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[PMID]:29330478
[Au] Autor:Williams JJL; Alotaiq N; Mullen W; Burchmore R; Liu L; Baillie GS; Schaper F; Pilch PF; Palmer TM
[Ad] Endereço:School of Pharmacy and Medical Sciences, University of Bradford, Bradford, BD7 1DP, UK. j.j.l.williams@bradford.ac.uk.
[Ti] Título:Interaction of suppressor of cytokine signalling 3 with cavin-1 links SOCS3 function and cavin-1 stability.
[So] Source:Nat Commun;9(1):168, 2018 01 12.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Effective suppression of JAK-STAT signalling by the inducible inhibitor "suppressor of cytokine signalling 3" (SOCS3) is essential for limiting signalling from cytokine receptors. Here we show that cavin-1, a component of caveolae, is a functionally significant SOCS3-interacting protein. Biochemical and confocal imaging demonstrate that SOCS3 localisation to the plasma membrane requires cavin-1. SOCS3 is also critical for cavin-1 stabilisation, such that deletion of SOCS3 reduces the expression of cavin-1 and caveolin-1 proteins, thereby reducing caveola abundance in endothelial cells. Moreover, the interaction of cavin-1 and SOCS3 is essential for SOCS3 function, as loss of cavin-1 enhances cytokine-stimulated STAT3 phosphorylation and abolishes SOCS3-dependent inhibition of IL-6 signalling by cyclic AMP. Together, these findings reveal a new functionally important mechanism linking SOCS3-mediated inhibition of cytokine signalling to localisation at the plasma membrane via interaction with and stabilisation of cavin-1.
[Mh] Termos MeSH primário: Proteínas de Membrana/metabolismo
Proteínas de Ligação a RNA/metabolismo
Proteína 3 Supressora da Sinalização de Citocinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Cavéolas/fisiologia
Deleção de Genes
Regulação da Expressão Gênica
Células HEK293
Seres Humanos
Janus Quinases/genética
Janus Quinases/metabolismo
Proteínas de Membrana/genética
Camundongos
Ligação Proteica
Proteínas de Ligação a RNA/genética
Fatores de Transcrição STAT/genética
Fatores de Transcrição STAT/metabolismo
Proteína 3 Supressora da Sinalização de Citocinas/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 (Membrane Proteins); 0 (PTRF protein, human); 0 (Ptrf protein, mouse); 0 (RNA-Binding Proteins); 0 (SOCS3 protein, human); 0 (STAT Transcription Factors); 0 (Socs3 protein, mouse); 0 (Suppressor of Cytokine Signaling 3 Protein); EC 2.7.10.2 (Janus Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180114
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02585-y


  2 / 1635 MEDLINE  
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[PMID]:29016674
[Au] Autor:Wilbers RHP; van Raaij DR; Westerhof LB; Bakker J; Smant G; Schots A
[Ad] Endereço:Wageningen University and Research, Plant Sciences Group, Laboratory of Nematology, Wageningen, The Netherlands.
[Ti] Título:Re-evaluation of IL-10 signaling reveals novel insights on the contribution of the intracellular domain of the IL-10R2 chain.
[So] Source:PLoS One;12(10):e0186317, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Interleukin-10 (IL-10) is an anti-inflammatory cytokine that plays a key role in maintaining immune homeostasis. IL-10-mediated responses are triggered upon binding to a heterodimeric receptor complex consisting of IL-10 receptor (IL-10R)1 and IL-10R2. Engagement of the IL-10R complex activates the intracellular kinases Jak1 and Tyk2, but the exact roles of IL-10R2 and IL-10R2-associated signaling via Tyk2 remain unclear. To elucidate the contribution of IL-10R2 and its signaling to IL-10 activity, we re-evaluated IL-10-mediated responses on bone marrow-derived dendritic cells, macrophages and mast cells. By using bone marrow from IL-10R-/- mice it was revealed that IL-10-mediated responses depend on both IL-10R1 and IL-10R2 in all three cell types. On the contrary, bone marrow-derived cells from Tyk2-/- mice showed similar responses to IL-10 as wild-type cells, indicating that signaling via this IL-10R2-associated kinase only plays a limited role. Tyk2 was shown to control the amplitude of STAT3 activation and the up-regulation of downstream SOCS3 expression. SOCS3 up-regulation was found to be cell-type dependent and correlated with the lack of early suppression of LPS-induced TNF-α in dendritic cells. Further investigation of the IL-10R complex revealed that both the extracellular and intracellular domains of IL-10R2 influence the conformation of IL-10R1 and that both domains were required for transducing IL-10 signals. This observation highlights a novel role for the intracellular domain of IL-10R2 in the molecular mechanisms of IL-10R activation.
[Mh] Termos MeSH primário: Células Dendríticas/imunologia
Interleucina-10/imunologia
Macrófagos/imunologia
Mastócitos/imunologia
Receptores de Interleucina-10/imunologia
Transdução de Sinais/imunologia
TYK2 Quinase/imunologia
[Mh] Termos MeSH secundário: Animais
Células da Medula Óssea/citologia
Células da Medula Óssea/efeitos dos fármacos
Células da Medula Óssea/imunologia
Clonagem Molecular
Células Dendríticas/citologia
Células Dendríticas/efeitos dos fármacos
Expressão Gênica
Regulação da Expressão Gênica
Interleucina-10/genética
Interleucina-10/farmacologia
Lipopolissacarídeos/farmacologia
Macrófagos/citologia
Macrófagos/efeitos dos fármacos
Mastócitos/citologia
Mastócitos/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Especificidade de Órgãos
Cultura Primária de Células
Ligação Proteica
Domínios e Motivos de Interação entre Proteínas
Isoformas de Proteínas/deficiência
Isoformas de Proteínas/genética
Isoformas de Proteínas/imunologia
Receptores de Interleucina-10/deficiência
Receptores de Interleucina-10/genética
Proteínas Recombinantes/química
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Fator de Transcrição STAT3/genética
Fator de Transcrição STAT3/imunologia
Proteína 3 Supressora da Sinalização de Citocinas/genética
Proteína 3 Supressora da Sinalização de Citocinas/imunologia
TYK2 Quinase/deficiência
TYK2 Quinase/genética
Tabaco/genética
Tabaco/metabolismo
Fator de Necrose Tumoral alfa/genética
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL10 protein, mouse); 0 (Lipopolysaccharides); 0 (Protein Isoforms); 0 (Receptors, Interleukin-10); 0 (Recombinant Proteins); 0 (STAT3 Transcription Factor); 0 (Socs3 protein, mouse); 0 (Stat3 protein, mouse); 0 (Suppressor of Cytokine Signaling 3 Protein); 0 (Tumor Necrosis Factor-alpha); 130068-27-8 (Interleukin-10); EC 2.7.10.2 (TYK2 Kinase); EC 2.7.10.2 (Tyk2 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171011
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0186317


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[PMID]:28976973
[Au] Autor:Qin Y; Wu L; Ouyang Y; Zhou P; Zhou H; Wang Y; Ma J; Zhang J; Chen Y; Qian J; Tang Y; Shen N
[Ad] Endereço:Department of Rheumatology and Shanghai Institute of Rheumatology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
[Ti] Título:MiR-125a Is a critical modulator for neutrophil development.
[So] Source:PLoS Genet;13(10):e1007027, 2017 Oct.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:MicroRNAs are universal post-transcriptional regulators in genomes. They have the ability of buffering gene expressional programs, contributing to robustness of biological systems and playing important roles in development, physiology and diseases. Here, we identified a microRNA, miR-125a, as a positive regulator of granulopoiesis. MiR125a knockout mice show reduced infiltration of neutrophils in the lung and alleviated tissue destruction after endotoxin challenge as a consequence of decreased neutrophil numbers. Furthermore, we demonstrated that this significant reduction of neutrophils was due to impaired development of granulocyte precursors to mature neutrophils in an intrinsic manner. We showed that Socs3, a critical repressor for granulopoiesis, was a target of miR-125a. Overall, our study revealed a new microRNA regulating granulocyte development and supported a model in which miR-125a acted as a fine-tuner of granulopoiesis.
[Mh] Termos MeSH primário: Leucopoese/genética
Leucopoese/fisiologia
MicroRNAs/genética
MicroRNAs/metabolismo
Neutrófilos/citologia
Neutrófilos/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Animais
Sítios de Ligação/genética
Morte Celular
Diferenciação Celular
Proliferação Celular
Fator Estimulador de Colônias de Granulócitos/metabolismo
Granulócitos/citologia
Granulócitos/metabolismo
Camundongos
Camundongos Knockout
Modelos Biológicos
Células Progenitoras Mieloides/citologia
Células Progenitoras Mieloides/metabolismo
Choque Séptico/genética
Choque Séptico/metabolismo
Choque Séptico/patologia
Transdução de Sinais
Proteína 3 Supressora da Sinalização de Citocinas/genética
Proteína 3 Supressora da Sinalização de Citocinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (MicroRNAs); 0 (Mirn125 microRNA, mouse); 0 (Socs3 protein, mouse); 0 (Suppressor of Cytokine Signaling 3 Protein); 143011-72-7 (Granulocyte Colony-Stimulating Factor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171031
[Lr] Data última revisão:
171031
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007027


  4 / 1635 MEDLINE  
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[PMID]:28926622
[Au] Autor:Cartoni R; Pekkurnaz G; Wang C; Schwarz TL; He Z
[Ad] Endereço:Department of Neurology, F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, Massachusetts, United States of America.
[Ti] Título:A high mitochondrial transport rate characterizes CNS neurons with high axonal regeneration capacity.
[So] Source:PLoS One;12(9):e0184672, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Improving axonal transport in the injured and diseased central nervous system has been proposed as a promising strategy to improve neuronal repair. However, the contribution of each cargo to the repair mechanism is unknown. DRG neurons globally increase axonal transport during regeneration. Because the transport of specific cargos after axonal insult has not been examined systematically in a model of enhanced regenerative capacity, it is unknown whether the transport of all cargos would be modulated equally in injured central nervous system neurons. Here, using a microfluidic culture system we compared neurons co-deleted for PTEN and SOCS3, an established model of high axonal regeneration capacity, to control neurons. We measured the axonal transport of three cargos (mitochondria, synaptic vesicles and late endosomes) in regenerating axons and found that the transport of mitochondria, but not the other cargos, was increased in PTEN/SOCS3 co-deleted axons relative to controls. The results reported here suggest a pivotal role for this organelle during axonal regeneration.
[Mh] Termos MeSH primário: Axônios/fisiologia
Mitocôndrias/metabolismo
Regeneração Nervosa/fisiologia
[Mh] Termos MeSH secundário: Animais
Transporte Biológico
Células Cultivadas
Córtex Cerebral/citologia
Feminino
Imuno-Histoquímica
Camundongos Transgênicos
Microscopia Confocal
Neurônios/citologia
Neurônios/metabolismo
PTEN Fosfo-Hidrolase/deficiência
PTEN Fosfo-Hidrolase/genética
Ratos
Proteína 3 Supressora da Sinalização de Citocinas/deficiência
Proteína 3 Supressora da Sinalização de Citocinas/genética
Imagem com Lapso de Tempo
Tubulina (Proteína)/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Suppressor of Cytokine Signaling 3 Protein); 0 (Tubulin); 0 (beta3 tubulin, mouse); EC 3.1.3.67 (PTEN Phosphohydrolase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170920
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184672


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[PMID]:28900038
[Au] Autor:Blumer T; Coto-Llerena M; Duong FHT; Heim MH
[Ad] Endereço:From the Department of Biomedicine, University of Basel, 4031 Basel, Switzerland and.
[Ti] Título:SOCS1 is an inducible negative regulator of interferon λ (IFN-λ)-induced gene expression .
[So] Source:J Biol Chem;292(43):17928-17938, 2017 Oct 27.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Type I (α and ß) and type III (λ) IFNs are induced upon viral infection through host sensory pathways that activate IFN regulatory factors (IRFs) and nuclear factor κB. Secreted IFNs induce autocrine and paracrine signaling through the JAK-STAT pathway, leading to the transcriptional induction of hundreds of IFN-stimulated genes, among them sensory pathway components such as cGAS, STING, RIG-I, MDA5, and the transcription factor IRF7, which enhance the induction of IFN-αs and IFN-λs. This positive feedback loop enables a very rapid and strong host response that, at some point, has to be controlled by negative regulators to maintain tissue homeostasis. Type I IFN signaling is controlled by the inducible negative regulators suppressor of cytokine signaling 1 (SOCS1), SOCS3, and ubiquitin-specific peptidase 18 (USP18). The physiological role of these proteins in IFN-γ signaling has not been clarified. Here we used knockout cell lines and mice to show that IFN-λ signaling is regulated by SOCS1 but not by SOCS3 or USP18. These differences were the basis for the distinct kinetic properties of type I and III IFNs. We found that IFN-α signaling is transient and becomes refractory after hours, whereas IFN-λ provides a long-lasting IFN-stimulated gene induction.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica/fisiologia
Interferons/metabolismo
Transdução de Sinais/fisiologia
Proteína 1 Supressora da Sinalização de Citocina/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Proteína DEAD-box 58/genética
Proteína DEAD-box 58/metabolismo
Endopeptidases/genética
Endopeptidases/metabolismo
Seres Humanos
Helicase IFIH1 Induzida por Interferon/genética
Helicase IFIH1 Induzida por Interferon/metabolismo
Interferons/genética
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Camundongos
Camundongos Knockout
Nucleotidiltransferases/genética
Nucleotidiltransferases/metabolismo
Proteína 1 Supressora da Sinalização de Citocina/genética
Proteína 3 Supressora da Sinalização de Citocinas/genética
Proteína 3 Supressora da Sinalização de Citocinas/metabolismo
Ubiquitina Tiolesterase/genética
Ubiquitina Tiolesterase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MPYS protein, human); 0 (MPYS protein, mouse); 0 (Membrane Proteins); 0 (SOCS1 protein, human); 0 (SOCS3 protein, human); 0 (Socs1 protein, mouse); 0 (Socs3 protein, mouse); 0 (Suppressor of Cytokine Signaling 1 Protein); 0 (Suppressor of Cytokine Signaling 3 Protein); 9008-11-1 (Interferons); EC 2.7.7.- (MB21D1 protein, human); EC 2.7.7.- (MB21D1 protein, mouse); EC 2.7.7.- (Nucleotidyltransferases); EC 3.4.- (Endopeptidases); EC 3.4.19.- (Usp18 protein, mouse); EC 3.4.19.12 (Ubiquitin Thiolesterase); EC 3.4.99.- (USP18 protein, human); EC 3.6.1.- (DDX58 protein, human); EC 3.6.1.- (Ddx58 protein, mouse); EC 3.6.1.- (IFIH1 protein, human); EC 3.6.1.- (Ifih1 protein, mouse); EC 3.6.4.13 (DEAD Box Protein 58); EC 3.6.4.13 (Interferon-Induced Helicase, IFIH1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170914
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.788877


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[PMID]:28899903
[Au] Autor:Pedroso JAB; de Mendonca POR; Fortes MAS; Tomaz I; Pecorali VL; Auricino TB; Costa IC; Lima LB; Furigo IC; Bueno DN; Ramos-Lobo AM; Lotfi CFP; Donato J
[Ad] Endereço:Department of Physiology and BiophysicsInstitute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
[Ti] Título:SOCS3 expression in SF1 cells regulates adrenal differentiation and exercise performance.
[So] Source:J Endocrinol;235(3):207-222, 2017 Dec.
[Is] ISSN:1479-6805
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Many hormones/cytokines are secreted in response to exercise and cytokine signaling may play a pivotal role in the training adaptations. To investigate the importance of cytokine signaling during vertical ladder climbing, a resistance exercise model, we produced mice lacking SOCS3 protein exclusively in steroidogenic factor-1 (SF1) cells (SF1 Socs3 KO mice). SF1 expression is found in steroidogenic cells of the adrenal cortex and gonads, as well as in neurons of the ventromedial nucleus of the hypothalamus. Histological markers of the fetal adrenal zone (or X-zone in rodents) were still present in adult males and postpartum SF1 Socs3 KO females, suggesting a previously unrecognized effect of SOCS3 on the terminal differentiation of the adrenal gland. This change led to a distinct distribution of lipid droplets along the adrenal cortex. Under basal conditions, adult SF1 Socs3 KO mice exhibited similar adrenal weight, and plasma ACTH and corticosterone concentrations. Nonetheless, SF1 Socs3 KO mice exhibited a blunted ACTH-induced corticosterone secretion. The overall metabolic responses induced by resistance training remained unaffected in SF1 Socs3 KO mice, including changes in body adiposity, glucose tolerance and energy expenditure. However, training performance and glucose control during intense resistance exercise were impaired in SF1 Socs3 KO mice. Furthermore, a reduced counter-regulatory response to 2-deoxy-d-glucose was observed in mutant mice. These findings revealed a novel participation of SOCS3 regulating several endocrine and metabolic aspects. Therefore, cytokine signaling in SF1 cells exerts an important role to sustain training performance possibly by promoting the necessary metabolic adjustments during exercise.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Fator Esteroidogênico 1/metabolismo
Proteína 3 Supressora da Sinalização de Citocinas/metabolismo
[Mh] Termos MeSH secundário: Adiposidade/genética
Adiposidade/fisiologia
Glândulas Suprarrenais/metabolismo
Animais
Diferenciação Celular/genética
Corticosterona/secreção
Desoxiglucose/metabolismo
Feminino
Masculino
Camundongos
Camundongos Knockout
Hipófise/metabolismo
Fator Esteroidogênico 1/genética
Proteína 3 Supressora da Sinalização de Citocinas/genética
Testículo/metabolismo
Testosterona/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Socs3 protein, mouse); 0 (Steroidogenic Factor 1); 0 (Suppressor of Cytokine Signaling 3 Protein); 0 (steroidogenic factor 1, mouse); 3XMK78S47O (Testosterone); 9G2MP84A8W (Deoxyglucose); W980KJ009P (Corticosterone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170914
[St] Status:MEDLINE
[do] DOI:10.1530/JOE-17-0255


  7 / 1635 MEDLINE  
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[PMID]:28710273
[Au] Autor:Zhang Y; Ma CA; Lawrence MG; Break TJ; O'Connell MP; Lyons JJ; López DB; Barber JS; Zhao Y; Barber DL; Freeman AF; Holland SM; Lionakis MS; Milner JD
[Ad] Endereço:Genetics and Pathogenesis of Allergy Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, Bethesda, MD.
[Ti] Título:PD-L1 up-regulation restrains Th17 cell differentiation in loss- and gain-of-function patients.
[So] Source:J Exp Med;214(9):2523-2533, 2017 Sep 04.
[Is] ISSN:1540-9538
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Patients with hypomorphic mutations in and patients with hypermorphic mutations in share several clinical and cellular phenotypes suggesting overlapping pathophysiologic mechanisms. We, therefore, examined cytokine signaling and CD4 T cell differentiation in these cohorts to characterize common pathways. As expected, differentiation of Th17 cells was impaired in both cohorts. We found that STAT1 was hyperphosphorylated in response to cytokine stimulation in both cohorts and that STAT1-dependent PD-L1 up-regulation-known to inhibit Th17 differentiation in mouse models-was markedly enhanced as well. Overexpression of SOCS3 strongly inhibited phosphorylation of STAT1 and PD-L1 up-regulation, suggesting that diminished SOCS3 expression may lead to the observed effects. Defects in Th17 differentiation could be partially overcome in vitro via PD-L1 inhibition and in a mouse model of STAT3 loss-of-function by crossing them with PD-1 knockout mice. PD-L1 may be a potential therapeutic target in several genetic diseases of immune deficiency affecting cytokine signaling.
[Mh] Termos MeSH primário: Antígeno B7-H1/fisiologia
Diferenciação Celular/fisiologia
Fator de Transcrição STAT1/fisiologia
Fator de Transcrição STAT3/fisiologia
Células Th17/fisiologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Animais
Criança
Citocinas/fisiologia
Feminino
Seres Humanos
Síndromes de Imunodeficiência/genética
Síndromes de Imunodeficiência/imunologia
Síndromes de Imunodeficiência/fisiopatologia
Interleucinas/fisiologia
Masculino
Camundongos
Camundongos Knockout
Meia-Idade
Fator de Transcrição STAT1/genética
Fator de Transcrição STAT3/genética
Transdução de Sinais/fisiologia
Proteína 3 Supressora da Sinalização de Citocinas/fisiologia
Regulação para Cima
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B7-H1 Antigen); 0 (CD274 protein, human); 0 (Cytokines); 0 (IL27 protein, human); 0 (Interleukins); 0 (SOCS3 protein, human); 0 (STAT1 Transcription Factor); 0 (STAT1 protein, human); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 0 (Suppressor of Cytokine Signaling 3 Protein)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170716
[St] Status:MEDLINE
[do] DOI:10.1084/jem.20161427


  8 / 1635 MEDLINE  
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[PMID]:28605567
[Au] Autor:Xu Z; Ji J; Xu J; Li D; Shi G; Liu F; Ding L; Ren J; Dou H; Wang T; Hou Y
[Ad] Endereço:The State Key Laboratory of Pharmaceutical Biotechnology, Division of Immunology, Medical School, Nanjing University, Nanjing, China.
[Ti] Título:MiR-30a increases MDSC differentiation and immunosuppressive function by targeting SOCS3 in mice with B-cell lymphoma.
[So] Source:FEBS J;284(15):2410-2424, 2017 Aug.
[Is] ISSN:1742-4658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Myeloid-derived suppressor cells (MDSCs), including granulocytic (G)-MDSCs and monocytic (M)-MDSCs, play a critical role in tumor-induced T cell tolerance. MDSC immunosuppressive function and differentiation are significantly promoted in patients and B-cell lymphoma model mice. However, the mechanisms regulating these processes remain largely unclear. In the present study, we observed increased microRNA (miR)-30a expression both in G-MDSCs and in M-MDSCs from B cell lymphoma model mice. After transfection with miR-30a mimics, the differentiation and suppressive capacities of MDSCs were significantly increased via up-regulation of arginase-1. Moreover, we showed that the 3'-UTR of suppressor of cytokine signaling 3 (SOCS3) mRNA is a direct target of miR-30a. Decreased SOCS3 expression and activated Janus kinase-signal transducer and activator of transcription 3 signaling promote MDSC differentiation and suppressive activities. These findings provide new insights into the molecular mechanisms underlying MDSC expansion and function during B cell lymphoma development.
[Mh] Termos MeSH primário: Regiões 3´ não Traduzidas
Diferenciação Celular
Linfoma de Células B/metabolismo
MicroRNAs/metabolismo
Células Supressoras Mieloides/metabolismo
Proteína 3 Supressora da Sinalização de Citocinas/metabolismo
Regulação para Cima
[Mh] Termos MeSH secundário: Animais
Arginase/genética
Arginase/metabolismo
Células da Medula Óssea/patologia
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD4-Positivos/metabolismo
Linfócitos T CD4-Positivos/patologia
Linhagem Celular Tumoral
Células Cultivadas
Regulação Neoplásica da Expressão Gênica
Células Precursoras de Granulócitos/imunologia
Células Precursoras de Granulócitos/metabolismo
Células Precursoras de Granulócitos/patologia
Imunossupressão
Linfoma de Células B/imunologia
Linfoma de Células B/patologia
Linfoma de Células B/terapia
Camundongos
Camundongos Endogâmicos BALB C
MicroRNAs/antagonistas & inibidores
Células Precursoras de Monócitos e Macrófagos/imunologia
Células Precursoras de Monócitos e Macrófagos/metabolismo
Células Precursoras de Monócitos e Macrófagos/patologia
Células Supressoras Mieloides/citologia
Células Supressoras Mieloides/imunologia
Células Supressoras Mieloides/patologia
Proteínas de Neoplasias/genética
Proteínas de Neoplasias/metabolismo
Transplante de Neoplasias
Baço/patologia
Proteína 3 Supressora da Sinalização de Citocinas/genética
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (MicroRNAs); 0 (Mirn30d microRNA, mouse); 0 (Neoplasm Proteins); 0 (Socs3 protein, mouse); 0 (Suppressor of Cytokine Signaling 3 Protein); EC 3.5.3.1 (Arg1 protein, mouse); EC 3.5.3.1 (Arginase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE
[do] DOI:10.1111/febs.14133


  9 / 1635 MEDLINE  
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[PMID]:28603075
[Au] Autor:Chu Q; Shen D; He L; Wang H; Liu C; Zhang W
[Ad] Endereço:Department of Anesthesiology, Zhengzhou University Affiliated First Hospital, 450052, He Nan, China.
[Ti] Título:Prognostic significance of SOCS3 and its biological function in colorectal cancer.
[So] Source:Gene;627:114-122, 2017 Sep 05.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Colorectal cancer (CRC) is a common malignant tumor, in which the inflammatory microenvironment plays an important role. STAT3 signaling pathway is regarded as the "bridge" between inflammation and cancer, and involved in the development of CRC. SOCS3 is a key negative feedback regulator of JAK/STAT signaling pathway. Studies about SOCS3 gene in CRC are rarely reported. The purpose of this study is to determine the expression of SOCS3 in CRC tissue and its correlation with the clinical pathological characteristics and prognosis of colorectal cancers. The effects of SOCS3 on biological behavior such as apoptosis, proliferation, migration, invasion and tumor formation in nude mice were studied. We observed that SOCS3 expression was down-regulated in CRC tissues, while IL-6, pSTAT3 were up-regulated. Inflammatory cytokines IL-6 can promote the expression of STAT3 signaling pathways while inhibit the expression of SOCS3 by promoting hypermethylation of SOCS3 gene promoters. 5-Aza-cdR treatment can reverse IL-6/STAT3 signaling pathway mediated down-regulation of SOCS3 in colorectal cancer cells. Low expression of SOCS3 was correlated with lymph node metastasis and advanced clinical stage. Patients with high expression of SOCS3 in colorectal cancers often indicated a relatively good prognosis. Overexpression of SOCS3 inhibited proliferation, migration, invasion and tumorigenic ability of CRC cells while increased cell apoptosis. This study demonstrated that IL-6/STAT3 signaling activation negatively regulated SOCS3 expression, which led to imbalance and sustained activation of STAT3 signaling pathway. Reduced expression of SOCS3 promoted the growth and metastasis of colorectal cancer. Thus, targeting IL-6/STAT3/SOCS3 signaling pathway may become an important treatment strategy of colorectal cancer.
[Mh] Termos MeSH primário: Neoplasias Colorretais/diagnóstico
Proteína 3 Supressora da Sinalização de Citocinas/metabolismo
[Mh] Termos MeSH secundário: Idoso
Animais
China
Neoplasias Colorretais/patologia
Neoplasias Colorretais/cirurgia
Feminino
Seres Humanos
Masculino
Camundongos
Camundongos Nus
Meia-Idade
Prognóstico
Regiões Promotoras Genéticas
Fator de Transcrição STAT3/análise
Proteína 3 Supressora da Sinalização de Citocinas/análise
Proteína 3 Supressora da Sinalização de Citocinas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (SOCS3 protein, human); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 0 (Suppressor of Cytokine Signaling 3 Protein)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170807
[Lr] Data última revisão:
170807
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE


  10 / 1635 MEDLINE  
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[PMID]:28582466
[Au] Autor:Lundtoft C; Afum-Adjei Awuah A; Rimpler J; Harling K; Nausch N; Kohns M; Adankwah E; Lang F; Olbrich L; Mayatepek E; Owusu-Dabo E; Jacobsen M
[Ad] Endereço:Department of General Pediatrics, Neonatology, and Pediatric Cardiology, University Children's Hospital, Medical Faculty, Duesseldorf, Germany.
[Ti] Título:Aberrant plasma IL-7 and soluble IL-7 receptor levels indicate impaired T-cell response to IL-7 in human tuberculosis.
[So] Source:PLoS Pathog;13(6):e1006425, 2017 Jun.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:T-cell proliferation and generation of protective memory during chronic infections depend on Interleukin-7 (IL-7) availability and receptivity. Regulation of IL-7 receptor (IL-7R) expression and signalling are key for IL-7-modulated T-cell functions. Aberrant expression of soluble (s) and membrane-associated (m) IL-7R molecules is associated with development of autoimmunity and immune failure in acquired immune deficiency syndrome (AIDS) patients. Here we investigated the role of IL-7/IL-7R on T-cell immunity in human tuberculosis. We performed two independent case-control studies comparing tuberculosis patients and healthy contacts. This was combined with follow-up examinations for a subgroup of tuberculosis patients under therapy and recovery. Blood plasma and T cells were characterised for IL-7/sIL-7R and mIL-7R expression, respectively. IL-7-dependent T-cell functions were determined by analysing STAT5 phosphorylation, antigen-specific cytokine release and by analysing markers of T-cell exhaustion and inflammation. Tuberculosis patients had lower soluble IL-7R (p < 0.001) and higher IL-7 (p < 0.001) plasma concentrations as compared to healthy contacts. Both markers were largely independent and aberrant expression normalised during therapy and recovery. Furthermore, tuberculosis patients had lower levels of mIL-7R in T cells caused by post-transcriptional mechanisms. Functional in vitro tests indicated diminished IL-7-induced STAT5 phosphorylation and impaired IL-7-promoted cytokine release of Mycobacterium tuberculosis-specific CD4+ T cells from tuberculosis patients. Finally, we determined T-cell exhaustion markers PD-1 and SOCS3 and detected increased SOCS3 expression during therapy. Only moderate correlation of PD-1 and SOCS3 with IL-7 expression was observed. We conclude that diminished soluble IL-7R and increased IL-7 plasma concentrations, as well as decreased membrane-associated IL-7R expression in T cells, reflect impaired T-cell sensitivity to IL-7 in tuberculosis patients. These findings show similarities to pathognomonic features of impaired T-cell functions and immune failure described in AIDS patients.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Interleucina-7/sangue
Receptores de Interleucina-7/sangue
Tuberculose/imunologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Estudos de Casos e Controles
Feminino
Seres Humanos
Interleucina-7/genética
Interleucina-7/imunologia
Masculino
Meia-Idade
Mycobacterium tuberculosis/genética
Mycobacterium tuberculosis/fisiologia
Fosforilação
Receptores de Interleucina-7/genética
Receptores de Interleucina-7/imunologia
Fator de Transcrição STAT5/genética
Fator de Transcrição STAT5/imunologia
Proteína 3 Supressora da Sinalização de Citocinas/genética
Proteína 3 Supressora da Sinalização de Citocinas/imunologia
Tuberculose/microbiologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interleukin-7); 0 (Receptors, Interleukin-7); 0 (STAT5 Transcription Factor); 0 (Suppressor of Cytokine Signaling 3 Protein)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170606
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006425



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