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Pesquisa : D12.776.260.725 [Categoria DeCS]
Referências encontradas : 3676 [refinar]
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[PMID]:29382818
[Au] Autor:Sánchez-Iranzo H; Galardi-Castilla M; Minguillón C; Sanz-Morejón A; González-Rosa JM; Felker A; Ernst A; Guzmán-Martínez G; Mosimann C; Mercader N
[Ad] Endereço:Development of the Epicardium and Its Role during Regeneration Group, Centro Nacional de Investigaciones Cardiovasculares (CNIC-ISCIII), Melchor Fernández Almagro 3, 28029, Madrid, Spain.
[Ti] Título:Tbx5a lineage tracing shows cardiomyocyte plasticity during zebrafish heart regeneration.
[So] Source:Nat Commun;9(1):428, 2018 01 30.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:During development, mesodermal progenitors from the first heart field (FHF) form a primitive cardiac tube, to which progenitors from the second heart field (SHF) are added. The contribution of FHF and SHF progenitors to the adult zebrafish heart has not been studied to date. Here we find, using genetic tbx5a lineage tracing tools, that the ventricular myocardium in the adult zebrafish is mainly derived from tbx5a cells, with a small contribution from tbx5a SHF progenitors. Notably, ablation of ventricular tbx5a -derived cardiomyocytes in the embryo is compensated by expansion of SHF-derived cells. In the adult, tbx5a expression is restricted to the trabeculae and excluded from the outer cortical layer. tbx5a-lineage tracing revealed that trabecular cardiomyocytes can switch their fate and differentiate into cortical myocardium during adult heart regeneration. We conclude that a high degree of cardiomyocyte cell fate plasticity contributes to efficient regeneration.
[Mh] Termos MeSH primário: Ventrículos do Coração/citologia
Miocárdio/citologia
Miócitos Cardíacos/citologia
Regeneração/genética
Proteínas com Domínio T-Box/genética
Peixe-Zebra/genética
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Diferenciação Celular
Linhagem da Célula/genética
Rastreamento de Células
Embrião não Mamífero
Regulação da Expressão Gênica no Desenvolvimento
Genes Reporter
Proteínas de Fluorescência Verde/genética
Proteínas de Fluorescência Verde/metabolismo
Ventrículos do Coração/crescimento & desenvolvimento
Ventrículos do Coração/metabolismo
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Miocárdio/metabolismo
Miócitos Cardíacos/metabolismo
Cadeias Leves de Miosina/genética
Cadeias Leves de Miosina/metabolismo
Organogênese/genética
Células-Tronco/citologia
Células-Tronco/metabolismo
Proteínas com Domínio T-Box/deficiência
Peixe-Zebra/crescimento & desenvolvimento
Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Luminescent Proteins); 0 (Myosin Light Chains); 0 (T-Box Domain Proteins); 0 (T-box transcription factor 5); 0 (red fluorescent protein); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02650-6


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[PMID]:28466692
[Au] Autor:Shimbo T; Dunnick JK; Brix A; Mav D; Shah R; Roberts JD; Wade PA
[Ad] Endereço:1 Epigenetics and Stem Cell Biology Laboratory, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA.
[Ti] Título:DNA Methylation Changes in Tbx3 in a Mouse Model Exposed to Polybrominated Diphenyl Ethers.
[So] Source:Int J Toxicol;36(3):229-238, 2017 May/Jun.
[Is] ISSN:1092-874X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:DE-71, a commercial mixture of polybrominated diphenyl ethers widely used in flame retardants, is a pervasive environmental contaminant due to its continuing release from waste material and its long half-life in humans. Although the genotoxic potential of DE-71 appears to be low based on bacterial mutagenicity, it remains a public health concern due to its reported involvement in tumor development. Molecular mechanisms by which DE-71 influences tumor incidence or progression remain understudied. We used liver carcinoma tissue from mice exposed to DE-71 to test the hypothesis that epigenetic alterations consistent with tumor development, specifically DNA methylation, result from long-term DE-71 exposure. We profiled DNA methylation status using the methylated-CpG island recovery assay coupled with microarray analysis of hepatocellular carcinoma DNA from animals exposed to DE-71. DE-71 exposure had little impact on global DNA methylation. However, we detected gene body-specific hypomethylation within the Tbx3 locus, a transcription factor important in liver tumorigenesis and in embryonic and cancer stem cell proliferation. This nonpromoter hypomethylation was accompanied by upregulation of Tbx3 mRNA and protein and by alterations in downstream cell cycle-associated marker expression. Thus, exposure to DE-71 may facilitate tumor development by inducing epigenetic programs that favor expansion of progenitor cell populations.
[Mh] Termos MeSH primário: Metilação de DNA/efeitos dos fármacos
Retardadores de Chama/toxicidade
Éteres Difenil Halogenados/toxicidade
Proteínas com Domínio T-Box/genética
[Mh] Termos MeSH secundário: Animais
Fígado/efeitos dos fármacos
Fígado/metabolismo
Fígado/patologia
Masculino
Camundongos
Proteínas com Domínio T-Box/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Flame Retardants); 0 (Halogenated Diphenyl Ethers); 0 (T-Box Domain Proteins); 0 (Tbx3 protein, mouse); 7REL09ZX35 (pentabromodiphenyl ether)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1177/1091581817706676


  3 / 3676 MEDLINE  
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[PMID]:29180489
[Au] Autor:Kaminuma O; Kitamura N; Nishito Y; Nemoto S; Tatsumi H; Mori A; Hiroi T
[Ad] Endereço:Allergy and Immunology Project, The Tokyo Metropolitan Institute of Medical Science, Tokyo 113-8613, Japan; osamuk@yamanashi.ac.jp.
[Ti] Título:Downregulation of NFAT3 Due to Lack of T-Box Transcription Factor TBX5 Is Crucial for Cytokine Expression in T Cells.
[So] Source:J Immunol;200(1):92-100, 2018 01 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The NFAT family transcription factors play crucial roles in immunological and other biological activities. NFAT3 is rarely expressed in T cells, and the mechanisms and significance of the specific NFAT3 downregulation in T cells have been unknown. In human CD4 T cells, overexpression of NFAT1 and NFAT3 enhanced and suppressed IL-2 expression, respectively. NFAT3 downregulation in Jurkat cells using RNA interference technology augmented IL-2 expression, whereas a knockdown of NFAT1, NFAT2, and NFAT4 suppressed it. The promoter/enhancer activity of the NFAT-binding site in the gene was upregulated and downregulated by NFAT1 and NFAT3, respectively. A study employing NFAT1/NFAT3 chimeric molecules revealed that the region in NFAT3 responsible for NFAT promoter activity inhibition was located within its N-terminal transactivation domain, Ca -regulatory domain, and DNA-binding domain. Downregulation of NFAT3 expression in T cells is mediated by lower chromatin accessibility and enhancer activity in its promoter in comparison with aortic smooth muscle cells expressing endogenous NFAT3. The binding sites of T-box transcription factor TBX5 and NK-2 transcription factor-related locus 5 Nkx2.5, which were expressed at higher levels in aortic smooth muscle cells than in T cells, were located within the -387 to +97 NFAT3 promoter region, exhibiting the maximum enhancer activity. Mutating the binding site of TBX5 but not Nkx2.5 diminished the NFAT3 promoter activity, whereas the overexpression of TBX5 enhanced it. Introduction of TBX5 into CD4 T cells enhanced the expression of NFAT3 and suppressed that of IL-2. TBX5 deficiency-mediated downregulation of NFAT3 is crucial for the high cytokine-producing activity of T cells.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Citocinas/metabolismo
Miócitos de Músculo Liso/fisiologia
Fatores de Transcrição NFATC/metabolismo
Proteínas com Domínio T-Box/metabolismo
[Mh] Termos MeSH secundário: Aorta/patologia
Células Cultivadas
Montagem e Desmontagem da Cromatina
Citocinas/genética
Regulação da Expressão Gênica
Proteína Homeobox Nkx-2.5/genética
Proteína Homeobox Nkx-2.5/metabolismo
Seres Humanos
Interleucina-2/genética
Interleucina-2/metabolismo
Fatores de Transcrição NFATC/genética
Regiões Promotoras Genéticas/genética
Ligação Proteica
Engenharia de Proteínas
Proteínas com Domínio T-Box/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (Homeobox Protein Nkx-2.5); 0 (Interleukin-2); 0 (NFATC Transcription Factors); 0 (NKX2-5 protein, human); 0 (T-Box Domain Proteins); 0 (T-box transcription factor 5)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1602113


  4 / 3676 MEDLINE  
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[PMID]:28461570
[Au] Autor:Bongiorno EK; Garcia SA; Sauma S; Hooper DC
[Ad] Endereço:Department of Cancer Biology, Thomas Jefferson University, Philadelphia, PA 19107; and.
[Ti] Título:Type 1 Immune Mechanisms Driven by the Response to Infection with Attenuated Rabies Virus Result in Changes in the Immune Bias of the Tumor Microenvironment and Necrosis of Mouse GL261 Brain Tumors.
[So] Source:J Immunol;198(11):4513-4523, 2017 06 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Immunotherapeutic strategies for malignant glioma have to overcome the immunomodulatory activities of M2 monocytes that appear in the circulation and as tumor-associated macrophages (TAMs). M2 cell products contribute to the growth-promoting attributes of the tumor microenvironment (TME) and bias immunity toward type 2, away from the type 1 mechanisms with antitumor properties. To drive type 1 immunity in CNS tissues, we infected GL261 tumor-bearing mice with attenuated rabies virus (RABV). These neurotropic viruses spread to CNS tissues -axonally, where they induce a strong type 1 immune response that involves Th1, CD8, and B cell entry across the blood-brain barrier and virus clearance in the absence of overt sequelae. Intranasal infection with attenuated RABV prolonged the survival of mice bearing established GL261 brain tumors. Despite the failure of virus spread to the tumor, infection resulted in significantly enhanced tumor necrosis, extensive CD4 T cell accumulation, and high levels of the proinflammatory factors IFN-γ, TNF-α, and inducible NO synthase in the TME merely 4 d postinfection, before significant virus spread or the appearance of RABV-specific immune mechanisms in CNS tissues. Although the majority of infiltrating CD4 cells appeared functionally inactive, the proinflammatory changes in the TME later resulted in the loss of accumulating M2 and increased M1 TAMs. Mice deficient in the Th1 transcription factor T-bet did not gain any survival advantage from RABV infection, exhibiting only limited tumor necrosis and no change in TME cytokines or TAM phenotype and highlighting the importance of type 1 mechanisms in this process.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/imunologia
Neoplasias Encefálicas/patologia
Encéfalo/virologia
Vírus da Raiva/imunologia
Microambiente Tumoral/imunologia
[Mh] Termos MeSH secundário: Animais
Linfócitos B/imunologia
Barreira Hematoencefálica/imunologia
Barreira Hematoencefálica/patologia
Barreira Hematoencefálica/virologia
Encéfalo/imunologia
Neoplasias Encefálicas/virologia
Linfócitos T CD4-Positivos
Citocinas/imunologia
Modelos Animais de Doenças
Feminino
Interferon gama/biossíntese
Interferon gama/imunologia
Camundongos
Necrose/virologia
Óxido Nítrico Sintase Tipo II/biossíntese
Óxido Nítrico Sintase Tipo II/metabolismo
Vírus da Raiva/genética
Vírus da Raiva/fisiologia
Proteínas com Domínio T-Box/deficiência
Proteínas com Domínio T-Box/metabolismo
Células Th2/imunologia
Fator de Necrose Tumoral alfa/biossíntese
Fator de Necrose Tumoral alfa/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Cytokines); 0 (T-Box Domain Proteins); 0 (T-box transcription factor TBX21); 0 (Tumor Necrosis Factor-alpha); 82115-62-6 (Interferon-gamma); EC 1.14.13.39 (Nitric Oxide Synthase Type II)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601444


  5 / 3676 MEDLINE  
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[PMID]:28455436
[Au] Autor:Singh R; Miao T; Symonds ALJ; Omodho B; Li S; Wang P
[Ad] Endereço:The Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, United Kingdom; and.
[Ti] Título:Egr2 and 3 Inhibit T-bet-Mediated IFN-γ Production in T Cells.
[So] Source:J Immunol;198(11):4394-4402, 2017 06 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:T-bet is important for differentiation of cytotoxic CD8 and Th1 CD4 T cells. We have discovered that Egr2 and 3 are potent inhibitors of T-bet function in CD4 and CD8 effector T cells. Egr2 and 3 were essential to suppress Th1 differentiation in Th2 and Th17 conditions in vitro and also to control IFN-γ-producing CD4 and CD8 T cells in response to virus infection. Together with Egr2 and 3, T-bet is induced in naive T cells by Ag stimulation, but Egr2 and 3 expression was inhibited by Th1-inducing cytokines. We found that Egr2 and 3 physically interact with the T-box domain of T-bet, blocking T-bet DNA binding and inhibiting T-bet-mediated production of IFN-γ. Thus, Egr2 and 3 are antagonists of T-bet function in effector T cells and are important for the control of inflammatory responses of T cells.
[Mh] Termos MeSH primário: Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD8-Positivos/imunologia
Proteína 2 de Resposta de Crescimento Precoce/metabolismo
Proteína 3 de Resposta de Crescimento Precoce/metabolismo
Interferon gama/biossíntese
Proteínas com Domínio T-Box/metabolismo
[Mh] Termos MeSH secundário: Animais
Linfócitos T CD4-Positivos/metabolismo
Linfócitos T CD8-Positivos/metabolismo
Citocinas/farmacologia
Proteína 2 de Resposta de Crescimento Precoce/antagonistas & inibidores
Proteína 2 de Resposta de Crescimento Precoce/genética
Proteína 3 de Resposta de Crescimento Precoce/antagonistas & inibidores
Proteína 3 de Resposta de Crescimento Precoce/genética
Interferon gama/imunologia
Camundongos
Células Th1/imunologia
Células Th1/fisiologia
Células Th17/imunologia
Células Th17/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (Early Growth Response Protein 2); 0 (Egr2 protein, mouse); 0 (Egr3 protein, mouse); 0 (T-Box Domain Proteins); 0 (T-box transcription factor TBX21); 144516-98-3 (Early Growth Response Protein 3); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180127
[Lr] Data última revisão:
180127
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1602010


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[PMID]:28457482
[Au] Autor:Frasca D; Diaz A; Romero M; D'Eramo F; Blomberg BB
[Ad] Endereço:Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL 33101, USA. Electronic address: dfrasca@med.miami.edu.
[Ti] Título:Aging effects on T-bet expression in human B cell subsets.
[So] Source:Cell Immunol;321:68-73, 2017 Nov.
[Is] ISSN:1090-2163
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:In order to compare human and mouse B cell subset markers, we evaluated T-bet expression in human B cell subsets from individuals of different ages. We found T-bet expressed in unstimulated memory more than naïve B cells, and more in young individuals. TLR7 stimulation up-regulated T-bet in all B cell subsets from young and elderly individuals, and more in the elderly. By fold-increase the best effect was seen in subsets of the elderly and especially in those that undergo class switch (naïve and IgM). We also evaluated CD11c expression, as T-bet+CD11c+ B cells are expanded in healthy elderly individuals and also in patients with autoimmunity. Similar to T-bet, CD11c expression was higher in memory than in naïve B cells, but no differences were observed between young and elderly individuals. After TLR7 stimulation, CD11c increases in all B cell subsets (especially in naïve and IgM) from the elderly.
[Mh] Termos MeSH primário: Envelhecimento
Subpopulações de Linfócitos B/metabolismo
Linfócitos B/metabolismo
Proteínas com Domínio T-Box/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Antígeno CD11c/metabolismo
Células Cultivadas
Feminino
Citometria de Fluxo
Seres Humanos
Imidazóis/farmacologia
Masculino
Meia-Idade
Receptor 7 Toll-Like/agonistas
Receptor 7 Toll-Like/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CD11c Antigen); 0 (Imidazoles); 0 (T-Box Domain Proteins); 0 (T-box transcription factor TBX21); 0 (TLR7 protein, human); 0 (Toll-Like Receptor 7); V3DMU7PVXF (resiquimod)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171227
[Lr] Data última revisão:
171227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


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[PMID]:29262349
[Au] Autor:Fu B; Zhou Y; Ni X; Tong X; Xu X; Dong Z; Sun R; Tian Z; Wei H
[Ad] Endereço:Institute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, School of Life Science and Medical Center, University of Science and Technology of China, Hefei, Anhui 230001, China; Hefei National Laboratory for Physical Sciences at Microscale, University of Science and Te
[Ti] Título:Natural Killer Cells Promote Fetal Development through the Secretion of Growth-Promoting Factors.
[So] Source:Immunity;47(6):1100-1113.e6, 2017 Dec 19.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Natural killer (NK) cells are present in large populations at the maternal-fetal interface during early pregnancy. However, the role of NK cells in fetal growth is unclear. Here, we have identified a CD49a Eomes subset of NK cells that secreted growth-promoting factors (GPFs), including pleiotrophin and osteoglycin, in both humans and mice. The crosstalk between HLA-G and ILT2 served as a stimulus for GPF-secreting function of this NK cell subset. Decreases in this GPF-secreting NK cell subset impaired fetal development, resulting in fetal growth restriction. The transcription factor Nfil3, but not T-bet, affected the function and the number of this decidual NK cell subset. Adoptive transfer of induced CD49a Eomes NK cells reversed impaired fetal growth and rebuilt an appropriate local microenvironment. These findings reveal properties of NK cells in promoting fetal growth. In addition, this research proposes approaches for therapeutic administration of NK cells in order to reverse restricted nourishments within the uterine microenvironment during early pregnancy.
[Mh] Termos MeSH primário: Aborto Habitual/imunologia
Transferência Adotiva
Proteínas de Transporte/secreção
Citocinas/secreção
Desenvolvimento Fetal/imunologia
Retardo do Crescimento Fetal/prevenção & controle
Peptídeos e Proteínas de Sinalização Intercelular/secreção
Células Matadoras Naturais/transplante
[Mh] Termos MeSH secundário: Aborto Habitual/genética
Aborto Habitual/patologia
Adulto
Animais
Antígenos CD/genética
Antígenos CD/imunologia
Fatores de Transcrição de Zíper de Leucina Básica/genética
Fatores de Transcrição de Zíper de Leucina Básica/imunologia
Proteínas de Transporte/genética
Proteínas de Transporte/imunologia
Microambiente Celular
Citocinas/genética
Citocinas/imunologia
Decídua/imunologia
Decídua/patologia
Feminino
Retardo do Crescimento Fetal/genética
Retardo do Crescimento Fetal/imunologia
Retardo do Crescimento Fetal/patologia
Feto
Regulação da Expressão Gênica no Desenvolvimento
Antígenos HLA-G/genética
Antígenos HLA-G/imunologia
Seres Humanos
Integrina alfa1/genética
Integrina alfa1/imunologia
Peptídeos e Proteínas de Sinalização Intercelular/genética
Peptídeos e Proteínas de Sinalização Intercelular/imunologia
Células Matadoras Naturais/citologia
Células Matadoras Naturais/imunologia
Receptor B1 de Leucócitos Semelhante a Imunoglobulina/genética
Receptor B1 de Leucócitos Semelhante a Imunoglobulina/imunologia
Camundongos
Camundongos Endogâmicos C57BL
Gravidez
Transdução de Sinais
Proteínas com Domínio T-Box/genética
Proteínas com Domínio T-Box/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Basic-Leucine Zipper Transcription Factors); 0 (Carrier Proteins); 0 (Cytokines); 0 (EOMES protein, human); 0 (HLA-G Antigens); 0 (Integrin alpha1); 0 (Intercellular Signaling Peptides and Proteins); 0 (LILRB1 protein, human); 0 (Leukocyte Immunoglobulin-like Receptor B1); 0 (NFIL3 protein, human); 0 (OGN protein, human); 0 (T-Box Domain Proteins); 0 (T-box transcription factor TBX21); 134034-50-7 (pleiotrophin)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171221
[St] Status:MEDLINE


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[PMID]:28740134
[Au] Autor:Zhang Y; Qin W; Lu X; Xu J; Huang H; Bai H; Li S; Lin S
[Ad] Endereço:Laboratory of Chemical Genomics, School of Chemical Biology and Biotechnology, Peking University Shenzhen Graduate School, Shenzhen, 518055, China.
[Ti] Título:Programmable base editing of zebrafish genome using a modified CRISPR-Cas9 system.
[So] Source:Nat Commun;8(1):118, 2017 07 25.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Precise genetic modifications in model animals are essential for biomedical research. Here, we report a programmable "base editing" system to induce precise base conversion with high efficiency in zebrafish. Using cytidine deaminase fused to Cas9 nickase, up to 28% of site-specific single-base mutations are achieved in multiple gene loci. In addition, an engineered Cas9-VQR variant with 5'-NGA PAM specificities is used to induce base conversion in zebrafish. This shows that Cas9 variants can be used to expand the utility of this technology. Collectively, the targeted base editing system represents a strategy for precise and effective genome editing in zebrafish.The use of base editing enables precise genetic modifications in model animals. Here the authors show high efficient single-base editing in zebrafish using modified Cas9 and its VQR variant with an altered PAM specificity.
[Mh] Termos MeSH primário: Sistemas CRISPR-Cas/genética
Edição de Genes/métodos
Mutagênese Sítio-Dirigida/métodos
Peixe-Zebra/genética
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Sequência de Bases
Proteínas Fetais/genética
Engenharia Genética/métodos
Fator 6 de Diferenciação de Crescimento/genética
Mutação Puntual
Reprodutibilidade dos Testes
Homologia de Sequência de Aminoácidos
Homologia de Sequência do Ácido Nucleico
Proteínas com Domínio T-Box/genética
Proteínas de Peixe-Zebra/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 (Brachyury protein); 0 (Fetal Proteins); 0 (Growth Differentiation Factor 6); 0 (T-Box Domain Proteins); 0 (Zebrafish Proteins); 0 (gdf6a protein, zebrafish)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-00175-6


  9 / 3676 MEDLINE  
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[PMID]:28981677
[Au] Autor:Wu HC; Yang HI; Wang Q; Chen CJ; Santella RM
[Ad] Endereço:Department of Environmental Health Sciences, Mailman School of Public Health of Columbia University, New York, NY 10032, USA.
[Ti] Título:Plasma DNA methylation marker and hepatocellular carcinoma risk prediction model for the general population.
[So] Source:Carcinogenesis;38(10):1021-1028, 2017 Oct 01.
[Is] ISSN:1460-2180
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Metastases in the later stages of hepatocellular carcinoma (HCC) cause the majority of deaths associated with the disease, making early detection crucial to patient survival. Risk models assessing HCC risk in the general population can be used for risk stratification for further HCC surveillance, however, none have been validated externally. Methylation of circulating DNA shows potential for non-invasive diagnosis of HCC. We conducted a prospective case-control study nested within a community-based cohort. We measured methylation levels in six genes (CDKN2A, RASSF1A, STEAP4, TBX2, VIM and ZNF154) which were identified in our previous work, using pre-diagnostic plasma DNA from 237 HCC cases and 257 matched controls. We found TBX2 hypermethylation was associated with increased HCC risk, with ORs (95% CI) of 3.2 (1.8-6.0). The associations were mainly among high-risk subjects; among subjects infected with HBV/HCV, the OR (95% CI) of TBX2 methylation was 5.3 (2.2-12.7). Among subjects with high risk scores, the ORs (95% CIs) were 7.8 (1.5-38.6) for Wen-HCC model ≥16, 5.8 (2.2-15.5) for Hung-HCC ≥15 and 7.5 (2.2-26.0) for Michikawa-HCC ≥8. Adding TBX2 methylation improved the accuracy of risk models for a high-risk population, with the area under the curve (AUC) of 76% for Wen-HCC score with TBX2 methylation compared with 69% with Wen-HCC alone. The AUCs were 63% for Hung-HCC score plus TBX2 methylation, and 53% for Hung-HCC alone, 65% for Michikawa-HCC score plus TBX2 methylation and 58% for Michikawa-HCC alone. Our findings suggest the potential increase in risk assessment discrimination and accuracy from incorporation of DNA methylation.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/genética
Metilação de DNA
Neoplasias Hepáticas/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Área Sob a Curva
Biomarcadores Tumorais/genética
Carcinoma Hepatocelular/sangue
Carcinoma Hepatocelular/patologia
Estudos de Casos e Controles
Inibidor de Quinase Dependente de Ciclina p18/genética
Feminino
Seres Humanos
Fatores de Transcrição Kruppel-Like/genética
Neoplasias Hepáticas/sangue
Neoplasias Hepáticas/patologia
Masculino
Proteínas de Membrana/genética
Meia-Idade
Oxirredutases/genética
Fatores de Risco
Proteínas com Domínio T-Box/genética
Proteínas Supressoras de Tumor/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CDKN2A protein, human); 0 (Cyclin-Dependent Kinase Inhibitor p18); 0 (Kruppel-Like Transcription Factors); 0 (Membrane Proteins); 0 (RASSF1 protein, human); 0 (T-Box Domain Protein 2); 0 (T-Box Domain Proteins); 0 (Tumor Suppressor Proteins); 0 (ZNF154 protein, human); EC 1.- (Oxidoreductases); EC 1.16.1.- (STEAP4 protein, human)
[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:171006
[St] Status:MEDLINE
[do] DOI:10.1093/carcin/bgx078


  10 / 3676 MEDLINE  
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[PMID]:28953967
[Au] Autor:Obeng-Adjei N; Portugal S; Holla P; Li S; Sohn H; Ambegaonkar A; Skinner J; Bowyer G; Doumbo OK; Traore B; Pierce SK; Crompton PD
[Ad] Endereço:Malaria Infection Biology and Immunity Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland, United States of America.
[Ti] Título:Malaria-induced interferon-γ drives the expansion of Tbethi atypical memory B cells.
[So] Source:PLoS Pathog;13(9):e1006576, 2017 Sep.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Many chronic infections, including malaria and HIV, are associated with a large expansion of CD21-CD27- 'atypical' memory B cells (MBCs) that exhibit reduced B cell receptor (BCR) signaling and effector functions. Little is known about the conditions or transcriptional regulators driving atypical MBC differentiation. Here we show that atypical MBCs in malaria-exposed individuals highly express the transcription factor T-bet, and that T-bet expression correlates inversely with BCR signaling and skews toward IgG3 class switching. Moreover, a longitudinal analysis of a subset of children suggested a correlation between the incidence of febrile malaria and the expansion of T-bethi B cells. The Th1-cytokine containing supernatants of malaria-stimulated PBMCs plus BCR cross linking induced T-bet expression in naïve B cells that was abrogated by neutralizing IFN-γ or blocking the IFN-γ receptor on B cells. Accordingly, recombinant IFN-γ plus BCR cross-linking drove T-bet expression in peripheral and tonsillar B cells. Consistent with this, Th1-polarized Tfh (Tfh-1) cells more efficiently induced T-bet expression in naïve B cells. These data provide new insight into the mechanisms underlying atypical MBC differentiation.
[Mh] Termos MeSH primário: Linfócitos B/citologia
Linfócitos B/imunologia
Diferenciação Celular/imunologia
Regulação da Expressão Gênica/imunologia
Memória Imunológica/imunologia
Interferon gama/biossíntese
Malária/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Criança
Pré-Escolar
Feminino
Proteínas Fetais/metabolismo
Seres Humanos
Lactente
Malária/metabolismo
Masculino
Receptores de Antígenos de Linfócitos B/metabolismo
Proteínas com Domínio T-Box/metabolismo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Brachyury protein); 0 (Fetal Proteins); 0 (Receptors, Antigen, B-Cell); 0 (T-Box Domain Proteins); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006576



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