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[PMID]:28930651
[Au] Autor:Li A; Jacks T
[Ad] Endereço:Koch Institute for Integrative Cancer Research and Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
[Ti] Título:Driving Rel-iant Tregs toward an Identity Crisis.
[So] Source:Immunity;47(3):391-393, 2017 Sep 19.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Inhibiting Treg cell function in tumors is an attractive strategy to improve anti-cancer immunity. In a pair of papers in Immunity and Cell, Ghosh and colleagues show that the canonical NF-κB subunits p65 and c-Rel have non-redundant, critical roles in promoting Treg cell development and function (Oh et al., 2017). Targeting c-Rel blunts Treg cell immunosuppressive activity in the tumor microenvironment and enhances anti-tumor T cell responses (Grinberg-Bleyer et al., 2017).
[Mh] Termos MeSH primário: NF-kappa B/imunologia
Proteínas Proto-Oncogênicas c-rel
[Mh] Termos MeSH secundário: Seres Humanos
Linfócitos T Reguladores/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (Proto-Oncogene Proteins c-rel)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE


  2 / 779 MEDLINE  
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[PMID]:28892661
[Au] Autor:Mohammadi SM; Mohammadnejad D; Hosseinpour Feizi AA; Movassaghpour AA; Montazersaheb S; Nozad Charoudeh H
[Ad] Endereço:Stem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
[Ti] Título:Inhibition of c-REL using siRNA increased apoptosis and decreased proliferation in pre-B ALL blasts: Therapeutic implications.
[So] Source:Leuk Res;61:53-61, 2017 Oct.
[Is] ISSN:1873-5835
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The c-Rel transcription factor is a unique member of the NF-kB family that has a role in apoptosis, proliferation and cell survival. Overexpression of c-Rel is detected in many human B cell tumors, including B-cell leukemia and several cancers. The study aimed to investigate the effects of c-Rel siRNA on the proliferation and apoptosis of relapsed pre-B acute leukemia cells. The c-Rel siRNA was transfected into Leukemia cells using an Amaxa cell line Nucleofector kit L (Lonza). Quantitative real-time RT-PCR (qRT-PCR) and western blot were done to measure the expression levels of mRNA and protein, respectively. The flow cytometry was used to analyze the effect of c-Rel siRNA on the apoptosis and proliferation of Leukemia cells. Observed c-Rel expression in the 5 pre-B Acute lymphoblastic leukemia (ALL) patients were higher than the normal cells. The c-Rel siRNA transfection significantly blocked the expression of c-Rel mRNA in a time-dependent manner, leading to a strong growth inhibition and enhanced apoptosis (P<0.05). Our results demonstrated that c-Rel plays a fundamental role in the survival. Therefore, c-Rel can be considered as an attractive target for gene therapy in ALL patients. Also siRNA-mediated silencing of this gene may be a novel strategy in ALL treatment.
[Mh] Termos MeSH primário: Apoptose/fisiologia
Técnicas de Silenciamento de Genes/métodos
Leucemia-Linfoma Linfoblástico de Células Precursoras B/patologia
Proteínas Proto-Oncogênicas c-rel/antagonistas & inibidores
[Mh] Termos MeSH secundário: Adolescente
Western Blotting
Proliferação Celular/genética
Células Cultivadas
Criança
Pré-Escolar
Feminino
Citometria de Fluxo
Terapia Genética/métodos
Seres Humanos
Masculino
Proteínas Proto-Oncogênicas c-rel/genética
RNA Interferente Pequeno
Reação em Cadeia da Polimerase em Tempo Real
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins c-rel); 0 (RNA, Small Interfering)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170912
[St] Status:MEDLINE


  3 / 779 MEDLINE  
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[PMID]:28886380
[Au] Autor:Grinberg-Bleyer Y; Oh H; Desrichard A; Bhatt DM; Caron R; Chan TA; Schmid RM; Klein U; Hayden MS; Ghosh S
[Ad] Endereço:Department of Microbiology & Immunology, College of Physicians & Surgeons, Columbia University, New York, NY 10032, USA.
[Ti] Título:NF-κB c-Rel Is Crucial for the Regulatory T Cell Immune Checkpoint in Cancer.
[So] Source:Cell;170(6):1096-1108.e13, 2017 Sep 07.
[Is] ISSN:1097-4172
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Regulatory T cells (Tregs) play a pivotal role in the inhibition of anti-tumor immune responses. Understanding the mechanisms governing Treg homeostasis may therefore be important for development of effective tumor immunotherapy. We have recently demonstrated a key role for the canonical nuclear factor κB (NF-κB) subunits, p65 and c-Rel, in Treg identity and function. In this report, we show that NF-κB c-Rel ablation specifically impairs the generation and maintenance of the activated Treg (aTreg) subset, which is known to be enriched at sites of tumors. Using mouse models, we demonstrate that melanoma growth is drastically reduced in mice lacking c-Rel, but not p65, in Tregs. Moreover, chemical inhibition of c-Rel function delayed melanoma growth by impairing aTreg-mediated immunosuppression and potentiated the effects of anti-PD-1 immunotherapy. Our studies therefore establish inhibition of NF-κB c-Rel as a viable therapeutic approach for enhancing checkpoint-targeting immunotherapy protocols.
[Mh] Termos MeSH primário: Imunoterapia/métodos
Melanoma/imunologia
Melanoma/patologia
NF-kappa B/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-rel/antagonistas & inibidores
Linfócitos T Reguladores/imunologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Feminino
Masculino
Melanoma/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
NF-kappa B/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (Proto-Oncogene Proteins c-rel)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE


  4 / 779 MEDLINE  
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[PMID]:28842469
[Au] Autor:Fischer JC; Otten V; Kober M; Drees C; Rosenbaum M; Schmickl M; Heidegger S; Beyaert R; van Loo G; Li XC; Peschel C; Schmidt-Supprian M; Haas T; Spoerl S; Poeck H
[Ad] Endereço:Klinik und Poliklinik für Innere Medizin III, Klinikum rechts der Isar, Technische Universität, 81675 Munich, Germany.
[Ti] Título:A20 Restrains Thymic Regulatory T Cell Development.
[So] Source:J Immunol;199(7):2356-2365, 2017 Oct 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Maintaining immune tolerance requires the production of Foxp3-expressing regulatory T (T ) cells in the thymus. Activation of NF-κB transcription factors is critically required for T cell development, partly via initiating Foxp3 expression. NF-κB activation is controlled by a negative feedback regulation through the ubiquitin editing enzyme A20, which reduces proinflammatory signaling in myeloid cells and B cells. In naive CD4 T cells, A20 prevents kinase RIPK3-dependent necroptosis. Using mice deficient for A20 in T lineage cells, we show that thymic and peripheral T cell compartments are quantitatively enlarged because of a cell-intrinsic developmental advantage of A20-deficient thymic T differentiation. A20-deficient thymic T cells exhibit reduced dependence on IL-2 but unchanged rates of proliferation and apoptosis. Activation of the NF-κB transcription factor RelA was enhanced, whereas nuclear translocation of c-Rel was decreased in A20-deficient thymic T cells. Furthermore, we found that the increase in T cells in T cell-specific A20-deficient mice was already observed in CD4 single-positive CD25 GITR Foxp3 thymic T cell progenitors. T cell precursors expressed high levels of the tumor necrosis factor receptor superfamily molecule GITR, whose stimulation is closely linked to thymic T cell development. A20-deficient T cells efficiently suppressed effector T cell-mediated graft-versus-host disease after allogeneic hematopoietic stem cell transplantation, suggesting normal suppressive function. Holding thymic production of natural T cells in check, A20 thus integrates T cell activity and increased effector T cell survival into an efficient CD4 T cell response.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Linfócitos T Reguladores/fisiologia
Timo/citologia
Timo/fisiologia
Proteína 3 Induzida por Fator de Necrose Tumoral alfa/genética
Proteína 3 Induzida por Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose
Diferenciação Celular
Citometria de Fluxo
Fatores de Transcrição Forkhead/genética
Fatores de Transcrição Forkhead/metabolismo
Regulação da Expressão Gênica
Proteína Relacionada a TNFR Induzida por Glucocorticoide/genética
Doença Enxerto-Hospedeiro/prevenção & controle
Interleucina-2/imunologia
Ativação Linfocitária
Camundongos
NF-kappa B/metabolismo
Proteínas Proto-Oncogênicas c-rel/genética
Transdução de Sinais
Transplante de Células-Tronco
Timo/imunologia
Fator de Transcrição RelA/genética
Proteína 3 Induzida por Fator de Necrose Tumoral alfa/deficiência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Glucocorticoid-Induced TNFR-Related Protein); 0 (Interleukin-2); 0 (NF-kappa B); 0 (Proto-Oncogene Proteins c-rel); 0 (Rela protein, mouse); 0 (Tnfrsf18 protein, mouse); 0 (Transcription Factor RelA); EC 3.4.19.12 (Tumor Necrosis Factor alpha-Induced Protein 3); EC 3.4.22.- (Tnfaip3 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170827
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1602102


  5 / 779 MEDLINE  
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[PMID]:28667172
[Au] Autor:Subramanian L; Khan AA; Allu PKR; Kiranmayi M; Sahu BS; Sharma S; Khullar M; Mullasari AS; Mahapatra NR
[Ad] Endereço:From the Department of Biotechnology, Bhupat and Jyoti Mehta School of Biosciences, Indian Institute of Technology Madras, Chennai 600036.
[Ti] Título:A haplotype variant of the human chromogranin A gene ( ) promoter increases CHGA expression and the risk for cardiometabolic disorders.
[So] Source:J Biol Chem;292(34):13970-13985, 2017 Aug 25.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The acidic glycoprotein chromogranin A (CHGA) is co-stored/co-secreted with catecholamines and crucial for secretory vesicle biogenesis in neuronal/neuroendocrine cells. CHGA is dysregulated in several cardiovascular diseases, but the underlying mechanisms are not well established. Here, we sought to identify common polymorphisms in the promoter and to explore the mechanistic basis of their plausible contribution to regulating CHGA protein levels in circulation. Resequencing of the promoter in an Indian population ( = 769) yielded nine single-nucleotide polymorphisms (SNPs): G-1106A, A-1018T, T-1014C, T-988G, G-513A, G-462A, T-415C, C-89A, and C-57T. Linkage disequilibrium (LD) analysis indicated strong LD among SNPs at the -1014, -988, -462, and -89 bp positions and between the -1018 and -57 bp positions. Haplotype analysis predicted five major promoter haplotypes that displayed differential promoter activities in neuronal cells; specifically, haplotype 2 (containing variant T alleles at -1018 and -57 bp) exhibited the highest promoter activity. Systematic computational and experimental analyses revealed that transcription factor c-Rel has a role in activating the promoter haplotype 2 under basal and pathophysiological conditions ( inflammation and hypoxia). Consistent with the higher promoter activity of haplotype 2, individuals carrying this haplotype had higher plasma CHGA levels, plasma glucose levels, diastolic blood pressure, and body mass index. In conclusion, these results suggest a functional role of the promoter haplotype 2 (occurring in a large proportion of the world population) in enhancing CHGA expression in haplotype 2 carriers who may be at higher risk for cardiovascular/metabolic disorders.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/genética
Cromogranina A/genética
Regulação da Expressão Gênica
Transtornos do Metabolismo de Glucose/genética
Polimorfismo de Nucleotídeo Único
Regiões Promotoras Genéticas
Proteínas Proto-Oncogênicas c-rel/metabolismo
[Mh] Termos MeSH secundário: Alelos
Doenças Cardiovasculares/sangue
Doenças Cardiovasculares/metabolismo
Linhagem Celular Tumoral
Imunoprecipitação da Cromatina
Cromogranina A/sangue
Cromogranina A/metabolismo
Biologia Computacional
Ensaio de Desvio de Mobilidade Eletroforética
Frequência do Gene
Estudos de Associação Genética
Predisposição Genética para Doença
Transtornos do Metabolismo de Glucose/sangue
Transtornos do Metabolismo de Glucose/metabolismo
Seres Humanos
Índia
Desequilíbrio de Ligação
Mutagênese Sítio-Dirigida
Mutação
Proteínas Proto-Oncogênicas c-rel/genética
Proteínas Recombinantes/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CHGA protein, human); 0 (Chromogranin A); 0 (HIVEN86A protein, human); 0 (Proto-Oncogene Proteins c-rel); 0 (Recombinant Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170702
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.778134


  6 / 779 MEDLINE  
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[PMID]:28652399
[Au] Autor:Schuster M; Plaza-Sirvent C; Matthies AM; Heise U; Jeron A; Bruder D; Visekruna A; Huehn J; Schmitz I
[Ad] Endereço:Systems-Oriented Immunology and Inflammation Research Group, Helmholtz Centre for Infection Research, 38124 Braunschweig, Germany.
[Ti] Título:c-REL and IκB Govern Common and Independent Steps of Regulatory T Cell Development from Novel CD122-Expressing Pre-Precursors.
[So] Source:J Immunol;199(3):920-930, 2017 Aug 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Foxp3-expressing regulatory T cells (Tregs) are essential regulators of immune homeostasis and, thus, are prime targets for therapeutic interventions of diseases such as cancer and autoimmunity. c-REL and IκB are important regulators of Foxp3 induction in Treg precursors upon γ-chain cytokine stimulation. In c-REL/IκB double-deficient mice, Treg numbers were dramatically reduced, indicating that together, c-REL and IκB are pivotal for Treg development. However, despite the highly reduced Treg compartment, double-deficient mice did not develop autoimmunity even when aged to more than 1 y, suggesting that c-REL and IκB are required for T cell effector function as well. Analyzing Treg development in more detail, we identified a CD122 subset within the CD25 Foxp3 precursor population, which gave rise to classical CD25 Foxp3 Treg precursors. Importantly, c-REL, but not IκB , controlled the generation of classical CD25 Foxp3 precursors via direct binding to the locus. Thus, we propose that CD4 GITR CD122 CD25 Foxp3 cells represent a Treg pre-precursor population, whose transition into Treg precursors is mediated via c-REL.
[Mh] Termos MeSH primário: Diferenciação Celular
Fatores de Transcrição Forkhead/metabolismo
Inibidor de NF-kappaB alfa/metabolismo
Proteínas Proto-Oncogênicas c-rel/metabolismo
Linfócitos T Reguladores/fisiologia
[Mh] Termos MeSH secundário: Animais
Autoimunidade
Fatores de Transcrição Forkhead/genética
Regulação da Expressão Gênica
Subunidade alfa de Receptor de Interleucina-2/imunologia
Subunidade alfa de Receptor de Interleucina-2/metabolismo
Subunidade beta de Receptor de Interleucina-2/genética
Subunidade beta de Receptor de Interleucina-2/imunologia
Camundongos
Inibidor de NF-kappaB alfa/deficiência
Inibidor de NF-kappaB alfa/genética
Ligação Proteica
Proteínas Proto-Oncogênicas c-rel/deficiência
Proteínas Proto-Oncogênicas c-rel/genética
Subpopulações de Linfócitos T/imunologia
Linfócitos T Reguladores/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Il2ra protein, mouse); 0 (Il2rb protein, mouse); 0 (Interleukin-2 Receptor alpha Subunit); 0 (Interleukin-2 Receptor beta Subunit); 0 (Proto-Oncogene Proteins c-rel); 139874-52-5 (NF-KappaB Inhibitor alpha)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170628
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1600877


  7 / 779 MEDLINE  
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[PMID]:28615451
[Au] Autor:Asatryan A; Bazan NG
[Ad] Endereço:From the Neuroscience Center of Excellence, School of Medicine, Louisiana State University Health New Orleans, New Orleans, Louisiana 70112-2223.
[Ti] Título:Molecular mechanisms of signaling via the docosanoid neuroprotectin D1 for cellular homeostasis and neuroprotection.
[So] Source:J Biol Chem;292(30):12390-12397, 2017 Jul 28.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Docosahexaenoic acid, enriched in the brain and retina, generates docosanoids in response to disruptions of cellular homeostasis. Docosanoids include neuroprotectin D1 (NPD1), which is decreased in the CA1 hippocampal area of patients with early-stage Alzheimer's disease (AD). We summarize here how NPD1 elicits neuroprotection by up-regulating c-REL, a nuclear factor (NF)-κB subtype that, in turn, enhances expression of BIRC3 (baculoviral inhibitor of apoptosis repeat-containing protein 3) in the retina and in experimental stroke, leading to neuroprotection. Elucidating the mechanisms of action of docosanoids will contribute to managing diseases, including stroke, AD, age-related macular degeneration, traumatic brain injury, Parkinson's disease, and other neurodegenerations.
[Mh] Termos MeSH primário: Ácidos Docosa-Hexaenoicos/metabolismo
Homeostase
Neuroproteção
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Proteínas Proto-Oncogênicas c-rel/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins c-rel); 0 (protectin D1); 25167-62-8 (Docosahexaenoic Acids)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170616
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.R117.783076


  8 / 779 MEDLINE  
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[PMID]:28328949
[Au] Autor:Lipert B; Wilamowski M; Gorecki A; Jura J
[Ad] Endereço:Jagiellonian University, Faculty of Biochemistry, Biophysics and Biotechnology, Department of General Biochemistry, Krakow, Poland.
[Ti] Título:MCPIP1, alias Regnase-1 binds and cleaves mRNA of C/EBPß.
[So] Source:PLoS One;12(3):e0174381, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CCAAT/enhancer-binding protein beta (C/EBPß) is a transcription factor controlling a broad range of genes essential for homeostasis, including genes related to immune functions, inflammation, metabolism and growth. Monocyte chemoattractant protein-1-induced protein 1 (MCPIP1) also called as Regnase-1 is an RNase and has been shown to decrease the stability of short-lived transcripts coding for inflammation-related proteins, including IL-1ß, IL-6, IL-2, IL-8, IL-12b, IER-3, c-Rel. We found previously that the half-life of the C/EBPß transcript is regulated by MCPIP. To understand the mechanism driving down-regulation of C/EBPß by MCPIP1, we applied an in vitro cleavage assay, followed by a luciferase-reporter assay and RNA immunoprecipitation (RIP). We demonstrated that MCPIP1 recognizes regions of the 3'UTR of C/EBPß mRNA and promotes its decay by introducing direct endonucleolytic cleavage.
[Mh] Termos MeSH primário: Proteína beta Intensificadora de Ligação a CCAAT/metabolismo
RNA Mensageiro/metabolismo
Ribonucleases/metabolismo
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas/genética
Proteínas Reguladoras de Apoptose/metabolismo
Linhagem Celular Tumoral
Regulação para Baixo/genética
Células Hep G2
Seres Humanos
Imunoprecipitação/métodos
Interleucina-12/metabolismo
Interleucina-1beta/metabolismo
Interleucina-2/metabolismo
Interleucina-6/metabolismo
Interleucina-8/metabolismo
Proteínas de Membrana/metabolismo
Proteínas Proto-Oncogênicas c-rel/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Apoptosis Regulatory Proteins); 0 (CCAAT-Enhancer-Binding Protein-beta); 0 (IER3 protein, human); 0 (Interleukin-1beta); 0 (Interleukin-2); 0 (Interleukin-6); 0 (Interleukin-8); 0 (Membrane Proteins); 0 (Proto-Oncogene Proteins c-rel); 0 (RNA, Messenger); 0 (Transcription Factors); 187348-17-0 (Interleukin-12); EC 3.1.- (Ribonucleases); EC 3.1.- (ZC3H12A protein, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170822
[Lr] Data última revisão:
170822
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170323
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0174381


  9 / 779 MEDLINE  
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[PMID]:28259870
[Au] Autor:Sekiya Y; Yamamoto E; Niimi K; Nishino K; Nakamura K; Kotani T; Kajiyama H; Shibata K; Kikkawa F
[Ad] Endereço:Department of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
[Ti] Título:c-Rel Promotes Invasion of Choriocarcinoma Cells via PI3K/AKT Signaling.
[So] Source:Oncology;92(5):299-310, 2017.
[Is] ISSN:1423-0232
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Choriocarcinoma is the most common epithelial cancer among gestational trophoblastic diseases (GTDs); the mechanism of trophoblastic carcinogenesis is unknown. This study aimed to examine the expression of NF-κB family proteins in GTDs and placental tissues as well as the roles of c-Rel in choriocarcinoma. METHODS: We examined the expression of NF-κB family proteins in normal placenta and hydatidiform mole tissues as well as extravillous trophoblast (EVT) and choriocarcinoma cell lines by Western blot and immunohistochemistry. Immunoprecipitation was performed to determine which proteins can bind with c-Rel in choriocarcinoma cells. To investigate the roles of c-Rel in choriocarcinoma, we examined the effects of c-Rel knockdown and overexpression on cell proliferation, migration, and invasion using small interfering RNAs and gene activation plasmid. RESULTS: The expression of c-Rel was strong in choriocarcinoma and EVTs, but very weak in villi of normal placenta and hydatidiform mole. Immunoprecipitation suggested that c-Rel heterodimerizes with p65 in choriocarcinoma. c-Rel knockdown reduced invasion, migration, and AKT phosphorylation in choriocarcinoma cells. c-Rel overexpression in choriocarcinoma increased migratory and invasive abilities, and the effect on invasion was inhibited by a PI3K inhibitor. CONCLUSION: These findings suggest that c-Rel might play a role in promoting the invasion of choriocarcinoma cells through PI3K/AKT signaling.
[Mh] Termos MeSH primário: Coriocarcinoma/metabolismo
Coriocarcinoma/patologia
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Proteínas Proto-Oncogênicas c-rel/metabolismo
Neoplasias Uterinas/metabolismo
Neoplasias Uterinas/patologia
[Mh] Termos MeSH secundário: Linhagem Celular
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Mola Hidatiforme/metabolismo
Mola Hidatiforme/patologia
Imuno-Histoquímica
NF-kappa B/metabolismo
Gravidez
Transdução de Sinais
Trofoblastos/metabolismo
Trofoblastos/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B); 0 (Proto-Oncogene Proteins c-rel); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170616
[Lr] Data última revisão:
170616
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170306
[St] Status:MEDLINE
[do] DOI:10.1159/000458529


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[PMID]:28090796
[Au] Autor:Fallahi S; Mohammadi SM; Tayefi Nasrabadi H; Alihemmati A; Samadi N; Gholami S; Shanehbandi D; Nozad Charoudeh H
[Ad] Endereço:a Stem Cell Research Center, Tabriz University of Medical Sciences , Tabriz , Iran.
[Ti] Título:Impact of C-rel inhibition of cord blood-derived B-, T-, and NK cells.
[So] Source:J Immunotoxicol;14(1):15-22, 2017 Dec.
[Is] ISSN:1547-6901
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The c-Rel transcription factor is a unique member of the nuclear factor (NF)-κB family that has a role in curtailing the proliferation, differentiation, cytokine production, and overall activity of B- and T-cells. In addition, c-Rel is a key regulator of apoptosis in that it influences the expression of anti-apoptotic genes such as Bcl-2 and Bcl-xL; conversely, inhibition of c-Rel increases cell apoptosis. To better understand the relationship between c-Rel expression and effects on B- and T-cell expansion, the current study evaluated c-Rel expression in cord blood mononuclear cells. This particular source was selected as cord blood is an important source of cells used for transplantation and immunotherapy, primarily in treating leukemias. As stem cell factor (SCF) and FLT3 are important agents for hematopoietic stem cell expansion, and cytokines like interleukin (IL)-2, -7, and -15 are essential for T- and B- (and also NK) cell development and proliferation, the current study evaluated c-Rel expression in cord blood mononuclear cells and CD34 cells, as well as effects on B-, T-, and NK cells associated with alterations in c-Rel expression, using flow cytometry and PCR. The results showed c-Rel expression increased among cells cultured in the presence of SCF and FLT3 but was reduced when IL-2, IL-7, and IL-15 were used all together. Further, inhibition of c-Rel expression by siRNA reduced cord blood-derived B-, T-, and NK cell differentiation and expansion. These results indicated that with cells isolated from cord blood, c-Rel has an important role in B-, T-, and NK cell differentiation and, further, that agents (select cytokines/growth factors) that could impact on its expression might not only affect immune cell profiles in a host but could potentially also limit apoptotic activities in (non-)immune cells in that host. In the context of cancer (immuno)therapy, in particular, when cord blood is used an important source in stem cell transplantation in leukemia patients, such down-regulating changes in c-Rel levels could be counter-productive.
[Mh] Termos MeSH primário: Linfócitos B/imunologia
Transplante de Células-Tronco Hematopoéticas
Imunoterapia/métodos
Células Matadoras Naturais/imunologia
Leucemia/terapia
Proteínas Proto-Oncogênicas c-rel/metabolismo
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Apoptose
Linfócitos B/transplante
Diferenciação Celular
Proliferação Celular
Células Cultivadas
Citocinas/metabolismo
Sangue Fetal/citologia
Seres Humanos
Células Matadoras Naturais/transplante
Leucemia/imunologia
Proteínas Proto-Oncogênicas c-rel/genética
RNA Interferente Pequeno/genética
Fator de Células-Tronco/metabolismo
Linfócitos T/transplante
Ativação Transcricional
Tirosina Quinase 3 Semelhante a fms/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Proto-Oncogene Proteins c-rel); 0 (RNA, Small Interfering); 0 (Stem Cell Factor); EC 2.7.10.1 (FLT3 protein, human); EC 2.7.10.1 (fms-Like Tyrosine Kinase 3)
[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:170117
[St] Status:MEDLINE
[do] DOI:10.1080/1547691X.2016.1250849



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