírus de DNA/genética
Infecções por Vírus de DNA/imunologia
Infecções por Vírus de DNA/virologia
Doenças dos Peixes/genética
Doenças dos Peixes/virologia
Proteínas de Peixes/metabolismo
Ranavirus/fisiologia
Análise de Sequência de DNA/veterinária
Peptídeos e Proteínas Associados a Receptores de Fatores de Necrose Tumoral/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fish Proteins); 0 (Tumor Necrosis Factor Receptor-Associated Peptides and Proteins)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170404
[Lr] Data última revisão:
170404
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161108
[St] Status:MEDLINE


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[PMID]:27808423
[Au] Autor:Zotti T; Scudiero I; Vito P; Stilo R
[Ad] Endereço:Dipartimento di Scienze e Tecnologie, Università degli Studi del Sannio, Benevento, Italy.
[Ti] Título:The Emerging Role of TRAF7 in Tumor Development.
[So] Source:J Cell Physiol;232(6):1233-1238, 2017 Jun.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The seven members of the tumor necrosis factor receptor (TNF-R)-associated factor (TRAF) family of intracellular proteins were originally discovered and characterized as signaling adaptor molecules coupled to the cytoplasmic regions of receptors of the TNF-R superfamily. Functionally, TRAFs act both as a scaffold and/or enzymatic proteins to regulate activation of mitogen-activated protein kinases (MAPKs) and transcription factors of nuclear factor-κB family (NF-κB). Given the wide variety of stimuli intracellularly conveyed by TRAF proteins, they are physiologically involved in multiple biological processes, including embryonic development, tissue homeostasis, and regulation of innate and adaptive immune responses. In the last few years, it has become increasingly evident the involvement of TRAF7, the last member of the TRAF family to be discovered, in the genesis and progression of several human cancers, placing TRAF7 in the spotlight as a novel tumor suppressor protein. In this paper, we review and discuss the literature recently produced on this subject. J. Cell. Physiol. 232: 1233-1238, 2017. © 2016 The Authors. Journal of Cellular Physiology Published by Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Carcinogênese/metabolismo
Carcinogênese/patologia
Neoplasias/metabolismo
Neoplasias/patologia
Peptídeos e Proteínas Associados a Receptores de Fatores de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Modelos Biológicos
Mutação/genética
Domínios Proteicos
Peptídeos e Proteínas Associados a Receptores de Fatores de Necrose Tumoral/química
Peptídeos e Proteínas Associados a Receptores de Fatores de Necrose Tumoral/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Tumor Necrosis Factor Receptor-Associated Peptides and Proteins)
[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:161104
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25676


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[PMID]:27847407
[Au] Autor:Kong QZ; Guo LT; Yang JN; Wang YF; Zhao JX; Kong SH; Zhang M; Yan S; Jin Y
[Ad] Endereço:Department of Orthopedic Trauma, Affiliated Hospital of Chengde Medical University, Chengde, Hebei 06700, China.
[Ti] Título:Anti-Inflammatory Effects of TRAF-Interacting Protein in Rheumatoid Arthritis Fibroblast-Like Synoviocytes.
[So] Source:Mediators Inflamm;2016:3906108, 2016.
[Is] ISSN:1466-1861
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease characterized by inflammatory cell infiltration, synovial inflammation, and cartilage destruction. Proliferative fibroblast-like synoviocytes (FLS) play crucial roles in both propagation of inflammation and joint damage because of their production of great amount of proinflammatory cytokines and proteolytic enzymes. In this study, we investigate the role of TRAF-interacting protein (TRIP) in regulating inflammatory process in RA-FLS. TRIP expression was attenuated in RA-FLS compared with osteoarthritis- (OA-) FLS. Overexpression of TRIP significantly inhibited the activation of NF- B signaling and decreased the production of proinflammatory cytokines and matrix metalloproteinases (MMPs) in TNF -stimulated RA-FLS. Furthermore, TRIP was found to interact with transforming growth factor -activated kinase 1 (TAK1) and promoting K48-linked polyubiquitination of TAK1 in RA-FLS. Our results demonstrate that TRIP has anti-inflammatory effects on RA-FLS and suggest TRIP as a potential therapeutic target for human RA.
[Mh] Termos MeSH primário: Artrite Reumatoide/metabolismo
Fibroblastos/metabolismo
MAP Quinase Quinase Quinases/metabolismo
Osteoartrite/metabolismo
Peptídeos e Proteínas Associados a Receptores de Fatores de Necrose Tumoral/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Citocinas/metabolismo
Ensaio de Imunoadsorção Enzimática
Seres Humanos
Inflamação
Interleucina-1beta/metabolismo
Interleucina-6/metabolismo
Lentivirus
Metaloproteinase 1 da Matriz/metabolismo
Metaloproteinase 13 da Matriz/metabolismo
NF-kappa B/metabolismo
Transdução de Sinais
Líquido Sinovial/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (IL1B protein, human); 0 (IL6 protein, human); 0 (Interleukin-1beta); 0 (Interleukin-6); 0 (NF-kappa B); 0 (Tumor Necrosis Factor Receptor-Associated Peptides and Proteins); EC 2.3.2.27 (TRAIP protein, human); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.11.25 (MAP Kinase Kinase Kinases); EC 2.7.11.25 (MAP kinase kinase kinase 7); EC 3.4.24.- (MMP13 protein, human); EC 3.4.24.- (Matrix Metalloproteinase 13); EC 3.4.24.7 (MMP1 protein, human); EC 3.4.24.7 (Matrix Metalloproteinase 1)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170811
[Lr] Data última revisão:
170811
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161117
[St] Status:MEDLINE


  9 / 452 MEDLINE  
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[PMID]:27723765
[Au] Autor:Velichko S; Zhou X; Zhu L; Anderson JD; Wu R; Chen Y
[Ad] Endereço:The Center for Comparative Respiratory Biology and Medicine, Department of Internal Medicine, University of California Davis, Davis, California, 95616, United States of America.
[Ti] Título:A Novel Nuclear Function for the Interleukin-17 Signaling Adaptor Protein Act1.
[So] Source:PLoS One;11(10):e0163323, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the context of the human airway, interleukin-17A (IL-17A) signaling is associated with severe inflammation, as well as protection against pathogenic infection, particularly at mucosal surfaces such as the airway. The intracellular molecule Act1 has been demonstrated to be an essential mediator of IL-17A signaling. In the cytoplasm, it serves as an adaptor protein, binding to both the intracellular domain of the IL-17 receptor as well as members of the canonical nuclear factor kappa B (NF-κB) pathway. It also has enzymatic activity, and serves as an E3 ubiquitin ligase. In the context of airway epithelial cells, we demonstrate for the first time that Act1 is also present in the nucleus, especially after IL-17A stimulation. Ectopic Act1 expression can also increase the nuclear localization of Act1. Act1 can up-regulate the expression and promoter activity of a subset of IL-17A target genes in the absence of IL-17A signaling in a manner that is dependent on its N- and C-terminal domains, but is NF-κB independent. Finally, we show that nuclear Act1 can bind to both distal and proximal promoter regions of DEFB4, one of the IL-17A responsive genes. This transcriptional regulatory activity represents a novel function for Act1. Taken together, this is the first report to describe a non-adaptor function of Act1 by directly binding to the promoter region of IL-17A responsive genes and directly regulate their transcription.
[Mh] Termos MeSH primário: Elementos de Resposta/fisiologia
Transdução de Sinais/fisiologia
Transcrição Genética/fisiologia
Peptídeos e Proteínas Associados a Receptores de Fatores de Necrose Tumoral/metabolismo
Regulação para Cima/fisiologia
[Mh] Termos MeSH secundário: Células A549
Seres Humanos
Interleucina-17/biossíntese
Interleucina-17/genética
NF-kappa B/genética
NF-kappa B/metabolismo
Domínios Proteicos
Peptídeos e Proteínas Associados a Receptores de Fatores de Necrose Tumoral/genética
beta-Defensinas/biossíntese
beta-Defensinas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DEFB4A protein, human); 0 (IL17A protein, human); 0 (Interleukin-17); 0 (NF-kappa B); 0 (TRAF3IP2 protein, human); 0 (Tumor Necrosis Factor Receptor-Associated Peptides and Proteins); 0 (beta-Defensins)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171028
[Lr] Data última revisão:
171028
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161011
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0163323


  10 / 452 MEDLINE  
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[PMID]:27660002
[Au] Autor:Tomuschat C; O'Donnell AM; Coyle D; Puri P
[Ad] Endereço:National Children's Research Centre, Our Lady's Children's Hospital, Crumlin, Dublin 12, Ireland.
[Ti] Título:Increased Act1/IL-17R expression in Hirschsprung's disease.
[So] Source:Pediatr Surg Int;32(12):1201-1207, 2016 Dec.
[Is] ISSN:1437-9813
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Hirschsprung's disease -associated enterocolitis (HAEC) is the most common cause of morbidity and mortality in Hirschsprung's disease (HSCR). Altered intestinal epithelial barrier function is implicated in the pathogenesis of HAEC. IL-17 is a proinflammatory cytokine that plays a crucial role in host defense against microbial organisms in the development of inflammatory diseases. Act1 is an essential adaptor molecule required for the IL-17-mediated inflammatory responses via interaction with IL-17 receptor (IL-17R). We designed this study to investigate the hypothesis that Act1/Il-17R expression is upregulated in HSCR. METHODS: We investigated Act1 and IL17R expression in ganglionic andaganglionic bowel of HD patients (n = 10) and controls (n = 10). qPCR, Western blotting and confocal immunofluorescence were performed. MAIN RESULTS: qPCR and Western blot analysis revealed that Act1 and IL17R are strongly expressed in the aganglionic and ganglionic colon of patients with HSCR. Act1 and IL17R expression was significantly increased in HSCR specimens compared to controls (p < 0.05). Confocal microscopy revealed a markedly increased expression of Act1 and IL17R in the colonic epithelium of patients with HSCR compared to controls. CONCLUSION: To our knowledge, we report, for the first time, the expression of Act1 in the human colon. The increased expression of Act1 and Il-17 in the aganglionic and ganglionic bowel in HSCR may result in IL-17-mediated increased inflammatory response leading to the development of HAEC.
[Mh] Termos MeSH primário: Doença de Hirschsprung/genética
Interleucina-17/genética
Peptídeos e Proteínas Associados a Receptores de Fatores de Necrose Tumoral/genética
[Mh] Termos MeSH secundário: Western Blotting
Feminino
Imunofluorescência
Gânglios/metabolismo
Gânglios/patologia
Expressão Gênica/genética
Doença de Hirschsprung/patologia
Seres Humanos
Lactente
Mucosa Intestinal/metabolismo
Mucosa Intestinal/patologia
Intestinos/metabolismo
Intestinos/patologia
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-17); 0 (TRAF3IP2 protein, human); 0 (Tumor Necrosis Factor Receptor-Associated Peptides and Proteins)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160924
[St] Status:MEDLINE



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