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  1 / 109 MEDLINE  
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[PMID]:28511095
[Au] Autor:Cho S; Jung SE; Hong SR; Lee EH; Lee JH; Lee SD; Lee HY
[Ad] Endereço:Institute of Forensic Science, Seoul National University College of Medicine, Seoul, Korea.
[Ti] Título:Independent validation of DNA-based approaches for age prediction in blood.
[So] Source:Forensic Sci Int Genet;29:250-256, 2017 Jul.
[Is] ISSN:1878-0326
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Numerous molecular biomarkers have been proposed as predictors of chronological age. Among them, T-cell specific DNA rearrangement and DNA methylation markers have been introduced as forensic age predictors in blood because of their high prediction accuracy. These markers appear highly promising, but for better application to forensic casework sample analysis the proposed markers and genotyping methods must be tested further. In the current study, signal-joint T-cell receptor excision circles (sjTRECs) and DNA methylation markers located in the ELOVL2, C1orf132, TRIM59, KLF14, and FHL2 genes were reanalyzed in 100 Korean blood samples to test their associations with chronological age, using the same analysis platform used in previous reports. Our study replicated the age association test for sjTREC and DNA methylation markers in the 5 genes in an independent validation set of 100 Koreans, and proved that the age predictive performance of the previous models is relatively consistent across different population groups. However, the extent of age association at certain CpG loci was not identical in the Korean and Polish populations; therefore, several age predictive models were retrained with the data obtained here. All of the 3 models retrained with DNA methylation and/or sjTREC data have a CpG site each from the ELOVL2 and FHL2 genes in common, and produced better prediction accuracy than previously reported models. This is attributable to the fact that the retrained model better fits the existing data and that the calculated prediction accuracy could be higher when the training data and the test data are the same. However, it is notable that the combination of different types of markers, i.e., sjTREC and DNA methylation, improved prediction accuracy in the eldest group. Our study demonstrates the usefulness of the proposed markers and the genotyping method in an independent dataset, and suggests the possibility of combining different types of DNA markers to improve prediction accuracy.
[Mh] Termos MeSH primário: Envelhecimento/genética
Metilação de DNA
Marcadores Genéticos
Receptores de Antígenos de Linfócitos T/sangue
[Mh] Termos MeSH secundário: Acetiltransferases/genética
Grupo com Ancestrais do Continente Asiático/genética
Ilhas de CpG/genética
Técnicas de Genotipagem
Seres Humanos
Proteínas com Homeodomínio LIM/genética
Proteínas de Membrana/genética
Metaloproteínas/genética
Proteínas Musculares/genética
Receptores de Antígenos de Linfócitos T/genética
República da Coreia
Fatores de Transcrição Sp/genética
Fatores de Transcrição/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (FHL2 protein, human); 0 (Genetic Markers); 0 (KLF14 protein, human); 0 (LIM-Homeodomain Proteins); 0 (Membrane Proteins); 0 (Metalloproteins); 0 (Muscle Proteins); 0 (Receptors, Antigen, T-Cell); 0 (Sp Transcription Factors); 0 (TRIM59 protein, human); 0 (Transcription Factors); EC 2.3.1.- (Acetyltransferases); EC 2.3.1.- (fatty acid elongases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170707
[Lr] Data última revisão:
170707
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170517
[St] Status:MEDLINE


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[PMID]:28366734
[Au] Autor:Kim CK; He P; Bialkowska AB; Yang VW
[Ad] Endereço:Department of Medicine, Stony Brook University School of Medicine, Stony Brook, New York.
[Ti] Título:SP and KLF Transcription Factors in Digestive Physiology and Diseases.
[So] Source:Gastroenterology;152(8):1845-1875, 2017 Jun.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Specificity proteins (SPs) and Krüppel-like factors (KLFs) belong to the family of transcription factors that contain conserved zinc finger domains involved in binding to target DNA sequences. Many of these proteins are expressed in different tissues and have distinct tissue-specific activities and functions. Studies have shown that SPs and KLFs regulate not only physiological processes such as growth, development, differentiation, proliferation, and embryogenesis, but pathogenesis of many diseases, including cancer and inflammatory disorders. Consistently, these proteins have been shown to regulate normal functions and pathobiology in the digestive system. We review recent findings on the tissue- and organ-specific functions of SPs and KLFs in the digestive system including the oral cavity, esophagus, stomach, small and large intestines, pancreas, and liver. We provide a list of agents under development to target these proteins.
[Mh] Termos MeSH primário: Doenças do Sistema Digestório/metabolismo
Sistema Digestório/metabolismo
Fatores de Transcrição Kruppel-Like/metabolismo
Fatores de Transcrição Sp/metabolismo
[Mh] Termos MeSH secundário: Animais
Sistema Digestório/patologia
Sistema Digestório/fisiopatologia
Doenças do Sistema Digestório/genética
Doenças do Sistema Digestório/patologia
Doenças do Sistema Digestório/fisiopatologia
Regulação da Expressão Gênica
Seres Humanos
Fatores de Transcrição Kruppel-Like/genética
Transdução de Sinais
Fatores de Transcrição Sp/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Kruppel-Like Transcription Factors); 0 (Sp Transcription Factors)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170404
[St] Status:MEDLINE


  3 / 109 MEDLINE  
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[PMID]:28275049
[Au] Autor:Jin UH; Cheng Y; Zhou B; Safe S
[Ad] Endereço:Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, Texas.
[Ti] Título:Bardoxolone Methyl and a Related Triterpenoid Downregulate cMyc Expression in Leukemia Cells.
[So] Source:Mol Pharmacol;91(5):438-450, 2017 May.
[Is] ISSN:1521-0111
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Structurally related pentacyclic triterpenoids methyl 2-cyano-3,12-dioxoolean-1,9-dien-28-oate [bardoxolone-methyl (Bar-Me)] and methyl 2-trifluoromethyl-3,11-dioxoolean-1,12-dien-30-oate (CF DODA-Me) contain 2-cyano-1-en-3-one and 2-trifluoromethyl-1-en-3-one moieties, respectively, in their A-rings and differ in the position of their en-one structures in ring C. Only Bar-Me forms a Michael addition adduct with glutathione (GSH) and inhibits IKK phosphorylation. These differences may be due to steric hindrance by the 11-keto group in CF DODA-Me, which prevents Michael addition by the conjugated en-one in the A-ring. In contrast, both Bar-Me and CF DODA-Me induce reactive oxygen species in HL-60 and Jurkat leukemia cells, inhibit cell growth, induce apoptosis and differentiation, and decrease expression of specificity proteins (Sp) 1, 3, and 4, and cMyc, and these effects are significantly attenuated after cotreatment with the antioxidant GSH. In contrast to solid tumor-derived cells, cMyc and Sp transcriptions are regulated independently and cMyc plays a more predominant role than Sp transcription factors in regulating HL-60 or Jurkat cell proliferation and differentiation compared with that observed in cells derived from solid tumors.
[Mh] Termos MeSH primário: Regulação para Baixo/efeitos dos fármacos
Leucemia/patologia
Ácido Oleanólico/análogos & derivados
Proteínas Proto-Oncogênicas c-myc/metabolismo
Triterpenos/farmacologia
[Mh] Termos MeSH secundário: Antineoplásicos/farmacologia
Morte Celular/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Proliferação Celular/efeitos dos fármacos
Glutationa/metabolismo
Seres Humanos
Quinase I-kappa B
Ácido Oleanólico/química
Ácido Oleanólico/farmacologia
Fosforilação/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-akt/metabolismo
Espécies Reativas de Oxigênio/metabolismo
Fatores de Transcrição Sp/metabolismo
Serina-Treonina Quinases TOR/metabolismo
Triterpenos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Proto-Oncogene Proteins c-myc); 0 (Reactive Oxygen Species); 0 (Sp Transcription Factors); 0 (Triterpenes); 6SMK8R7TGJ (Oleanolic Acid); CEG1Q6OGU1 (methyl 2-cyano-3,12-dioxoolean-1,9-dien-28-oate); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.10 (I-kappa B Kinase); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170509
[Lr] Data última revisão:
170509
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE
[do] DOI:10.1124/mol.116.106245


  4 / 109 MEDLINE  
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[PMID]:27811009
[Au] Autor:Hedrick E; Li X; Safe S
[Ad] Endereço:Department of Veterinary Physiology & Pharmacology, Texas A&M University, College Station, Texas.
[Ti] Título:Penfluridol Represses Integrin Expression in Breast Cancer through Induction of Reactive Oxygen Species and Downregulation of Sp Transcription Factors.
[So] Source:Mol Cancer Ther;16(1):205-216, 2017 Jan.
[Is] ISSN:1538-8514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It was recently demonstrated the penfluridol inhibited breast tumor growth and metastasis and this was associated with downregulation of α6- and ß4-integrins. In this study, we observed the penfluridol induced reactive oxygen species (ROS) and this was the primary mechanism of action. Penfluridol-mediated growth inhibition, induction of apoptosis, and inhibition of breast cancer cell migration was attenuated after cotreatment with glutathione. Penfluridol also downregulated Sp transcription factors Sp1, Sp3, and Sp4 through epigenetic downregulation of cMyc and cMyc-regulated miRNAs (miR27a and miR20a/miR17) and induction of the miR-regulated Sp transcriptional repressors ZBTB10 and ZBTB4. α6- and ß4-integrins as well as α5- and ß1-integrins are Sp-regulated genes that are also coregulated by the orphan nuclear receptor NR4A1 and these integrins can be targeted by agents such as penfluridol that suppress Sp1, Sp3, and Sp4 and also by NR4A1 antagonists. Mol Cancer Ther; 16(1); 205-16. ©2016 AACR.
[Mh] Termos MeSH primário: Neoplasias da Mama/genética
Neoplasias da Mama/metabolismo
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Integrinas/genética
Penfluridol/farmacologia
Espécies Reativas de Oxigênio/metabolismo
Fatores de Transcrição Sp/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Modelos Animais de Doenças
Feminino
Genes myc
Seres Humanos
MicroRNAs/genética
Membro 1 do Grupo A da Subfamília 4 de Receptores Nucleares/metabolismo
Ligação Proteica
Transdução de Sinais/efeitos dos fármacos
Ensaios Antitumorais Modelo de Xenoenxerto
Dedos de Zinco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrins); 0 (MicroRNAs); 0 (NR4A1 protein, human); 0 (Nuclear Receptor Subfamily 4, Group A, Member 1); 0 (Reactive Oxygen Species); 0 (Sp Transcription Factors); 25TLU22Q8H (Penfluridol)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161105
[St] Status:MEDLINE
[do] DOI:10.1158/1535-7163.MCT-16-0451


  5 / 109 MEDLINE  
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[PMID]:27697431
[Au] Autor:Suske G
[Ad] Endereço:Institute of Molecular Biology and Tumor Research (IMT), Philipps-University Marburg, Emil-Mannkopff-Str. 2, D-35032-Marburg, Germany. Electronic address: Suske@imt.uni-marburg.de.
[Ti] Título:NF-Y and SP transcription factors - New insights in a long-standing liaison.
[So] Source:Biochim Biophys Acta;1860(5):590-597, 2017 05.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:For long it has been recognized that CCAAT boxes and GC-rich elements co-occur in many human and murine promoters within 100bp upstream of the transcription start site. The trimeric transcription factor NF-Y is the major CCAAT box-binding factor, and members of the SP family of transcription factors are the major GC box-binding proteins. Recent chromatin immunoprecipitations coupled with high throughput sequencing (ChIP-seq) have examined binding of NF-Y and the ubiquitous SP factors SP1, SP2 and SP3 genome-wide, allowing for comprehensive comparison of NF-Y and SP factor actions in the context of chromatin. Here, I attempt a synthesis of the earlier single-promoter type of analysis with the more recent genome-wide studies. In particular, I also discuss different modes of genomic interactions between SP factors and NF-Y that have emerged recently, and identify a key technical issue, which needs to be taken into account in a critical evaluation of genome-wide studies. This article is part of a Special Issue entitled: Nuclear Factor Y in Development and Disease, edited by Prof. Roberto Mantovani.
[Mh] Termos MeSH primário: Fator de Ligação a CCAAT/metabolismo
Elementos de Resposta/fisiologia
Fatores de Transcrição Sp/metabolismo
[Mh] Termos MeSH secundário: Animais
Fator de Ligação a CCAAT/genética
Imunoprecipitação da Cromatina
Estudo de Associação Genômica Ampla
Seres Humanos
Camundongos
Fatores de Transcrição Sp/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (CCAAT-Binding Factor); 0 (Sp Transcription Factors)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170814
[Lr] Data última revisão:
170814
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161005
[St] Status:MEDLINE


  6 / 109 MEDLINE  
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[PMID]:27875298
[Au] Autor:Kasiappan R; Jutooru I; Karki K; Hedrick E; Safe S
[Ad] Endereço:From the Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, Texas 77843-4466.
[Ti] Título:Benzyl Isothiocyanate (BITC) Induces Reactive Oxygen Species-dependent Repression of STAT3 Protein by Down-regulation of Specificity Proteins in Pancreatic Cancer.
[So] Source:J Biol Chem;291(53):27122-27133, 2016 12 30.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The antineoplastic agent benzyl isothiocyanate (BITC) acts by targeting multiple pro-oncogenic pathways/genes, including signal transducer and activator of transcription 3 (STAT3); however, the mechanism of action is not well known. As reported previously, BITC induced reactive oxygen species (ROS) in Panc1, MiaPaCa2, and L3.6pL pancreatic cancer cells. This was accompanied by induction of apoptosis and inhibition of cell growth and migration, and these responses were attenuated in cells cotreated with BITC plus glutathione (GSH). BITC also decreased expression of specificity proteins (Sp) Sp1, Sp3, and Sp4 transcription factors (TFs) and several pro-oncogenic Sp-regulated genes, including STAT3 and phospho-STAT3 (pSTAT3), and GSH attenuated these responses. Knockdown of Sp TFs by RNA interference also decreased STAT3/pSTAT3 expression. BITC-induced ROS activated a cascade of events that included down-regulation of c-Myc, and it was also demonstrated that c-Myc knockdown decreased expression of Sp TFs and STAT3 These results demonstrate that in pancreatic cancer cells, STAT3 is an Sp-regulated gene that can be targeted by BITC and other ROS inducers, thereby identifying a novel therapeutic approach for targeting STAT3.
[Mh] Termos MeSH primário: Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Isotiocianatos/farmacologia
Neoplasias Pancreáticas/tratamento farmacológico
Espécies Reativas de Oxigênio/metabolismo
Fator de Transcrição STAT3/antagonistas & inibidores
Fatores de Transcrição Sp/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Antineoplásicos/farmacologia
Apoptose/efeitos dos fármacos
Western Blotting
Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Seres Humanos
Camundongos
Camundongos Nus
Neoplasias Pancreáticas/metabolismo
Neoplasias Pancreáticas/patologia
RNA Mensageiro/genética
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fator de Transcrição STAT3/genética
Fator de Transcrição STAT3/metabolismo
Fator de Transcrição STAT3/uso terapêutico
Fatores de Transcrição Sp/genética
Fatores de Transcrição Sp/metabolismo
Células Tumorais Cultivadas
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Isothiocyanates); 0 (RNA, Messenger); 0 (Reactive Oxygen Species); 0 (STAT3 Transcription Factor); 0 (STAT3 protein, human); 0 (Sp Transcription Factors); 871J6YOR8Q (benzyl isothiocyanate)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161123
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.746339


  7 / 109 MEDLINE  
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[PMID]:27384261
[Au] Autor:Safe S; Kasiappan R
[Ad] Endereço:Department of Veterinary Physiology and Pharmacology, Texas A&M University, College Station, TX, 77843-4466, USA. ssafe@cvm.tamu.edu.
[Ti] Título:Natural Products as Mechanism-based Anticancer Agents: Sp Transcription Factors as Targets.
[So] Source:Phytother Res;30(11):1723-1732, 2016 Nov.
[Is] ISSN:1099-1573
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Naturally occurring anticancer agents and their derivatives act on multiple pathways to inhibit carcinogenesis and their inhibition of migration, invasion, growth, survival, and metastasis is associated with downregulation of genes associated with these responses. Several phytochemical-derived anticancer drugs including curcumin, betulinic acid, phenethylisothiocyanate and celastrol, and many others induce reactive oxygen species, and their effects on gene regulation show some overlap in various cancer cell lines. We hypothesize that reactive oxygen species-inducing anticancer agents and many other natural products target a common pathway in cancer cells, which initially involves downregulation of specificity protein 1 (Sp1), Sp3, and Sp4, which are highly expressed in tumors/cell lines derived from solid tumors. This hypothesis is supported by several published reports showing that a large number of phytochemical-derived anticancer agents downregulate Sp1, Sp3, Sp4, and pro-oncogenic Sp-regulated genes involved in cell growth (cyclin D1 and growth factor receptors), survival (bcl-2 and survivin), angiogenesis and migration (MMP-9, vascular endothelial growth factor and its receptors), and inflammation (NF-kB). The contribution of this pathway to the anticancer activity of drugs such as curcumin, celastrol, betulinic acid, and phenethylisothiocyanate must be determined in order to optimize clinical applications of drug combinations containing these compounds. Copyright © 2016 John Wiley & Sons, Ltd.
[Mh] Termos MeSH primário: Antineoplásicos/química
Produtos Biológicos/química
Fatores de Transcrição Sp/metabolismo
[Mh] Termos MeSH secundário: Antineoplásicos/farmacologia
Produtos Biológicos/farmacologia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Biological Products); 0 (Sp Transcription Factors)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160708
[St] Status:MEDLINE
[do] DOI:10.1002/ptr.5669


  8 / 109 MEDLINE  
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[PMID]:27265324
[Au] Autor:Boot A; Oosting J; de Miranda NF; Zhang Y; Corver WE; van de Water B; Morreau H; van Wezel T
[Ad] Endereço:Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands.
[Ti] Título:Imprinted survival genes preclude loss of heterozygosity of chromosome 7 in cancer cells.
[So] Source:J Pathol;240(1):72-83, 2016 09.
[Is] ISSN:1096-9896
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The genomes of a wide range of cancers, including colon, breast, and thyroid cancers, frequently show copy number gains of chromosome 7 and rarely show loss of heterozygosity. The molecular basis for this phenomenon is unknown. Strikingly, oncocytic follicular thyroid carcinomas can display an extreme genomic profile, with homozygosity of all chromosomes except for chromosome 7. The observation that homozygosity of chromosome 7 is never observed suggests that retention of heterozygosity is essential for cells. We hypothesized that cell survival genes are genetically imprinted on either of two copies of chromosome 7, which thwarts loss of heterozygosity at this chromosome in cancer cells. By employing a DNA methylation screen and gene expression analysis, we identified six imprinted genes that force retention of heterozygosity on chromosome 7. Subsequent knockdown of gene expression showed that CALCR, COPG2, GRB10, KLF14, MEST, and PEG10 were essential for cancer cell survival, resulting in reduced cell proliferation, G1 -phase arrest, and increased apoptosis. We propose that imprinted cell survival genes provide a genetic basis for retention of chromosome 7 heterozygosity in cancer cells. The monoallelically expressed cell survival genes identified in this study, and the cellular pathways that they are involved in, offer new therapeutic targets for the treatment of tumours showing retention of heterozygosity on chromosome 7. Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
[Mh] Termos MeSH primário: Carcinoma Medular/genética
Sobrevivência Celular/genética
Cromossomos Humanos Par 7
Regulação Neoplásica da Expressão Gênica
Impressão Genômica
Perda de Heterozigosidade
Neoplasias da Glândula Tireoide/genética
[Mh] Termos MeSH secundário: Proteína Semelhante a Receptor de Calcitonina/genética
Carcinoma Medular/patologia
Proliferação Celular/genética
Proteína Coatomer/genética
Metilação de DNA
Proteína Adaptadora GRB10/genética
Seres Humanos
Proteínas/genética
Fatores de Transcrição Sp/genética
Glândula Tireoide/patologia
Neoplasias da Glândula Tireoide/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CALCRL protein, human); 0 (COPG2 protein, human); 0 (Calcitonin Receptor-Like Protein); 0 (Coatomer Protein); 0 (KLF14 protein, human); 0 (PEG10 protein, human); 0 (Proteins); 0 (Sp Transcription Factors); 0 (mesoderm specific transcript protein); 151441-47-3 (GRB10 Adaptor Protein)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160607
[St] Status:MEDLINE
[do] DOI:10.1002/path.4756


  9 / 109 MEDLINE  
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[PMID]:27060138
[Au] Autor:Thakur BK; Dasgupta N; Ta A; Das S
[Ad] Endereço:Division of Clinical Medicine, National Institute of Cholera and Enteric Diseases, P-33, CIT Road, Scheme XM, Beliaghata, Kolkata 700010, India.
[Ti] Título:Physiological TLR5 expression in the intestine is regulated by differential DNA binding of Sp1/Sp3 through simultaneous Sp1 dephosphorylation and Sp3 phosphorylation by two different PKC isoforms.
[So] Source:Nucleic Acids Res;44(12):5658-72, 2016 Jul 08.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Toll-like receptor 5 (TLR5) expression in the intestinal epithelial cells (IECs) is critical to maintain health, as underscored by multiple intestinal and extra-intestinal diseases in mice genetically engineered for IEC-specific TLR5 knockout. A gradient of expression exists in the colonic epithelial cells from the cecum to the distal colon. Intriguingly, an identical gradient for the dietary metabolite, butyrate also exists in the luminal contents. However, both being critical for intestinal homeostasis and immune response, no studies examined the role of butyrate in the regulation of TLR5 expression. We showed that butyrate transcriptionally upregulates TLR5 in the IECs and augments flagellin-induced immune responses. Both basal and butyrate-induced transcription is regulated by differential binding of Sp-family transcription factors to the GC-box sequences over the TLR5 promoter. Butyrate activates two different protein kinase C isoforms to dephosphorylate/acetylate Sp1 by serine/threonine phosphatases and phosphorylate Sp3 by ERK-MAPK, respectively. This resulted in Sp1 displacement from the promoter and binding of Sp3 to it, leading to p300 recruitment and histone acetylation, activating transcription. This is the first study addressing the mechanisms of physiological TLR5 expression in the intestine. Additionally, a novel insight is gained into Sp1/Sp3-mediated gene regulation that may apply to other genes.
[Mh] Termos MeSH primário: Imunidade Celular/genética
Fatores de Transcrição Sp/genética
Fator de Transcrição Sp3/genética
Receptor 5 Toll-Like/biossíntese
[Mh] Termos MeSH secundário: Acetilação/efeitos dos fármacos
Animais
Butiratos/farmacologia
MAP Quinases Reguladas por Sinal Extracelular/genética
Flagelina/farmacologia
Regulação da Expressão Gênica/genética
Histonas/metabolismo
Seres Humanos
Imunidade Celular/efeitos dos fármacos
Mucosa Intestinal/metabolismo
Camundongos
Camundongos Knockout
Regiões Promotoras Genéticas
Ligação Proteica/genética
Fatores de Transcrição Sp/metabolismo
Fator de Transcrição Sp3/metabolismo
Receptor 5 Toll-Like/genética
Fatores de Transcrição de p300-CBP/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Butyrates); 0 (Histones); 0 (Sp Transcription Factors); 0 (Sp3 protein, mouse); 0 (Toll-Like Receptor 5); 12777-81-0 (Flagellin); 148710-94-5 (Sp3 Transcription Factor); EC 2.3.1.48 (p300-CBP Transcription Factors); EC 2.3.1.48 (p300-CBP-associated factor); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170613
[Lr] Data última revisão:
170613
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160410
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkw189


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[PMID]:26927145
[Au] Autor:Gao K; Wang J; Li L; Zhai Y; Ren Y; You H; Wang B; Wu X; Li J; Liu Z; Li X; Huang Y; Luo XP; Hu D; Ohno K; Wang C
[Ad] Endereço:Department of Preventive Medicine, School of Medicine, Shenzhen University, Shenzhen 518060, China. gao_kp@szu.edu.cn.
[Ti] Título:Polymorphisms in Four Genes (KCNQ1 rs151290, KLF14 rs972283, GCKR rs780094 and MTNR1B rs10830963) and Their Correlation with Type 2 Diabetes Mellitus in Han Chinese in Henan Province, China.
[So] Source:Int J Environ Res Public Health;13(3), 2016 Feb 26.
[Is] ISSN:1660-4601
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Genetic variants at KCNQ1 rs151290, KLF14 rs972283, GCKR rs780094 and MTNR1B rs10830963 have been associated with type 2 diabetes mellitus (T2DM), but the results are contradictory in Chinese populations. The aim of the present study was to investigate the association of these four SNPs with T2DM in a large population of Han Chinese at Henan province, China. Seven-hundred-thirty-six patients with T2DM (cases) and Seven-hundred-sixty-eight healthy glucose-tolerant controls were genotyped for KCNQ1 rs151290, KLF14 rs972283, GCKR rs780094 and MTNR1B rs10830963. The association of genetic variants in these four genes with T2DM was analyzed using multivariate logistic regression. Genotypes and allele distributions of KCNQ1 rs151290 were significantly different between the cases and controls (p < 0.05). The AC and CC genotypes and the combined AC + CC genotype of rs151290 in KCNQ1 were associated with increases risk of T2DM before (OR = 1.482, 95% CI = 1.062-2.069; p = 0.021; OR = 1.544, 95% CI = 1.097-2.172, p = 0.013; and OR = 1.509, 95% CI = 1.097-2.077, p = 0.011, respectively) and after (OR = 1.539, 95% CI = 1.015-2.332, p = 0.042; OR = 1.641, 95% CI = 1.070-2.516, p = 0.023; and OR = 1.582, 95% CI = 1.061-2.358, p = 0.024; respectively) adjustment for sex, age, anthropometric measurements, biochemical indexes, smoking and alcohol consumption. Consistent with results of genotype analysis, the C allele of rs151290 in KCNQ1 was also associated with increased risk of T2DM (OR = 1.166, 95% CI = 1.004-1.355, p = 0.045). No associations between genetic variants of KLF14 rs972283, GCKR rs780094 or MTNR1B rs10830963 and T2DM were detected. The AC and CC genotypes and the C allele of rs151290 in KCNQ1 may be risk factors for T2DM in Han Chinese in Henan province.
[Mh] Termos MeSH primário: Diabetes Mellitus Tipo 2/genética
Predisposição Genética para Doença/epidemiologia
Polimorfismo de Nucleotídeo Único/genética
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal
Idoso
Grupo com Ancestrais do Continente Asiático/genética
China/epidemiologia
Diabetes Mellitus Tipo 2/epidemiologia
Feminino
Variação Genética
Genótipo
Seres Humanos
Canal de Potássio KCNQ1
Masculino
Meia-Idade
Receptor MT2 de Melatonina
Fatores de Transcrição Sp
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (GCKR protein, human); 0 (KCNQ1 Potassium Channel); 0 (KCNQ1 protein, human); 0 (KLF14 protein, human); 0 (MTNR1B protein, human); 0 (Receptor, Melatonin, MT2); 0 (Sp Transcription Factors)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160302
[St] Status:MEDLINE



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