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[PMID]:27779203
[Au] Autor:Villalobos-Hernandez A; Bobbala D; Kandhi R; Khan MG; Mayhue M; Dubois CM; Ferbeyre G; Saucier C; Ramanathan S; Ilangumaran S
[Ad] Endereço:Immunology Division, Department of Pediatrics, Faculty of Medicine and Health Sciences, University of Sherbrooke, Sherbrooke, Quebec, Canada.
[Ti] Título:SOCS1 inhibits migration and invasion of prostate cancer cells, attenuates tumor growth and modulates the tumor stroma.
[So] Source:Prostate Cancer Prostatic Dis;20(1):36-47, 2017 Mar.
[Is] ISSN:1476-5608
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The suppressor of cytokine signaling 1 (SOCS1) gene is repressed in prostate cancer (PCa) by epigenetic silencing and microRNA miR30d. Increased expression of the SOCS1-targeting miR30d correlates with higher biochemical recurrence, suggesting a tumor suppressor role of SOCS1 in PCa, but the underlying mechanisms are unclear. We have shown that SOCS1 inhibits MET receptor kinase signaling, a key oncogenic pathway in cancer progression. Here we evaluated the role of SOCS1 in attenuating MET signaling in PCa cells and tumor growth in vivo. METHODS: MET-overexpressing human DU145 and PC3 PCa cell lines were stably transduced with SOCS1, and their growth, migration and invasion of collagen matrix were evaluated in vitro. Cells expressing SOCS1 or the control vector were evaluated for tumor growth in NOD.scid.gamma mice as xenograft or orthotopic tumors. RESULTS: HGF-induced MET signaling was attenuated in SOCS1-expressing DU145 and PC3 cells. Compared with vector control cells, SOCS1-expressing cells showed reduced proliferation and impaired migration following HGF stimulation. DU145 and PC3 cells showed marked ability to invade the collagen matrix following HGF stimulation and this was attenuated by SOCS1. As xenografts, SOCS1-expressing PCa cells showed significantly reduced tumor growth compared with vector control cells. In the orthotopic tumor model, SOCS1 reduced the growth of primary tumors and metastatic spread. Intriguingly, the SOCS1-expressing DU145 and PC3 tumors showed increased collagen deposition, associated with increased frequency of myofibroblasts. CONCLUSIONS: Our findings support the tumor suppressor role of SOCS1 in PCa and suggest that attenuation of MET signaling is one of the underlying mechanisms. SOCS1 in PCa cells also appears to prevent the tumor-promoting functions of cancer-associated fibroblasts.
[Mh] Termos MeSH primário: Neoplasias da Próstata/metabolismo
Neoplasias da Próstata/patologia
Células Estromais/metabolismo
Proteína 1 Supressora da Sinalização de Citocina/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Movimento Celular
Proliferação Celular
Transformação Celular Neoplásica/genética
Transformação Celular Neoplásica/metabolismo
Colágeno/metabolismo
Metilação de DNA
Modelos Animais de Doenças
Epigênese Genética
Expressão Gênica
Fator de Crescimento de Hepatócito/metabolismo
Xenoenxertos
Seres Humanos
Masculino
Camundongos
Invasividade Neoplásica
Metástase Neoplásica
Neoplasias da Próstata/genética
Proteínas Proto-Oncogênicas c-met/metabolismo
Transdução de Sinais
Células Estromais/patologia
Proteína 1 Supressora da Sinalização de Citocina/genética
Carga Tumoral
Microambiente Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HGF protein, human); 0 (SOCS1 protein, human); 0 (Suppressor of Cytokine Signaling 1 Protein); 67256-21-7 (Hepatocyte Growth Factor); 9007-34-5 (Collagen); EC 2.7.10.1 (Proto-Oncogene Proteins c-met)
[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:161026
[St] Status:MEDLINE
[do] DOI:10.1038/pcan.2016.50


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[PMID]:28469732
[Au] Autor:Cohen SA; Yu M; Baker K; Redman M; Wu C; Heinzerling TJ; Wirtz RM; Charalambous E; Pentheroudakis G; Kotoula V; Kalogeras KT; Fountzilas G; Grady WM
[Ad] Endereço:Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109 USA.
[Ti] Título:The CpG island methylator phenotype is concordant between primary colorectal carcinoma and matched distant metastases.
[So] Source:Clin Epigenetics;9:46, 2017.
[Is] ISSN:1868-7083
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The CpG island methylator phenotype (CIMP) in stage III colon cancer (CRC) has been associated with improved survival after treatment with adjuvant irinotecan-based chemotherapy. In this analysis, we determine whether CIMP status in the primary CRC is concordant with the CIMP status of matched metastases in order to determine if assessment of CIMP status in the primary tumor can be used to predict CIMP status of metastatic disease, which is relevant for patient management as well as for understanding the biology of CIMP CRCs. METHODS: We assessed the CIMP status of 70 pairs of primary CRC and matched metastases using a CRC-specific panel of five markers ( , , , , and ) where CIMP positive was defined as 3/5 positive markers at a percent methylated reference threshold of ≥10%. Concordance was compared using the Fisher's exact test and < 0.05 was considered significant. RESULTS: Sixty-nine of the pairs (98.6%) showed concordant CIMP status in the primary tumor and matched metastasis; five (7.0%) of the pairs were concordantly CIMP positive. Only one pair (1.4%) had divergent CIMP status, demonstrating CIMP positivity (4/5 markers positive) in the primary tumor, while the matched metastasis was CIMP negative (0 markers positive). CONCLUSIONS: CIMP status is generally concordant between primary CRCs and matched metastases. Thus, CIMP status in the primary tumor is maintained in matched metastases and can be used to inform CIMP-based therapy options for the metastases.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/genética
Neoplasias Colorretais/genética
Metilação de DNA
[Mh] Termos MeSH secundário: Adulto
Idoso
Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Canais de Cálcio Tipo T/genética
Neoplasias Colorretais/patologia
Subunidade alfa 3 de Fator de Ligação ao Core/genética
Ilhas de CpG
Epigênese Genética
Feminino
Seres Humanos
Fator de Crescimento Insulin-Like II/genética
Masculino
Meia-Idade
Metástase Neoplásica
Proteínas do Tecido Nervoso/genética
Fenótipo
Proteína 1 Supressora da Sinalização de Citocina/genética
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Biomarkers, Tumor); 0 (CACNA1G protein, human); 0 (Calcium Channels, T-Type); 0 (Core Binding Factor Alpha 3 Subunit); 0 (IGF2 protein, human); 0 (NEUROG1 protein, human); 0 (Nerve Tissue Proteins); 0 (Runx3 protein, human); 0 (SOCS1 protein, human); 0 (Suppressor of Cytokine Signaling 1 Protein); 67763-97-7 (Insulin-Like Growth Factor II)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180122
[Lr] Data última revisão:
180122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1186/s13148-017-0347-1


  3 / 1076 MEDLINE  
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[PMID]:27770564
[Au] Autor:Liu D; Zhou JL; Hong F; Zhang YQ
[Ad] Endereço:Department of Applied Biology, School of Basic Medical and Biological Sciences, Soochow University, RM702-2303, Renai Road No. 199, Dushuhu Higher Edu. Town, Suzhou, 215123, People's Republic of China.
[Ti] Título:Lung inflammation caused by long-term exposure to titanium dioxide in mice involving in NF-κB signaling pathway.
[So] Source:J Biomed Mater Res A;105(3):720-727, 2017 03.
[Is] ISSN:1552-4965
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Titanium dioxide nanoparticles (TiO NPs) are used in many fields, such as paints, medicine additives, food additives, sunscreens, and agriculture. The aim of this study was to investigate the mechanism behind the formation of inflammation induced by TiO NPs. ICR mice were exposed to TiO NPs through intragastric administration at 2.5, 5, and 10 mg/kg body weight every day for 90 consecutive days. The experiment suggested that long-term exposure to TiO NPs resulted in an obvious inflammatory response in mice lung tissues, which led to a thickened alveoli septum, lung hyperemia, and titanium accumulation. Furthermore, our results show that TiO NPs exposure remarkably altered the expression of inflammation-related cytokines, with increases in proinflammatory cytokines-such as nucleic factor-κB, interferon-α, interferon-ß, interleukin-1ß, interleukin-6, cyclo-oxygen-ase, interleukin-8, interferon-inducible protein-10, and platelet-derived growth factor AB-and decreases in anti-inflammatory cytokines-such as inhibitor of NF-κB suppressor of cytokine signaling 1, endothelin 1, peroxisome proliferators-activated receptors-γ, and peroxisome proliferators-activated receptors coactivator-1α. This finding indicated that TiO NPs cause lung inflammation in mice after intragastric administration, primarily through the NF-κB signaling pathways. Therefore, more attention should be placed on the application of TiO NPs and their potential long-term effects, especially in human beings. © 2016 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 105A: 720-727, 2017.
[Mh] Termos MeSH primário: NF-kappa B/toxicidade
Pneumonia
Transdução de Sinais/efeitos dos fármacos
Titânio/toxicidade
[Mh] Termos MeSH secundário: Animais
Citocinas/metabolismo
Endotelina-1/metabolismo
Feminino
Camundongos
Camundongos Endogâmicos ICR
PPAR gama/metabolismo
Pneumonia/induzido quimicamente
Pneumonia/metabolismo
Pneumonia/patologia
Proteína 1 Supressora da Sinalização de Citocina/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (Endothelin-1); 0 (NF-kappa B); 0 (PPAR gamma); 0 (Socs1 protein, mouse); 0 (Suppressor of Cytokine Signaling 1 Protein); 15FIX9V2JP (titanium dioxide); D1JT611TNE (Titanium)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171225
[Lr] Data última revisão:
171225
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161023
[St] Status:MEDLINE
[do] DOI:10.1002/jbm.a.35945


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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


  5 / 1076 MEDLINE  
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[PMID]:28762092
[Au] Autor:Youssef SS; Hamdy NM
[Ad] Endereço:Genetic Engineering Division, Microbial Biotechnology Department, National Research Centre, El Behous st, Dokki, Cairo, Giza, 12311, Egypt. youssefsamar1969@yahoo.com.
[Ti] Título:SOCS1 and pattern recognition receptors: TLR9 and RIG-I; novel haplotype associations in Egyptian fibrotic/cirrhotic patients with HCV genotype 4.
[So] Source:Arch Virol;162(11):3347-3354, 2017 Nov.
[Is] ISSN:1432-8798
[Cp] País de publicação:Austria
[La] Idioma:eng
[Ab] Resumo:In this paper we explore the role of suppressor of cytokine signaling 1 (SOCS1) (rs243327), the regulator of toll-like receptor-9 (TLR9) (rs352140), retinoic acid inducible gene-I (RIG-I) (rs669260), and cluster of differentiation 152 (CD152) (rs231776) in fibrotic/cirrhotic patients. Single nucleotide polymorphisms (SNPs) within these genes as well as haplotype analyses were performed on a cohort of 120 Egyptian fibrotic patients. Fibrosis had progressed from HCV genotype 4 infections. Using RT-PCR, SNPs were evaluated in the DNA collected from each patient using TaqMan genotyping assays. A regression model was used to evaluate allelic and haplotypic associations with a fibrosis/cirrhotic scale. The necroinflammatory A score was adjusted for non-genetic covariates. The genotype distributions for SOCS1 (rs243327) and TLR-9 (rs352140) differed significantly between the F1-F3 and F3-F4 groups. On the other hand, the genotype distributions for RIG-I (rs669260) and CD152 (rs231776) genes did not significantly differ. The allele frequency was calculated using Hardy-Weinberg Equilibrium (HWE) for the SOCS1 (rs243327), RIG-I (rs669260), and CD152 (rs231776) genes. These calculated frequency values indicated the need to compare them to another population for that locus. However, TLR9 (rs352140) did not show similar results. The A allele in SOCS1, TLR9, and RIG-I SNPs was an adverse prognostic factor for liver fibrosis and liver activity. Haplotype analysis revealed a significant association between SOCS1 and TLR9 in fibrotic/cirrhotic patients. This indicated the presence of the A allele in either gene, which is considered a risk factor for the progression of liver disease to cirrhosis. SOCS1 rs243327, TLR9 rs352140, and RIG-I rs669260 polymorphisms might affect liver pathophysiology and the cirrhotic outcome following genotype 4 HCV infection. Therefore, performing this specific SNP testing may be of value for the stratification of the population at risk.
[Mh] Termos MeSH primário: Proteína DEAD-box 58/metabolismo
Hepacivirus/classificação
Cirrose Hepática/virologia
Proteína 1 Supressora da Sinalização de Citocina/metabolismo
Receptor Toll-Like 9/metabolismo
[Mh] Termos MeSH secundário: Adulto
Estudos de Coortes
Proteína DEAD-box 58/genética
Egito/epidemiologia
Feminino
Haplótipos
Hepatite C/epidemiologia
Hepatite C/metabolismo
Hepatite C/virologia
Seres Humanos
Cirrose Hepática/epidemiologia
Cirrose Hepática/metabolismo
Cirrose Hepática/patologia
Masculino
Meia-Idade
Polimorfismo de Nucleotídeo Único
Proteína 1 Supressora da Sinalização de Citocina/genética
Receptor Toll-Like 9/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (SOCS1 protein, human); 0 (Suppressor of Cytokine Signaling 1 Protein); 0 (TLR9 protein, human); 0 (Toll-Like Receptor 9); EC 3.6.1.- (DDX58 protein, human); EC 3.6.4.13 (DEAD Box Protein 58)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171025
[Lr] Data última revisão:
171025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170802
[St] Status:MEDLINE
[do] DOI:10.1007/s00705-017-3498-7


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[PMID]:28753604
[Au] Autor:Demirel Ö; Balló O; Reddy PNG; Vakhrusheva O; Zhang J; Eichler A; Fernandes R; Badura S; Serve H; Brandts C
[Ad] Endereço:Department of Medicine, Hematology/Oncology, Goethe University, Frankfurt, Germany.
[Ti] Título:SOCS1 function in BCR-ABL mediated myeloproliferative disease is dependent on the cytokine environment.
[So] Source:PLoS One;12(7):e0180401, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Treatment with tyrosine kinase inhibitors is the standard of care for Philadelphia chromosome positive leukemias. However the eradication of leukemia initiating cells remains a challenge. Circumstantial evidence suggests that the cytokine microenvironment may play a role in BCR-ABL mediated leukemogenesis and in imatinib resistance. Gene expression analyses of BCR-ABL positive ALL long-term cultured cells revealed strong reduction of SOCS mRNA expression after imatinib treatment, thereby demonstrating a strong inhibition of cytokine signaling. In this study we employed SOCS1-a strong inhibitor of cytokine signaling-as a tool to terminate external cytokine signals in BCR-ABL transformed cells in vitro and in vivo. In colony formation assays with primary bone marrow cells, expression of SOCS1 decreased colony numbers under pro-proliferative cytokines, while it conferred growth resistance to anti-proliferative cytokines. Importantly, co-expression of SOCS1 with BCR-ABL led to the development of a MPD phenotype with a prolonged disease latency compared to BCR-ABL alone in a murine bone marrow transplantation model. Interestingly, SOCS1 co-expression protected 20% of mice from MPD development. In summary, we conclude that under pro-proliferative cytokine stimulation at the onset of myeloproliferative diseases SOCS1 acts as a tumor suppressor, while under anti-proliferative conditions it exerts oncogenic function. Therefore SOCS1 can promote opposing functions depending on the cytokine environment.
[Mh] Termos MeSH primário: Citocinas/metabolismo
Proteínas de Fusão bcr-abl/metabolismo
Transtornos Mieloproliferativos/metabolismo
Proteína 1 Supressora da Sinalização de Citocina/metabolismo
[Mh] Termos MeSH secundário: Animais
Medula Óssea/metabolismo
Transplante de Medula Óssea
Linhagem Celular
Feminino
Proteínas de Fusão bcr-abl/genética
Interleucina-3/metabolismo
Camundongos
Transtornos Mieloproliferativos/genética
Fosforilação
Fator de Transcrição STAT5/metabolismo
Baço/metabolismo
Proteína 1 Supressora da Sinalização de Citocina/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Interleukin-3); 0 (STAT5 Transcription Factor); 0 (Socs1 protein, mouse); 0 (Suppressor of Cytokine Signaling 1 Protein); EC 2.7.10.2 (Fusion Proteins, bcr-abl)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170729
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180401


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[PMID]:28704535
[Au] Autor:López-Rodríguez R; Hernández-Bartolomé Á; Borque MJ; Rodríguez-Muñoz Y; Martín-Vílchez S; García-Buey L; González-Moreno L; Real-Martínez Y; Muñoz de Rueda P; Salmerón J; Vidal-Castiñeira JR; López-Larrea C; Rodrigo L; Moreno-Otero R; Sanz-Cameno P
[Ad] Endereço:Liver Unit, Gastroenterology Service, Instituto Investigación Sanitaria Princesa, IIS-IP, Madrid, Spain.
[Ti] Título:Interferon-related genetic markers of necroinflammatory activity in chronic hepatitis C.
[So] Source:PLoS One;12(7):e0180927, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Chronic hepatitis C (CHC) is a major cause of liver disease worldwide which often leads to progressive liver inflammation, fibrosis, cirrhosis and hepatocellular carcinoma (HCC). CHC displays heterogeneous progression depending on a broad set of factors, some of them intrinsic to each individual such as the patient's genetic profile. This study aims to evaluate the contribution of certain genetic variants of crucial interferon alpha and lambda signaling pathways to the hepatic necroinflammatory activity (NIA) grade of CHC patients. METHODS: NIA was evaluated in 119 CHC patients by METAVIR scale and classified as low (NIA = 0-2, n = 80) or high grade (NIA = 3, n = 39). In a candidate gene approach, 64 SNPs located in 30 different genes related to interferon pathways (IL-28B, IFNAR1-2, JAK-STAT and OAS1-3, among others) were genotyped using the Illumina GoldenGate® Genotyping Assay. Statistical association was determined by logistic regression and expressed as OR and 95% CI. Those SNPs significantly associated were further adjusted by other covariates. RESULTS: Seven SNPs located in IL-28B (rs12979860), JAK1 (rs11576173 and rs1497056), TYK2 (rs280519), OAS1 (rs2057778), SOCS1 (rs33932899) and RNASEL (rs3738579) genes were significantly related to severe NIA grade (p<0.05). Regarding to clinical variables, elevated NIA was notably associated with aspartate aminotransferase (AST) serum levels >40 IU/L (p<0.05) but not with other clinical factors. Multivariate logistic regression analysis of these factors reflected that AST (>40 IU/L), TYK2 rs280519 (G allele) and RNASEL rs3738579 (G allele) were factors independently associated with elevated NIA (p<0.05). AST concentration showed a moderate AUC value (AUC = 0.63), similar to TYK2 (rs280519) and RNASEL (rs3738579) SNPs (AUC = 0.61, both) in the ROC_AUC analysis. Interestingly, the model including all significant variables reached a considerable predictive value (AUC = 0.74). CONCLUSION: The identified genetic variants in interferon signaling pathways may constitute useful prognostic markers of CHC progression. Further validation in larger cohorts of patients is needed.
[Mh] Termos MeSH primário: Hepatite C Crônica/genética
Interleucinas/genética
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: 2',5'-Oligoadenilato Sintetase/genética
Adulto
Idoso
Aspartato Aminotransferases/sangue
Endorribonucleases/genética
Feminino
Hepatite C Crônica/sangue
Hepatite C Crônica/patologia
Seres Humanos
Janus Quinase 1/genética
Masculino
Meia-Idade
Proteína 1 Supressora da Sinalização de Citocina/genética
TYK2 Quinase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL28B protein, human); 0 (Interleukins); 0 (SOCS1 protein, human); 0 (Suppressor of Cytokine Signaling 1 Protein); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.7.10.2 (JAK1 protein, human); EC 2.7.10.2 (Janus Kinase 1); EC 2.7.10.2 (TYK2 Kinase); EC 2.7.10.2 (TYK2 protein, human); EC 2.7.7.- (OAS1 protein, human); EC 2.7.7.84 (2',5'-Oligoadenylate Synthetase); EC 3.1.- (Endoribonucleases); EC 3.1.26.- (2-5A-dependent ribonuclease)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170714
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0180927


  8 / 1076 MEDLINE  
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[PMID]:28550203
[Au] Autor:Takahashi R; Nakatsukasa H; Shiozawa S; Yoshimura A
[Ad] Endereço:Department of Immunology, Research Institute, Nozaki Tokushukai, Daitou, Osaka 574-0074, Japan; rtakahas@tokushukai.jp.
[Ti] Título:SOCS1 Is a Key Molecule That Prevents Regulatory T Cell Plasticity under Inflammatory Conditions.
[So] Source:J Immunol;199(1):149-158, 2017 Jul 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We previously showed that regulatory T cells (Tregs) from T cell-specific -deficient mice ( mice) easily convert into Th1- or Th17-like cells (ex-Tregs), which lose Foxp3 expression and suppressive functions in vivo. Because Tregs in mice are constantly exposed to a large amount of inflammatory cytokines produced by non-Tregs in vivo, in this study we analyzed Treg-specific -deficient mice ( mice). These mice developed dermatitis, splenomegaly, and lymphadenopathy that were much milder than those in mice. A fate mapping study revealed that deficiency accelerated the conversion of Tregs to Foxp3 IFN-γ ex-Tregs in the tumor microenvironment and suppressed tumor growth. When transferred into mice, Tregs from mice easily lost Foxp3 expression, whereas those from mice maintained Foxp3 expression. Although Tregs from mice produced IFN-γ after a 3-d culture in response to anti-CD3/CD28 Ab stimulation in vitro, Tregs from mice did not. This finding suggested that the inflammatory conditions in mice modified the born nature of -deficient Tregs. To investigate this mechanism, Tregs from mice were cultured with APCs from mice. These APCs facilitated STAT4 phosphorylation, IFN-γ production, and loss of Foxp3 expression in Tregs from mice in an IL-12-dependent manner. The results indicate that -deficient Tregs tend to convert into ex-Tregs under the inflammatory conditions in which APCs are highly activated, and that SOCS1 could be a useful target for enhancement of anti-tumor immunity.
[Mh] Termos MeSH primário: Plasticidade Celular
Inflamação/imunologia
Proteína 1 Supressora da Sinalização de Citocina/metabolismo
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Animais
Citocinas/imunologia
Fatores de Transcrição Forkhead/deficiência
Fatores de Transcrição Forkhead/genética
Fatores de Transcrição Forkhead/metabolismo
Interferon gama/biossíntese
Interferon gama/imunologia
Camundongos
Camundongos Knockout
Esplenomegalia/imunologia
Proteína 1 Supressora da Sinalização de Citocina/deficiência
Linfócitos T Reguladores/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Socs1 protein, mouse); 0 (Suppressor of Cytokine Signaling 1 Protein); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170528
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600441


  9 / 1076 MEDLINE  
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[PMID]:28419615
[Au] Autor:Sato Y; Koshizuka T; Ishibashi K; Hashimoto K; Ishioka K; Ikuta K; Yokota SI; Fujii N; Suzutani T
[Ad] Endereço:Department of Microbiology, Fukushima Medical University School of Medicine, Fukushima, Japan.
[Ti] Título:Involvement of herpes simplex virus type 1 UL13 protein kinase in induction of SOCS genes, the negative regulators of cytokine signaling.
[So] Source:Microbiol Immunol;61(5):159-167, 2017 May.
[Is] ISSN:1348-0421
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:The suppressor of cytokine signaling (SOCS) family has eight members and suppresses various cytokine signaling pathways, including IFN signaling. Therefore, some viruses have evolved molecular mechanisms for inducing SOCS proteins and thus escaping host immunity. Herpes simplex virus type 1 (HSV-1) has a mechanism for escaping from type I IFN by induction of both SOCS1 and SOCS3. In this study, expression of the eight members of the SOCS family stimulated by HSV-1 infection was comparatively analyzed by qRT-PCR. It was found that SOCS1 and SOCS3 are induced by HSV-1-infection at 4 hr post infection. However, such induction was not observed in UL13 deficient virus-infected cells, suggesting that UL13 protein kinase participates in induction of both genes. The transcription factor Sp1-binding sites of SOCS3 promoter/enhancer region were identified as the regulatory elements for induction of SOCS3 in HSV-1 infected cells. Accumulation of activated Sp1 was detectable in the nuclei of HSV-1-infected cells before induction of SOCS3. Taken together, these results suggest that HSV-1 has a potent mechanism for escaping from the IFN system.
[Mh] Termos MeSH primário: Herpesvirus Humano 1/genética
Evasão da Resposta Imune/imunologia
Interferon Tipo I/metabolismo
Proteínas Quinases/genética
Proteína 1 Supressora da Sinalização de Citocina/metabolismo
Proteína 3 Supressora da Sinalização de Citocinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação/genética
Linhagem Celular
Cercopithecus aethiops
Seres Humanos
Evasão da Resposta Imune/genética
Regiões Promotoras Genéticas/genética
Elementos Reguladores de Transcrição/genética
Transdução de Sinais/genética
Fator de Transcrição Sp1/metabolismo
Proteína 1 Supressora da Sinalização de Citocina/genética
Proteína 3 Supressora da Sinalização de Citocinas/genética
Células Vero
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Interferon Type I); 0 (SOCS1 protein, human); 0 (SOCS3 protein, human); 0 (Sp1 Transcription Factor); 0 (Sp1 protein, human); 0 (Suppressor of Cytokine Signaling 1 Protein); 0 (Suppressor of Cytokine Signaling 3 Protein); EC 2.7.- (Protein Kinases); EC 2.7.1.- (UL13 protein, Simplexvirus)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170419
[St] Status:MEDLINE
[do] DOI:10.1111/1348-0421.12483


  10 / 1076 MEDLINE  
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[PMID]:28378729
[Au] Autor:Sorokina LN; Mineev VN; Lim VV
[Ad] Endereço:I.P. Pavlov First Saint Petersburg State Medical University, Ministry of Health of Russia, Saint Petersburg, Russia.
[Ti] Título:[Role of negative regulators of SOCS1, SOCS3, and SOCS5 gene transcription in the negative cell signaling regulation system in asthma].
[Ti] Título:Rol' negativnykh regulyatorov transkriptsii genov SOCS1, SOCS3 i SOCS5 v sisteme negativnoi regulyatsii kletochnoi signalizatsii pri bronkhial'noi astme..
[So] Source:Ter Arkh;89(3):43-47, 2017.
[Is] ISSN:0040-3660
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:AIM: To conduct a comprehensive study of the components of negative cell signaling regulation in different types of asthma. SUBJECTS AND METHODS: A total of 171 people, including 80 patients with allergic asthma (AA), 60 patients with non-allergic asthma (NAA), and 31 apparently healthy individuals, were examined. SOCS5 mRNA expression was assessed by reverse-transcription polymerase chain reaction. The expression of SOCS1 and SOCS3 proteins was investigated by immunoblotting. The concentration of total serum IgE was determined by enzyme immunoassay; the level of cytokines was measured according to the standard protocol using a Bio-Plex fluorometer. RESULTS: The findings show that the patients with AA generally display more marked changes in the expression of all three investigated SOCSes (SOCS1, SOCS3, and SOCS5) at baseline and when interleukin 4 (IL-4) acts. In NAA, there are pronounced changes in the expression of SOCS3 only and, to a lesser extent, SOCS5. The results of investigating the concentrations of IL-4 in the examined groups demonstrate its significant decrease in the AA group, whereas in the NAA group, it is similar to those in healthy individuals. On the contrary, IL-10 concentrations in AA tend towards those in the control group, but much exceed in NAA. CONCLUSION: The findings allow one to consider the complexity of regulatory disorders arising at various levels of cell signaling in the context of the multifunctional nature of the molecules from the family of negative regulators of transcription of the SOCS1, SOCS3, and SOCS5 genes, which provide the comprehensive control of cytokine signaling simultaneously in different signal pathways.
[Mh] Termos MeSH primário: Asma
Interleucina-4/metabolismo
Proteína 1 Supressora da Sinalização de Citocina/metabolismo
Proteína 3 Supressora da Sinalização de Citocinas/metabolismo
Proteínas Supressoras da Sinalização de Citocinas/metabolismo
[Mh] Termos MeSH secundário: Adulto
Asma/diagnóstico
Asma/etiologia
Asma/metabolismo
Asma/fisiopatologia
Feminino
Perfilação da Expressão Gênica/métodos
Seres Humanos
Hipersensibilidade/metabolismo
Interleucina-10/metabolismo
Masculino
Transdução de Sinais/fisiologia
Transcrição Genética/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (IL10 protein, human); 0 (IL4 protein, human); 0 (SOCS1 protein, human); 0 (SOCS3 protein, human); 0 (SOCS5 protein, human); 0 (Suppressor of Cytokine Signaling 1 Protein); 0 (Suppressor of Cytokine Signaling 3 Protein); 0 (Suppressor of Cytokine Signaling Proteins); 130068-27-8 (Interleukin-10); 207137-56-2 (Interleukin-4)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE
[do] DOI:10.17116/terarkh201789343-47



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