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[PMID]:27110068
[Au] Autor:Shang J; Li L; Wang X; Pan H; Liu S; He R; Li J; Zhao Q
[Ad] Endereço:Department of Gastroenterology/Hepatology, Zhongnan Hospital of Wuhan University, Wuhan 430071, China; The Hubei Clinical Center & Key Laboratory of Intestinal & Colorectal Diseases, Wuhan 430071, China.
[Ti] Título:Disruption of Tumor Necrosis Factor Receptor-Associated Factor 5 Exacerbates Murine Experimental Colitis via Regulating T Helper Cell-Mediated Inflammation.
[So] Source:Mediators Inflamm;2016:9453745, 2016.
[Is] ISSN:1466-1861
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tumor necrosis factor (TNF) receptor-associated factor 5 (TRAF5) is a key mediator of TNF receptor superfamily members and is important in both T helper (Th) cell immunity and the regulation of multiple signaling pathways. To clarify TRAF5's influence on inflammatory bowel diseases (IBDs), we investigated TRAF5 deficiency's effect on dextran sulfate sodium- (DSS-) induced colitis. Colitis was induced in TRAF5 knockout (KO) mice and their wild-type (WT) littermates by administering 3% DSS orally for 7 days. The mice were then sacrificed, and their colons were removed. Our data suggested that KO mice were more susceptible to DSS-induced colitis. TRAF5 deficiency significantly enhanced IFN-γ, IL-4, and IL-17a mRNA and protein levels in the colons of DSS-fed mice, and the mRNA expression of T-bet and GATA-3 was also markedly elevated. However, ROR-α and ROR-γt mRNA levels did not differ between DSS-induced KO and WT mice. Flow cytometry showed increased frequencies of Th2 and IFN-γ/IL-17a-coproducing CD4(+) T cells in the colons of DSS-induced KO mice. Additionally, TRAF5 deficiency significantly enhanced the activation of NF-κB in CD4(+) T cells after DSS administration. These results indicated that TRAF5 deficiency significantly aggravated DSS-induced colitis, most likely by regulating Th cell-mediated inflammation.
[Mh] Termos MeSH primário: Inflamação/metabolismo
Linfócitos T Auxiliares-Indutores/metabolismo
Fator 5 Associado a Receptor de TNF/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Linfócitos T CD4-Positivos/metabolismo
Colite
Sulfato de Dextrana/farmacologia
Modelos Animais de Doenças
Eletroforese em Gel de Poliacrilamida
Feminino
Citometria de Fluxo
Inflamação/genética
Interleucina-17/metabolismo
Masculino
Camundongos
Camundongos Knockout
Peroxidase/genética
Peroxidase/metabolismo
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
Fator 5 Associado a Receptor de TNF/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-17); 0 (RNA, Messenger); 0 (TNF Receptor-Associated Factor 5); 9042-14-2 (Dextran Sulfate); EC 1.11.1.7 (Peroxidase)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170117
[Lr] Data última revisão:
170117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160426
[St] Status:MEDLINE
[do] DOI:10.1155/2016/9453745


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[PMID]:27076680
[Au] Autor:Nagashima H; Okuyama Y; Hayashi T; Ishii N; So T
[Ad] Endereço:Department of Microbiology and Immunology, Tohoku University Graduate School of Medicine, Sendai 980-8575, Japan.
[Ti] Título:TNFR-Associated Factors 2 and 5 Differentially Regulate the Instructive IL-6 Receptor Signaling Required for Th17 Development.
[So] Source:J Immunol;196(10):4082-9, 2016 05 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:IL-17-producing CD4(+) T cells (Th17 cells) regulate host defense and immune pathogenesis, and IL-6 plays an important role for the differentiation of Th17 cells. We have previously identified that TNFR-associated factor (TRAF)5 binds to the signal-transducing receptor gp130 through the C-terminal TRAF domain and inhibits Th17 development mediated by IL-6. Although gp130 has TRAF-binding motifs that can be recognized by other TRAF family proteins, it is unclear how TRAFs regulate IL-6-driven Th17 differentiation in general. Using retrovirus-mediated gene complementation and gene silencing approaches, we found that not only TRAF5 but also TRAF2 restrained the IL-6R signaling, whereas TRAF1, TRAF3, TRAF4, and TRAF6 did not. Traf2 silencing further promoted the ability of naive CD4(+) T cells from Traf5(-/-) mice to differentiate into Th17 cells. Notably, TRAF5 but not TRAF2 expressed in naive CD4(+) T cells was rapidly downregulated after TCR triggering, which indicates that TRAF5 specifically inhibits instructive IL-6 signals in the initial stage of Th17 development. Collectively, our results demonstrate a dedicated role for TRAF2 and TRAF5 in the process of IL-6-mediated Th17 development and a differential role for TCR signaling in regulation of TRAF2 and TRAF5. Therefore, both TRAF2 and TRAF5 work as important regulators of the IL-6R signaling needed for Th17 development.
[Mh] Termos MeSH primário: Receptor gp130 de Citocina/metabolismo
Interleucina-6/metabolismo
Fator 2 Associado a Receptor de TNF/metabolismo
Fator 5 Associado a Receptor de TNF/metabolismo
Células Th17/fisiologia
[Mh] Termos MeSH secundário: Transferência Adotiva
Animais
Linfócitos B/imunologia
Diferenciação Celular
Linhagem Celular
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
RNA Interferente Pequeno/genética
Transdução de Sinais
Fator 2 Associado a Receptor de TNF/genética
Fator 5 Associado a Receptor de TNF/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-6); 0 (RNA, Small Interfering); 0 (TNF Receptor-Associated Factor 2); 0 (TNF Receptor-Associated Factor 5); 133483-10-0 (Cytokine Receptor gp130)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160415
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1501610


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[PMID]:26872784
[Au] Autor:Zhang L; Blackwell K; Workman LM; Gibson-Corley KN; Olivier AK; Bishop GA; Habelhah H
[Ad] Endereço:Department of Pathology, Carver College of Medicine, University of Iowa, and the Iowa City Veterans Affairs Medical Center, Iowa City, IA 52242, USA.
[Ti] Título:TRAF2 exerts opposing effects on basal and TNFα-induced activation of the classic IKK complex in hematopoietic cells in mice.
[So] Source:J Cell Sci;129(7):1455-67, 2016 Apr 01.
[Is] ISSN:1477-9137
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The role of TRAF2 and TRAF5 in TNFα-induced NF-κB activation has become complicated owing to the accumulation of conflicting data. Here, we report that 7-day-old TRAF2-knockout (KO) and TRAF2 TRAF5 double KO (TRAF2/5-DKO) mice exhibit enhanced canonical IκB kinase (IKK) and caspase-8 activation in spleen and liver, and that subsequent knockout of TNFα suppresses the basal activity of caspase-8, but not of IKK. In primary TRAF2 KO and TRAF2/5-DKO cells, TNFα-induced immediate IKK activation is impaired, whereas delayed IKK activation occurs normally; as such, owing to elevated basal and TNFα-induced delayed IKK activation, TNFα stimulation leads to significantly increased induction of a subset of NF-κB-dependent genes in these cells. In line with this, both TRAF2 KO and TRAF2/5-DKO mice succumb to a sublethal dose of TNFα owing to increased expression of NF-κB target genes, diarrhea and bradypnea. Notably, depletion of IAP1 and IAP2 (also known as BIRC2 and BIRC3, respectively) also results in elevated basal IKK activation that is independent of autocrine TNFα production and that impairs TNFα-induced immediate IKK activation. These data reveal that TRAF2, IAP1 and IAP2, but not TRAF5, cooperatively regulate basal and TNFα-induced immediate IKK activation.
[Mh] Termos MeSH primário: Caspase 8/metabolismo
Quinase I-kappa B/metabolismo
NF-kappa B/metabolismo
Fator 2 Associado a Receptor de TNF/metabolismo
Fator 5 Associado a Receptor de TNF/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/genética
Proteína 3 com Repetições IAP de Baculovírus
Células Cultivadas
Quimiocina CCL5/metabolismo
Ativação Enzimática/genética
Quinase I-kappa B/genética
Proteínas Inibidoras de Apoptose/deficiência
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Knockout
Óxido Nítrico Sintase Tipo II/metabolismo
Fator 2 Associado a Receptor de TNF/genética
Fator 5 Associado a Receptor de TNF/genética
Fator de Necrose Tumoral alfa/genética
Ubiquitina-Proteína Ligases/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Ccl5 protein, mouse); 0 (Chemokine CCL5); 0 (Inhibitor of Apoptosis Proteins); 0 (NF-kappa B); 0 (TNF Receptor-Associated Factor 2); 0 (TNF Receptor-Associated Factor 5); 0 (Tumor Necrosis Factor-alpha); EC 1.14.13.39 (Nitric Oxide Synthase Type II); EC 1.14.13.39 (Nos2 protein, mouse); EC 2.3.2.27 (Baculoviral IAP Repeat-Containing 3 Protein); EC 2.3.2.27 (Birc2 protein, mouse); EC 2.3.2.27 (Birc3 protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.11.10 (I-kappa B Kinase); EC 3.4.22.- (Caspase 8)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160214
[St] Status:MEDLINE
[do] DOI:10.1242/jcs.180554


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[PMID]:26872428
[Au] Autor:Li M; Long C; Yang G; Luo Y; Du H
[Ad] Endereço:Chinese PLA General Hospital of Lanzhou Military Command, Department of Dermatology, 333 Road Nanbinhe, District Qilihe, Lanzhou, 730000, China.
[Ti] Título:MiR-26b inhibits melanoma cell proliferation and enhances apoptosis by suppressing TRAF5-mediated MAPK activation.
[So] Source:Biochem Biophys Res Commun;471(3):361-7, 2016 Mar 11.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alterations in microRNA-26b (miR-26b) expression have been shown to participate in various malignant tumor developments. However, the possible function of miR-26b in human melanoma cells remains unclarified. In this study, quantitative polymerase chain reaction was used to explore the expression profiles of miR-26b in melanoma cells. The effect of miR-26b on cell viability was determined by using MTT assays and colony formation assay. The apoptosis levels were evaluated by using Annexin V/fluorescein isothiocyanate (FITC) apoptosis detection kit and the apoptosis cells were confirmed by Transmission Electron Microscopy (TEM). Luciferase reporter plasmids were constructed to confirm direct targeting. Our study found that the expression of miR-26b was downregulated in human melanoma specimens. Overexpression of miR-26b significantly increased the anti-proliferative effects and apoptosis in A375 and B16F10 melanoma cells. In addition, luciferase gene reporter assays confirmed that TRAF5 was a direct target gene of miR-26b and the anti-tumor effect of miR-26b in melanoma cells was significantly counteracted by treatment with TRAF5 overexpression. Furthermore, the molecular mechanisms underlying the tumor suppressor of miR-26b in malignant melanomas may be due to the dephosphorylation of MAPK pathway caused by the decrease in TRAF5 expression when miR-26b is up-regulated in melanoma cells. These findings indicate that miR-26b might influence TRAF5-MAPK signaling pathways to facilitate the malignant progression of melanoma cells.
[Mh] Termos MeSH primário: Apoptose/genética
Melanoma/metabolismo
Melanoma/patologia
MicroRNAs/metabolismo
Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo
Fator 5 Associado a Receptor de TNF/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Proliferação Celular
Regulação para Baixo/genética
Ativação Enzimática
Seres Humanos
Sistema de Sinalização das MAP Quinases/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN26A microRNA, human); 0 (MicroRNAs); 0 (TNF Receptor-Associated Factor 5); EC 2.7.12.2 (Mitogen-Activated Protein Kinase Kinases)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:160227
[Lr] Data última revisão:
160227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160214
[St] Status:MEDLINE


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[PMID]:26779844
[Au] Autor:Foight GW; Keating AE
[Ad] Endereço:Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts, 02139.
[Ti] Título:Comparison of the peptide binding preferences of three closely related TRAF paralogs: TRAF2, TRAF3, and TRAF5.
[So] Source:Protein Sci;25(7):1273-89, 2016 07.
[Is] ISSN:1469-896X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tumor necrosis factor receptor-associated factors (TRAFs) constitute a family of adapter proteins that act in numerous signaling pathways important in human biology and disease. The MATH domain of TRAF proteins binds peptides found in the cytoplasmic domains of signaling receptors, thereby connecting extracellular signals to downstream effectors. Beyond several very general motifs, the peptide binding preferences of TRAFs have not been extensively characterized, and differences between the binding preferences of TRAF paralogs are poorly understood. Here we report a screening system that we established to explore TRAF peptide-binding specificity using deep mutational scanning of TRAF-peptide ligands. We displayed single- and double-mutant peptide libraries based on the TRAF-binding sites of CD40 or TANK on the surface of Escherichia coli and screened them for binding to TRAF2, TRAF3, and TRAF5. Enrichment analysis of the library sequencing results showed differences in the permitted substitution patterns in the TANK versus CD40 backgrounds. The three TRAF proteins also demonstrated different preferences for binding to members of the CD40 library, and three peptides from that library that were analyzed individually showed striking differences in affinity for the three TRAFs. These results illustrate a previously unappreciated level of binding specificity between these close paralogs and demonstrate that established motifs are overly simplistic. The results from this work begin to outline differences between TRAF family members, and the experimental approach established herein will enable future efforts to investigate and redesign TRAF peptide-binding specificity.
[Mh] Termos MeSH primário: Análise Mutacional de DNA/métodos
Peptídeos/metabolismo
Fator 2 Associado a Receptor de TNF/metabolismo
Fator 3 Associado a Receptor de TNF/metabolismo
Fator 5 Associado a Receptor de TNF/metabolismo
Peptídeos e Proteínas Associados a Receptores de Fatores de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Sítios de Ligação
Antígenos CD40/metabolismo
Seres Humanos
Modelos Moleculares
Ligação Proteica
Estrutura Secundária de Proteína
Fator 2 Associado a Receptor de TNF/química
Fator 2 Associado a Receptor de TNF/genética
Fator 3 Associado a Receptor de TNF/química
Fator 3 Associado a Receptor de TNF/genética
Fator 5 Associado a Receptor de TNF/química
Fator 5 Associado a Receptor de TNF/genética
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:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (CD40 Antigens); 0 (PSMD2 protein, human); 0 (Peptides); 0 (TANK protein, human); 0 (TNF Receptor-Associated Factor 2); 0 (TNF Receptor-Associated Factor 3); 0 (TNF Receptor-Associated Factor 5); 0 (TRAF3 protein, human); 0 (TRAF5 protein, human); 0 (Tumor Necrosis Factor Receptor-Associated Peptides and Proteins)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160119
[St] Status:MEDLINE
[do] DOI:10.1002/pro.2881


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[PMID]:26454171
[Au] Autor:Chiba Y; Matsumiya T; Satoh T; Hayakari R; Furudate K; Xing F; Yoshida H; Tanji K; Mizukami H; Imaizumi T; Ito E
[Ad] Endereço:Department of Pediatrics, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
[Ti] Título:Retinoic acid-inducible gene-I-like receptor (RLR)-mediated antiviral innate immune responses in the lower respiratory tract: Roles of TRAF3 and TRAF5.
[So] Source:Biochem Biophys Res Commun;467(2):191-6, 2015 Nov 13.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Upon viral infection, the cytoplasmic viral sensor retinoic acid-inducible gene-I (RIG-I) recognizes viral RNA to activate antiviral signaling to induce type I interferon (IFN). RIG-I-like receptors (RLRs) activate antiviral signaling in a tissue-specific manner. The molecular mechanism underlying antiviral signaling in the respiratory system remains unclear. We studied antiviral signaling in the lower respiratory tract (LRT), which is the site of many harmful viral infections. Epithelial cells of the LRT can be roughly divided into two groups: bronchial epithelial cells (BECs) and pulmonary alveolar epithelial cells (AECs). These two cell types exhibit different phenotypes; therefore, we hypothesized that these cells may play different roles in antiviral innate immunity. We found that BECs exhibited higher antiviral activity than AECs. TNF receptor-associated factor 3 (TRAF3) has been shown to be a crucial molecule in RLR signaling. The expression levels of TRAF3 and TRAF5, which have conserved domains that are nearly identical, in the LRT were examined. We found that the bronchus exhibited the highest expression levels of TRAF3 and TRAF5 in the LRT. These findings suggest the importance of the bronchus in antiviral innate immunity in the LRT and indicate that TRAF3 and TRAF5 may contribute to RLR signaling.
[Mh] Termos MeSH primário: RNA Helicases DEAD-box/genética
Células Epiteliais/efeitos dos fármacos
Fator 3 Associado a Receptor de TNF/genética
Fator 5 Associado a Receptor de TNF/genética
[Mh] Termos MeSH secundário: Brônquios/citologia
Brônquios/efeitos dos fármacos
Brônquios/imunologia
Linhagem Celular
Proteína DEAD-box 58
RNA Helicases DEAD-box/imunologia
Células Epiteliais/citologia
Células Epiteliais/imunologia
Esôfago/química
Esôfago/efeitos dos fármacos
Esôfago/imunologia
Regulação da Expressão Gênica
Seres Humanos
Imunidade Inata
Interferon beta/biossíntese
Interferon beta/imunologia
Laringe/química
Laringe/efeitos dos fármacos
Laringe/imunologia
Leucócitos Mononucleares/química
Leucócitos Mononucleares/efeitos dos fármacos
Leucócitos Mononucleares/imunologia
Especificidade de Órgãos
Poli I-C/farmacologia
Alvéolos Pulmonares/citologia
Alvéolos Pulmonares/efeitos dos fármacos
Alvéolos Pulmonares/imunologia
Transdução de Sinais
Fator 3 Associado a Receptor de TNF/imunologia
Fator 5 Associado a Receptor de TNF/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (TNF Receptor-Associated Factor 3); 0 (TNF Receptor-Associated Factor 5); 0 (TRAF3 protein, human); 77238-31-4 (Interferon-beta); EC 3.6.1.- (DDX58 protein, human); EC 3.6.4.13 (DEAD Box Protein 58); EC 3.6.4.13 (DEAD-box RNA Helicases); O84C90HH2L (Poly I-C)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151011
[St] Status:MEDLINE


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[PMID]:26453305
[Au] Autor:Wang X; Yang J; Han L; Zhao K; Wu Q; Bao L; Li Z; Lv L; Li B
[Ad] Endereço:From the Division of Rheumatology, Huashan Hospital, Fudan University, 12 Middle Wulumuqi Road, Shanghai 200040, China.
[Ti] Título:TRAF5-mediated Lys-63-linked Polyubiquitination Plays an Essential Role in Positive Regulation of RORγt in Promoting IL-17A Expression.
[So] Source:J Biol Chem;290(48):29086-94, 2015 Nov 27.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Retinoid-related orphan nuclear receptor γt (RORγt) is a key transcription factor for the development and function of Th17 cells. In this study, we show that tumor necrosis factor receptor-associated factor 5 (TRAF5), known as an E3 ubiquitin protein ligase and signal transducer, interacts with and ubiquitinates RORγt via Lys-63-linked polyubiquitination. TRAF5 stabilizes the RORγt protein level depending on its RING finger domain. Depletion of TRAF5 in Th17 cells destabilizes RORγt protein and down-regulates Th17-related genes, including IL-17A, an inflammatory cytokine involved in pathogenic mechanisms of several autoimmune diseases such as systemic lupus erythematosus. Moreover, up-regulation of the TRAF5 mRNA level was found in systemic lupus erythematosus patient CD4(+) T cells. Our findings reveal a direct link between TRAF5-mediated ubiquitination and RORγt protein regulation, which may aggravate inflammatory progress and provide new therapeutic drug targets for autoimmune diseases.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica/fisiologia
Interleucina-17/biossíntese
Membro 3 do Grupo F da Subfamília 1 de Receptores Nucleares/metabolismo
Fator 5 Associado a Receptor de TNF/metabolismo
Células Th17/metabolismo
Ubiquitinação/fisiologia
[Mh] Termos MeSH secundário: Células HEK293
Seres Humanos
Interleucina-17/genética
Lisina/genética
Lisina/metabolismo
Membro 3 do Grupo F da Subfamília 1 de Receptores Nucleares/genética
Estabilidade Proteica
Fator 5 Associado a Receptor de TNF/genética
Células Th17/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (IL17A protein, human); 0 (Interleukin-17); 0 (Nuclear Receptor Subfamily 1, Group F, Member 3); 0 (RORC protein, human); 0 (TNF Receptor-Associated Factor 5); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151011
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M115.664573


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[PMID]:25710910
[Au] Autor:Somma D; Mastrovito P; Grieco M; Lavorgna A; Pignalosa A; Formisano L; Salzano AM; Scaloni A; Pacifico F; Siebenlist U; Leonardi A
[Ad] Endereço:Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università Federico II di Napoli, 80131 Naples, Italy;
[Ti] Título:CIKS/DDX3X interaction controls the stability of the Zc3h12a mRNA induced by IL-17.
[So] Source:J Immunol;194(7):3286-94, 2015 Apr 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:IL-17 is a proinflammatory cytokine that promotes the expression of different cytokines and chemokines via the induction of gene transcription and the posttranscriptional stabilization of mRNAs. In this study, we show that IL-17 increases the half-life of the Zc3h12a mRNA via interaction of the adaptor protein CIKS with the DEAD box protein DDX3X. IL-17 stimulation promotes the formation of a complex between CIKS and DDX3X, and this interaction requires the helicase domain of DDX3X but not its ATPase activity. DDX3X knockdown decreases the IL-17-induced stability of Zc3h12a without affecting the stability of other mRNAs. IKKε, TNFR-associated factor 2, and TNFR-associated factor 5 were also required to mediate the IL-17-induced Zc3h12a stabilization. DDX3X directly binds the Zc3h12a mRNA after IL-17 stimulation. Collectively, our findings define a novel, IL-17-dependent mechanism regulating the stabilization of a selected mRNA.
[Mh] Termos MeSH primário: RNA Helicases DEAD-box/metabolismo
Regulação da Expressão Gênica
Interleucina-17/metabolismo
Estabilidade de RNA
Ribonucleases/genética
Fatores de Transcrição/genética
Peptídeos e Proteínas Associados a Receptores de Fatores de Necrose Tumoral/metabolismo
[Mh] Termos MeSH secundário: Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Quinase I-kappa B/metabolismo
Interleucina-17/farmacologia
Complexos Multiproteicos/metabolismo
Ligação Proteica/efeitos dos fármacos
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Fator 2 Associado a Receptor de TNF/metabolismo
Fator 5 Associado a Receptor de TNF/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., INTRAMURAL
[Nm] Nome de substância:
0 (Interleukin-17); 0 (Multiprotein Complexes); 0 (RNA, Messenger); 0 (TNF Receptor-Associated Factor 2); 0 (TNF Receptor-Associated Factor 5); 0 (TRAF3IP2 protein, human); 0 (Transcription Factors); 0 (Tumor Necrosis Factor Receptor-Associated Peptides and Proteins); EC 2.7.11.10 (I-kappa B Kinase); EC 3.1.- (Ribonucleases); EC 3.1.- (ZC3H12A protein, human); EC 3.6.1.- (DDX3X protein, human); EC 3.6.4.13 (DEAD-box RNA Helicases)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:161025
[Lr] Data última revisão:
161025
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150225
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1401589


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[PMID]:25062762
[Au] Autor:Magnusson-Lind A; Davidsson M; Silajdzic E; Hansen C; McCourt AC; Tabrizi SJ; Björkqvist M
[Ad] Endereço:Brain Disease Biomarker Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden.
[Ti] Título:Skeletal muscle atrophy in R6/2 mice - altered circulating skeletal muscle markers and gene expression profile changes.
[So] Source:J Huntingtons Dis;3(1):13-24, 2014.
[Is] ISSN:1879-6397
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In addition to classical neurological symptoms, Huntington's disease (HD) is complicated by peripheral pathology, including progressive skeletal muscle wasting, and common skeletal muscle gene expression changes have been shown in HD mice and human HD. OBJECTIVE: To highlight possible mechanisms underlying muscle wasting in HD, we examined gene expression in pathways governing skeletal muscle contractility, skeletal myogenesis, skeletal muscle wasting, apoptosis and the NFκB signaling pathway in two HD mouse models (the transgenic R6/2 and full-length knock-in Q175). In addition, we assessed circulating markers that increase in response to skeletal muscle injury, skeletal Troponin I (sTnI), fatty acid binding protein 3 (FABP3), and Myosin light chain 3 (Myl3). METHODS: We measured gene expression in muscle tissue as well as in cultured primary myocytes using qPCR. Concentrations of cytokines and muscle proteins were obtained using multiplex ELISA. RESULTS: Circulating markers of muscle injury (sTnI, FABP3, and Myl3) were significantly increased in mouse serum. In skeletal muscle, we observed reduced gene expression of components involved in muscle contractility, with pronounced downregulation of Acta1, Myh2 and Tnni2, among others. Alongside, we found increased expression of caspases (3 and 8) and key elements of the NFκB signaling pathway, p65/RelA, Tradd, and TRAF5. We also found similar gene expression alterations in cultured primary myocytes from R6/2 mice stimulated with TNF-α. CONCLUSIONS: Our results indicate that activation of apoptotic and NFκB pathways occur alongside down-regulation of key compartments of the muscle contractility unit in skeletal muscle of HD mice, and muscle atrophy could possibly be a source of circulating disease progression markers.
[Mh] Termos MeSH primário: Doença de Huntington/genética
Músculo Esquelético/metabolismo
Atrofia Muscular/genética
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Caspase 3/genética
Caspase 3/metabolismo
Caspase 8/genética
Caspase 8/metabolismo
Modelos Animais de Doenças
Regulação para Baixo
Proteína 3 Ligante de Ácido Graxo
Proteínas de Ligação a Ácido Graxo/genética
Proteínas de Ligação a Ácido Graxo/metabolismo
Doença de Huntington/complicações
Doença de Huntington/metabolismo
Camundongos
Camundongos Transgênicos
Contração Muscular/genética
Atrofia Muscular/etiologia
Atrofia Muscular/metabolismo
Cadeias Pesadas de Miosina/genética
Cadeias Pesadas de Miosina/metabolismo
Cadeias Leves de Miosina/genética
Cadeias Leves de Miosina/metabolismo
NF-kappa B/genética
NF-kappa B/metabolismo
Transdução de Sinais
Proteína de Domínio de Morte Associada a Receptor de TNF/genética
Proteína de Domínio de Morte Associada a Receptor de TNF/metabolismo
Fator 5 Associado a Receptor de TNF/genética
Fator 5 Associado a Receptor de TNF/metabolismo
Fator de Transcrição RelA/genética
Fator de Transcrição RelA/metabolismo
Transcriptoma
Troponina I/genética
Troponina I/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Fabp3 protein, mouse); 0 (Fatty Acid Binding Protein 3); 0 (Fatty Acid-Binding Proteins); 0 (Myosin Light Chains); 0 (NF-kappa B); 0 (TNF Receptor-Associated Death Domain Protein); 0 (TNF Receptor-Associated Factor 5); 0 (Tradd protein, mouse); 0 (Transcription Factor RelA); 0 (Troponin I); EC 3.4.22.- (Casp3 protein, mouse); EC 3.4.22.- (Casp8 protein, mouse); EC 3.4.22.- (Caspase 3); EC 3.4.22.- (Caspase 8); EC 3.6.4.1 (Myosin Heavy Chains)
[Em] Mês de entrada:1410
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140727
[St] Status:MEDLINE
[do] DOI:10.3233/JHD-130075


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[PMID]:24681564
[Au] Autor:Nagashima H; Okuyama Y; Asao A; Kawabe T; Yamaki S; Nakano H; Croft M; Ishii N; So T
[Ad] Endereço:Department of Microbiology and Immunology, Tohoku University Graduate School of Medicine, Sendai, Japan.
[Ti] Título:The adaptor TRAF5 limits the differentiation of inflammatory CD4(+) T cells by antagonizing signaling via the receptor for IL-6.
[So] Source:Nat Immunol;15(5):449-56, 2014 May.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The physiological functions of members of the tumor-necrosis factor (TNF) receptor (TNFR)-associated factor (TRAF) family in T cell immunity are not well understood. We found that in the presence of interleukin 6 (IL-6), naive TRAF5-deficient CD4(+) T cells showed an enhanced ability to differentiate into the TH17 subset of helper T cells. Accordingly, TH17 cell-associated experimental autoimmune encephalomyelitis (EAE) was greatly exaggerated in Traf5(-/-) mice. Although it is normally linked with TNFR signaling pathways, TRAF5 constitutively associated with a cytoplasmic region in the signal-transducing receptor gp130 that overlaps with the binding site for the transcription activator STAT3 and suppressed the recruitment and activation of STAT3 in response to IL-6. Our results identify TRAF5 as a negative regulator of the IL-6 receptor signaling pathway that limits the induction of proinflammatory CD4(+) T cells that require IL-6 for their development.
[Mh] Termos MeSH primário: Receptor gp130 de Citocina/metabolismo
Encefalomielite Autoimune Experimental/imunologia
Subpopulações de Linfócitos T/imunologia
Fator 5 Associado a Receptor de TNF/metabolismo
Células Th17/imunologia
[Mh] Termos MeSH secundário: Animais
Antígenos CD4/metabolismo
Diferenciação Celular/genética
Células Cultivadas
Progressão da Doença
Interleucina-6/imunologia
Camundongos
Camundongos Endogâmicos
Camundongos Knockout
Glicoproteína Mielina-Oligodendrócito/imunologia
Fragmentos de Peptídeos/imunologia
Fator de Transcrição STAT3/metabolismo
Transdução de Sinais/genética
Fator 5 Associado a Receptor de TNF/genética
Ativação Transcricional/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CD4 Antigens); 0 (Interleukin-6); 0 (Myelin-Oligodendrocyte Glycoprotein); 0 (Peptide Fragments); 0 (STAT3 Transcription Factor); 0 (TNF Receptor-Associated Factor 5); 0 (myelin oligodendrocyte glycoprotein (34-56)); 133483-10-0 (Cytokine Receptor gp130)
[Em] Mês de entrada:1407
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140401
[St] Status:MEDLINE
[do] DOI:10.1038/ni.2863



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