Base de dados : MEDLINE
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[PMID]:28235042
[Au] Autor:McFadden VC; Shalaby RE; Iram S; Oropeza CE; Landolfi JA; Lyubimov AV; Maienschein-Cline M; Green SJ; Kaestner KH; McLachlan A
[Ad] Endereço:Department of Microbiology and Immunology College of Medicine University of Illinois at Chicago 909 South Wolcott Avenue Chicago, IL, United States of America.
[Ti] Título:Hepatic deficiency of the pioneer transcription factor FoxA restricts hepatitis B virus biosynthesis by the developmental regulation of viral DNA methylation.
[So] Source:PLoS Pathog;13(2):e1006239, 2017 Feb.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The FoxA family of pioneer transcription factors regulates hepatitis B virus (HBV) transcription, and hence viral replication. Hepatocyte-specific FoxA-deficiency in the HBV transgenic mouse model of chronic infection prevents the transcription of the viral DNA genome as a result of the failure of the developmentally controlled conversion of 5-methylcytosine residues to cytosine during postnatal hepatic maturation. These observations suggest that pioneer transcription factors such as FoxA, which mark genes for expression at subsequent developmental steps in the cellular differentiation program, mediate their effects by reversing the DNA methylation status of their target genes to permit their ensuing expression when the appropriate tissue-specific transcription factor combinations arise during development. Furthermore, as the FoxA-deficient HBV transgenic mice are viable, the specific developmental timing, abundance and isoform type of pioneer factor expression must permit all essential liver gene expression to occur at a level sufficient to support adequate liver function. This implies that pioneer transcription factors can recognize and mark their target genes in distinct developmental manners dependent upon, at least in part, the concentration and affinity of FoxA for its binding sites within enhancer and promoter regulatory sequence elements. This selective marking of cellular genes for expression by the FoxA pioneer factor compared to HBV may offer the opportunity for the specific silencing of HBV gene expression and hence the resolution of chronic HBV infections which are responsible for approximately one million deaths worldwide annually due to liver cirrhosis and hepatocellular carcinoma.
[Mh] Termos MeSH primário: DNA Viral/metabolismo
Regulação Viral da Expressão Gênica/fisiologia
Vírus da Hepatite B/fisiologia
Hepatite B Crônica/virologia
Fatores Nucleares de Hepatócito/deficiência
[Mh] Termos MeSH secundário: Animais
Metilação de DNA/fisiologia
Modelos Animais de Doenças
Hepatite B Crônica/genética
Fígado/metabolismo
Fígado/virologia
Camundongos
Camundongos Transgênicos
Reação em Cadeia da Polimerase
Fatores de Transcrição/metabolismo
Replicação Viral/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Viral); 0 (Hepatocyte Nuclear Factors); 0 (Transcription Factors)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170803
[Lr] Data última revisão:
170803
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170225
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006239


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[PMID]:27610013
[Au] Autor:Kim DH; Kang HS; Kim KH
[Ad] Endereço:Doo Hyun Kim, Hong Seok Kang, Kyun-Hwan Kim, Department of Pharmacology, and Center for Cancer Research and Diagnostic Medicine, IBST, School of Medicine, Konkuk University, Seoul 143-701, South Korea.
[Ti] Título:Roles of hepatocyte nuclear factors in hepatitis B virus infection.
[So] Source:World J Gastroenterol;22(31):7017-29, 2016 Aug 21.
[Is] ISSN:2219-2840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Approximately 350 million people are estimated to be persistently infected with hepatitis B virus (HBV) worldwide. HBV maintains persistent infection by employing covalently closed circular DNA (cccDNA), a template for all HBV RNAs. Chronic hepatitis B (CHB) patients are currently treated with nucleos(t)ide analogs such as lamivudine, adefovir, entecavir, and tenofovir. However, these treatments rarely cure CHB because they are unable to inhibit cccDNA transcription and inhibit only a late stage in the HBV life cycle (the reverse transcription step in the nucleocapsid). Therefore, an understanding of the factors regulating cccDNA transcription is required to stop this process. Among numerous factors, hepatocyte nuclear factors (HNFs) play the most important roles in cccDNA transcription, especially in the generation of viral genomic RNA, a template for HBV replication. Therefore, proper control of HNF function could lead to the inhibition of HBV replication. In this review, we summarize and discuss the current understanding of the roles of HNFs in the HBV life cycle and the upstream factors that regulate HNFs. This knowledge will enable the identification of new therapeutic targets to cure CHB.
[Mh] Termos MeSH primário: Hepatite B Crônica/etiologia
Fatores Nucleares de Hepatócito/fisiologia
[Mh] Termos MeSH secundário: Proteínas Estimuladoras de Ligação a CCAAT/fisiologia
DNA Circular/fisiologia
Elementos Facilitadores Genéticos
Regulação Viral da Expressão Gênica
Vírus da Hepatite B/genética
Vírus da Hepatite B/fisiologia
Seres Humanos
MicroRNAs/fisiologia
Fatores de Transcrição/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (CCAAT-Enhancer-Binding Proteins); 0 (DNA, Circular); 0 (Hepatocyte Nuclear Factors); 0 (MicroRNAs); 0 (Transcription Factors)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170419
[Lr] Data última revisão:
170419
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160910
[St] Status:MEDLINE
[do] DOI:10.3748/wjg.v22.i31.7017


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[PMID]:27561454
[Au] Autor:De Mattia E; Cecchin E; Roncato R; Toffoli G
[Ad] Endereço:Experimental & Clinical Pharmacology, Centro di Riferimento Oncologico- National Cancer Institute, Aviano, Italy.
[Ti] Título:Pregnane X receptor, constitutive androstane receptor and hepatocyte nuclear factors as emerging players in cancer precision medicine.
[So] Source:Pharmacogenomics;17(14):1547-71, 2016 Sep.
[Is] ISSN:1744-8042
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Great research effort has been focused on elucidating the contribution of host genetic variability on pharmacological outcomes in cancer. Nuclear receptors have emerged as mediators between environmental stimuli and drug pharmacokinetics and pharmacodynamics. The pregnane X receptor, constitutive androstane receptor and hepatocyte nuclear factors have been reported to regulate transcription of genes that encode drug metabolizing enzymes and transporters. Altered nuclear receptor expression has been shown to affect the metabolism and pharmacological profile of traditional chemotherapeutics and targeted agents. Accordingly, polymorphic variants in these genes have been studied as pharmacogenetic markers of outcome variability. This review summarizes the state of knowledge about the roles played by pregnane X receptor, constitutive androstane receptor and hepatocyte nuclear factor expression and genetics as predictive markers of anticancer drug toxicity and efficacy, which can improve cancer precision medicine.
[Mh] Termos MeSH primário: Fatores Nucleares de Hepatócito/fisiologia
Neoplasias/tratamento farmacológico
Medicina de Precisão
Receptores Citoplasmáticos e Nucleares/fisiologia
Receptores de Esteroides/fisiologia
[Mh] Termos MeSH secundário: Antineoplásicos/efeitos adversos
Antineoplásicos/uso terapêutico
Fatores Nucleares de Hepatócito/genética
Seres Humanos
Neoplasias/genética
Receptores Citoplasmáticos e Nucleares/genética
Receptores de Esteroides/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Hepatocyte Nuclear Factors); 0 (Receptors, Cytoplasmic and Nuclear); 0 (Receptors, Steroid); 0 (constitutive androstane receptor); 0 (pregnane X receptor)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160827
[St] Status:MEDLINE
[do] DOI:10.2217/pgs-2016-0095


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[PMID]:27124543
[Au] Autor:Wu N; Zhang YL; Wang HT; Li DW; Dai HJ; Zhang QQ; Zhang J; Ma Y; Xia Q; Bian JM; Hang HL
[Ad] Endereço:a Department of Liver Surgery , RenJi Hospital, School of Medicine, Shanghai Jiao Tong University , Shanghai , China.
[Ti] Título:Overexpression of hepatocyte nuclear factor 4α in human mesenchymal stem cells suppresses hepatocellular carcinoma development through Wnt/ß-catenin signaling pathway downregulation.
[So] Source:Cancer Biol Ther;17(5):558-65, 2016 May 03.
[Is] ISSN:1555-8576
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mesenchymal stem cells (MSCs) hold promise as cellular vehicles for the delivery of therapeutic gene products because they can be isolated, expanded, and genetically modified in vitro and possess tumor-oriented homing capacity in vivo. (1) Hepatocyte nuclear factor 4α (HNF4α) is a dominant transcriptional regulator of hepatocyte differentiation and hepatocellular carcinogenesis (HCC). (2,3) We have previously demonstrated that overexpression of HNF4α activates various hepatic-specific genes and enhances MSC differentiation. (4) However, the extent that overexpression of HNF4α in MSCs influences HCC progression has yet to be examined. Here we sought to investigate what effect MSCs overexpressing HNF4α (MSC-HNF4α) have on human hepatoma cells in vitro and in vivo. Conditioned medium collected from in vitro MSC-HNF4α cultures significantly inhibited hepatoma cell growth and metastasis compared with controls. Additionally, nude mice administered MSC-HNF4α exhibited significantly smaller tumors compared with controls in vivo. Immunoblot analysis of HCC cells treated with MSC-HNF4α displayed downregulated ß-catenin, cyclinD1, c-Myc, MMP2 and MMP9. Taken together, our results demonstrate that MSC-HNF4α inhibits HCC progression by reducing hepatoma cell growth and metastasis through downregulation of the Wnt/ß-catenin signaling pathway.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/genética
Fatores Nucleares de Hepatócito/metabolismo
Neoplasias Hepáticas/genética
Células Mesenquimais Estromais/metabolismo
Via de Sinalização Wnt/genética
[Mh] Termos MeSH secundário: Animais
Carcinoma Hepatocelular/patologia
Proliferação Celular
Regulação para Baixo
Seres Humanos
Neoplasias Hepáticas/patologia
Masculino
Camundongos
Camundongos Nus
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hepatocyte Nuclear Factors)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170906
[Lr] Data última revisão:
170906
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160429
[St] Status:MEDLINE
[do] DOI:10.1080/15384047.2016.1177675


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[PMID]:27103109
[Au] Autor:Timsit J; Saint-Martin C; Dubois-Laforgue D; Bellanné-Chantelot C
[Ad] Endereço:Department of Diabetology, Hôpital Cochin-Port-Royal, Paris, France. Electronic address: jose.timsit@aphp.fr.
[Ti] Título:Searching for Maturity-Onset Diabetes of the Young (MODY): When and What for?
[So] Source:Can J Diabetes;40(5):455-461, 2016 Oct.
[Is] ISSN:2352-3840
[Cp] País de publicação:Canada
[La] Idioma:eng
[Ab] Resumo:Maturity-onset diabetes of the young (MODY) is a group of monogenic diseases that results in primary defects in insulin secretion and dominantly inherited forms of nonautoimmune diabetes. Although many genes may be associated with monogenic diabetes, heterozygous mutations in 6 of them are responsible for the majority of cases of MODY. Glucokinase (GCK)-MODY is due to mutations in the glucokinase gene, 3 MODY subtypes are associated with mutations in the hepatocyte nuclear factor (HNF) transcription factors, and 2 others with mutations in ABCC8 and KCNJ11, which encode the subunits of the ATP-dependent potassium channel in pancreatic beta cells. GCK-MODY and HNF1A-MODY are the most common subtypes. The clinical presentation of MODY subtypes has been reported to differ according to the gene involved, and the diagnosis of MODY may be considered in various clinical circumstances. However, except in patients with GCK-MODY whose phenotype is very homogeneous, in most cases the penetrance and expressivity of a given molecular abnormality vary greatly among patients and, conversely, alterations in various genes may lead to similar phenotypes. Moreover, differential diagnosis among more common forms of diabetes may be difficult, particularly with type 2 diabetes. Thus, careful assessment of the personal and family histories of patients with diabetes is mandatory to select those in whom genetic screening is worthwhile. The diagnosis of monogenic diabetes has many consequences in terms of prognosis, therapeutics and family screening.
[Mh] Termos MeSH primário: Diabetes Mellitus/diagnóstico
Doenças Raras/diagnóstico
[Mh] Termos MeSH secundário: Adolescente
Criança
Diabetes Mellitus/genética
Diabetes Mellitus/terapia
Diagnóstico Diferencial
Erros de Diagnóstico
Feminino
Regulação da Expressão Gênica
Testes Genéticos
Glucoquinase/genética
Fatores Nucleares de Hepatócito/genética
Seres Humanos
Masculino
Canais de Potássio Corretores do Fluxo de Internalização/genética
Guias de Prática Clínica como Assunto
Doenças Raras/genética
Doenças Raras/terapia
Receptores Sulfonilureia/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (ABCC8 protein, human); 0 (Hepatocyte Nuclear Factors); 0 (Kir6.2 channel); 0 (Potassium Channels, Inwardly Rectifying); 0 (Sulfonylurea Receptors); EC 2.7.1.2 (Glucokinase)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170206
[Lr] Data última revisão:
170206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160423
[St] Status:MEDLINE


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[PMID]:26409214
[Au] Autor:Park YK; Park ES; Kim DH; Ahn SH; Park SH; Lee AR; Park S; Kang HS; Lee JH; Kim JM; Lee SK; Lim KH; Isorce N; Tong S; Zoulim F; Kim KH
[Ad] Endereço:Department of Pharmacology, Center for Cancer Research and Diagnostic Medicine, IBST, School of Medicine, Konkuk University, Seoul, Republic of Korea; KU Open Innovation Center, Konkuk University, Seoul, Republic of Korea.
[Ti] Título:Cleaved c-FLIP mediates the antiviral effect of TNF-α against hepatitis B virus by dysregulating hepatocyte nuclear factors.
[So] Source:J Hepatol;64(2):268-277, 2016 Feb.
[Is] ISSN:1600-0641
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND & AIMS: Cytokines are key molecules implicated in the defense against virus infection. Tumor necrosis factor-alpha (TNF-α) is well known to block the replication of hepatitis B virus (HBV). However, the molecular mechanism and the downstream effector molecules remain largely unknown. METHODS: In this study, we investigated the antiviral effect and mechanism of p22-FLIP (FLICE-inhibitory protein) by ectopic expression in vitro and in vivo. In addition, to provide the biological relevance of our study, we examined that the p22-FLIP is involved in TNF-α-mediated suppression of HBV in primary human hepatocytes. RESULTS: We found that p22-FLIP, a newly discovered c-FLIP cleavage product, inhibited HBV replication at the transcriptional level in both hepatoma cells and primary human hepatocytes, and that c-FLIP conversion to p22-FLIP was stimulated by the TNF-α/NF-κB pathway. p22-FLIP inhibited HBV replication through the upregulation of HNF3ß but downregulation of HNF4α, thus inhibiting both HBV enhancer elements. Finally, p22-FLIP potently inhibited HBV DNA replication in a mouse model of HBV replication. CONCLUSIONS: Taken together, these findings suggest that the anti-apoptotic p22-FLIP serves a novel function of inhibiting HBV transcription, and mediates the antiviral effect of TNF-α against HBV replication.
[Mh] Termos MeSH primário: Proteína Reguladora de Apoptosis Semelhante a CASP8 e FADD/metabolismo
Vírus da Hepatite B
Fator de Necrose Tumoral alfa
Replicação Viral/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Antivirais/farmacologia
Linhagem Celular
DNA Viral/metabolismo
Vírus da Hepatite B/efeitos dos fármacos
Vírus da Hepatite B/fisiologia
Fatores Nucleares de Hepatócito/metabolismo
Hepatócitos/metabolismo
Seres Humanos
Camundongos
Modelos Animais
Transdução de Sinais/efeitos dos fármacos
Fator de Necrose Tumoral alfa/metabolismo
Fator de Necrose Tumoral alfa/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antiviral Agents); 0 (CASP8 and FADD-Like Apoptosis Regulating Protein); 0 (DNA, Viral); 0 (Hepatocyte Nuclear Factors); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150927
[St] Status:MEDLINE


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[PMID]:26166417
[Au] Autor:Wang K
[Ad] Endereço:Departments of Surgery, University of Illinois College of Medicine, One Illini Drive, Peoria, IL 61605, USA. kewang@uic.edu.
[Ti] Título:Pathophysiological Role of Hepatocyte Nuclear Factor 6 in Negative Regulation of Hepatic Apoptosis: A Novel Hypothesis.
[So] Source:Curr Mol Med;15(5):412-7, 2015.
[Is] ISSN:1875-5666
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Apoptosis is a prominent characteristic in the pathogenesis of liver disease. The molecular mechanism of hepatic apoptosis is not well understood. Liver injury induces a downregulation of hepatocyte nuclear factor 6 (HNF6) that is negatively correlated with the degree of apoptosis. However, an enhancement of HNF6 can relieve hepatic apoptosis and impede the progression of liver disease. HNF6 has distinct mechanisms to modulate hepatic apoptosis. Pathophysiological role of HNF6 may be apoptosis-resistant and liver-protective during different types of liver injury. The enhancing modality of HNF6 is a novel therapeutic intervention for liver disease.
[Mh] Termos MeSH primário: Apoptose
Fator 6 Nuclear de Hepatócito/metabolismo
Hepatócitos/metabolismo
Fígado/metabolismo
[Mh] Termos MeSH secundário: Animais
Apoptose/genética
Expressão Gênica
Regulação da Expressão Gênica
Fator 6 Nuclear de Hepatócito/genética
Fatores Nucleares de Hepatócito/metabolismo
Hepatócitos/patologia
Seres Humanos
Fígado/patologia
Hepatopatias/genética
Hepatopatias/metabolismo
Hepatopatias/patologia
Ligação Proteica
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Hepatocyte Nuclear Factor 6); 0 (Hepatocyte Nuclear Factors)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:150713
[Lr] Data última revisão:
150713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150714
[St] Status:MEDLINE


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[PMID]:25254346
[Au] Autor:Scimone ML; Kravarik KM; Lapan SW; Reddien PW
[Ad] Endereço:Howard Hughes Medical Institute, MIT Biology, and Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, MA 02142, USA.
[Ti] Título:Neoblast specialization in regeneration of the planarian Schmidtea mediterranea.
[So] Source:Stem Cell Reports;3(2):339-52, 2014 Aug 12.
[Is] ISSN:2213-6711
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Planarians can regenerate any missing body part in a process requiring dividing cells called neoblasts. Historically, neoblasts have largely been considered a homogeneous stem cell population. Most studies, however, analyzed neoblasts at the population rather than the single-cell level, leaving the degree of heterogeneity in this population unresolved. We combined RNA sequencing of neoblasts from wounded planarians with expression screening and identified 33 transcription factors transcribed in specific differentiated cells and in small fractions of neoblasts during regeneration. Many neoblast subsets expressing distinct tissue-associated transcription factors were present, suggesting candidate specification into many lineages. Consistent with this possibility, klf, pax3/7, and FoxA were required for the differentiation of cintillo-expressing sensory neurons, dopamine-ß-hydroxylase-expressing neurons, and the pharynx, respectively. Together, these results suggest that specification of cell fate for most-to-all regenerative lineages occurs within neoblasts, with regenerative cells of blastemas being generated from a highly heterogeneous collection of lineage-specified neoblasts.
[Mh] Termos MeSH primário: Células-Tronco/citologia
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Diferenciação Celular
Fatores Nucleares de Hepatócito/genética
Fatores Nucleares de Hepatócito/metabolismo
Fatores de Transcrição Kruppel-Like/antagonistas & inibidores
Fatores de Transcrição Kruppel-Like/genética
Fatores de Transcrição Kruppel-Like/metabolismo
Dados de Sequência Molecular
Fatores de Transcrição Box Pareados/antagonistas & inibidores
Fatores de Transcrição Box Pareados/genética
Fatores de Transcrição Box Pareados/metabolismo
Planárias
Interferência de RNA
RNA Interferente Pequeno/metabolismo
Regeneração
Células Receptoras Sensoriais/citologia
Células Receptoras Sensoriais/metabolismo
Análise de Sequência de RNA
Células-Tronco/metabolismo
Fatores de Transcrição/antagonistas & inibidores
Fatores de Transcrição/química
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Hepatocyte Nuclear Factors); 0 (Kruppel-Like Transcription Factors); 0 (Paired Box Transcription Factors); 0 (RNA, Small Interfering); 0 (Transcription Factors)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140926
[St] Status:MEDLINE


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[PMID]:25198130
[Au] Autor:Shen N; Gong J; Wang Y; Tian J; Qian J; Zou L; Chen W; Zhu B; Lu X; Zhong R; Guo A; Wang L; Miao X
[Ad] Endereço:State Key Laboratory of Environment Health (Incubation), MOE (Ministry of Education) Key Laboratory of Environment & Health, Ministry of Environmental Protection Key Laboratory of Environment and Health (Wuhan), and Department of Epidemiology and Biostatistics, School of Public Health, Tongji Me
[Ti] Título:Integrative genomic analysis identifies that SERPINA6-rs1998056 regulated by FOXA/ERα is associated with female hepatocellular carcinoma.
[So] Source:PLoS One;9(9):e107246, 2014.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The human forkhead box A1 (FOXA1) and A2 (FOXA2) transcription factors have been found to control estrogen and androgen signaling through co-regulating target genes with sex hormone receptors. Here we used an integrative strategy to examine the hypothesis that genetic variants at FOXA1/2 binding elements may be associated with sexual dimorphism of hepatocellular carcinoma (HCC) risk. Firstly we extracted chromatin immunoprecipitation-sequencing (ChIP-seq) data of FOXA1, FOXA2 and estrogen receptor 1(ERα) from ENCODE database to obtain dual target regions of FOXA/ERα, and further intersected these regions with genes' promoters. Then we used MATCH program to predict FOXA binding elements, in which genetic variants were retrieved by dbSNP database (NCBI, build 134). A total of 15 candidate variants were identified in this stage. Secondly we performed a case-control study with 1,081 HCC patients and 2,008 matched controls and found a significant association of SERPINA6-rs1998056 with female HCC risk under common genetic models (e.g. GG versus CC: OR = 2.03, 95% CI = 1.26-3.27, P = 0.004). Moreover, results from our real-time quantitative polymerase chain reaction (qPCR) using 72 normal liver tissues adjacent to the tumors showed that SERPINA6 expression was significantly different among different genotypes of this variant (GG versus CC: P = 0.032; Group test: P = 0.060). In summary, our study suggested that SERPINA6-rs1998056 regulated by FOXA/ERα might be associated with female HCC risk.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/genética
Receptor alfa de Estrogênio/metabolismo
Genômica
Fatores Nucleares de Hepatócito/metabolismo
Neoplasias Hepáticas/genética
Polimorfismo de Nucleotídeo Único
Transcortina/genética
[Mh] Termos MeSH secundário: Carcinoma Hepatocelular/patologia
Estudos de Casos e Controles
Feminino
Predisposição Genética para Doença/genética
Células Hep G2
Fator 3-alfa Nuclear de Hepatócito/metabolismo
Fator 3-beta Nuclear de Hepatócito/metabolismo
Seres Humanos
Fígado/metabolismo
Fígado/patologia
Neoplasias Hepáticas/patologia
Meia-Idade
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Estrogen Receptor alpha); 0 (Hepatocyte Nuclear Factor 3-alpha); 0 (Hepatocyte Nuclear Factors); 0 (RNA, Messenger); 0 (SERPINA6 protein, human); 135845-92-0 (Hepatocyte Nuclear Factor 3-beta); 9010-38-2 (Transcortin)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140909
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0107246


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[PMID]:24103914
[Au] Autor:Rastinejad F; Huang P; Chandra V; Khorasanizadeh S
[Ad] Endereço:Metabolic Signaling and Disease Program, Sanford-Burnham Medical Research Institute, Orlando, Florida 32827, USA.
[Ti] Título:Understanding nuclear receptor form and function using structural biology.
[So] Source:J Mol Endocrinol;51(3):T1-T21, 2013 Dec.
[Is] ISSN:1479-6813
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Nuclear receptors (NRs) are a major transcription factor family whose members selectively bind small-molecule lipophilic ligands and transduce those signals into specific changes in gene programs. For over two decades, structural biology efforts were focused exclusively on the individual ligand-binding domains (LBDs) or DNA-binding domains of NRs. These analyses revealed the basis for both ligand and DNA binding and also revealed receptor conformations representing both the activated and repressed states. Additionally, crystallographic studies explained how NR LBD surfaces recognize discrete portions of transcriptional coregulators. The many structural snapshots of LBDs have also guided the development of synthetic ligands with therapeutic potential. Yet, the exclusive structural focus on isolated NR domains has made it difficult to conceptualize how all the NR polypeptide segments are coordinated physically and functionally in the context of receptor quaternary architectures. Newly emerged crystal structures of the peroxisome proliferator-activated receptor-γ-retinoid X receptor α (PPARγ-RXRα) heterodimer and hepatocyte nuclear factor (HNF)-4α homodimer have recently revealed the higher order organizations of these receptor complexes on DNA, as well as the complexity and uniqueness of their domain-domain interfaces. These emerging structural advances promise to better explain how signals in one domain can be allosterically transmitted to distal receptor domains, also providing much better frameworks for guiding future drug discovery efforts.
[Mh] Termos MeSH primário: Receptores Citoplasmáticos e Nucleares/metabolismo
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Animais
Fatores Nucleares de Hepatócito/metabolismo
Seres Humanos
PPAR gama/metabolismo
Receptor X Retinoide alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; REVIEW
[Nm] Nome de substância:
0 (Hepatocyte Nuclear Factors); 0 (PPAR gamma); 0 (Receptors, Cytoplasmic and Nuclear); 0 (Retinoid X Receptor alpha); 0 (Transcription Factors)
[Em] Mês de entrada:1407
[Cu] Atualização por classe:161025
[Lr] Data última revisão:
161025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131010
[St] Status:MEDLINE
[do] DOI:10.1530/JME-13-0173



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