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Pesquisa : A11.872.700.250 [Categoria DeCS]
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  1 / 15296 MEDLINE  
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[PMID]:29364956
[Au] Autor:Winzi M; Casas Vila N; Paszkowski-Rogacz M; Ding L; Noack S; Theis M; Butter F; Buchholz F
[Ad] Endereço:Medical Systems Biology, Faculty of Medicine Carl Gustav Carus, University Cancer Center, TU Dresden, Dresden, Germany.
[Ti] Título:The long noncoding RNA lncR492 inhibits neural differentiation of murine embryonic stem cells.
[So] Source:PLoS One;13(1):e0191682, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RNA interference (RNAi) screens have been shown to be valuable to study embryonic stem cell (ESC) self-renewal and they have been successfully applied to identify coding as well as noncoding genes required for maintaining pluripotency. Here, we used an RNAi library targeting >640 long noncoding RNAs (lncRNA) to probe for their role in early cell differentiation. Utilizing a Sox1-GFP ESC reporter cell line, we identified the lncRNA lncR492 as lineage-specific inhibitor of neuroectodermal differentiation. Molecular characterization showed that lncR492 interacts with the mRNA binding protein HuR and facilitates its inhibitory function by activation of Wnt signaling. Thus, lncRNAs modulate the fate decision of pluripotent stem cells.
[Mh] Termos MeSH primário: Diferenciação Celular
Células-Tronco Embrionárias/citologia
Neurônios/citologia
RNA Longo não Codificante/genética
[Mh] Termos MeSH secundário: Animais
Camundongos
Interferência de RNA
Reação em Cadeia da Polimerase Via Transcriptase Reversa
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA, Long Noncoding)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180125
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191682


  2 / 15296 MEDLINE  
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[PMID]:29311541
[Au] Autor:Stremmel C; Schuchert R; Wagner F; Thaler R; Weinberger T; Pick R; Mass E; Ishikawa-Ankerhold HC; Margraf A; Hutter S; Vagnozzi R; Klapproth S; Frampton J; Yona S; Scheiermann C; Molkentin JD; Jeschke U; Moser M; Sperandio M; Massberg S; Geissmann F; Schulz C
[Ad] Endereço:Medizinische Klinik und Poliklinik I, Klinikum der Universität, Ludwig-Maximilians-Universität, Marchioninistrasse 15, 81377, Munich, Germany.
[Ti] Título:Yolk sac macrophage progenitors traffic to the embryo during defined stages of development.
[So] Source:Nat Commun;9(1):75, 2018 01 08.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tissue macrophages in many adult organs originate from yolk sac (YS) progenitors, which invade the developing embryo and persist by means of local self-renewal. However, the route and characteristics of YS macrophage trafficking during embryogenesis are incompletely understood. Here we show the early migration dynamics of YS-derived macrophage progenitors in vivo using fate mapping and intravital microscopy. From embryonic day 8.5 (E8.5) CX CR1+ pre-macrophages are present in the mouse YS where they rapidly proliferate and gain access to the bloodstream to migrate towards the embryo. Trafficking of pre-macrophages and their progenitors from the YS to tissues peaks around E10.5, dramatically decreases towards E12.5 and is no longer evident from E14.5 onwards. Thus, YS progenitors use the vascular system during a restricted time window of embryogenesis to invade the growing fetus. These findings close an important gap in our understanding of the development of the innate immune system.
[Mh] Termos MeSH primário: Movimento Celular
Células-Tronco Embrionárias/citologia
Macrófagos/citologia
Saco Vitelino/citologia
[Mh] Termos MeSH secundário: Animais
Circulação Sanguínea
Linhagem da Célula
Proliferação Celular
Embrião de Mamíferos/irrigação sanguínea
Embrião de Mamíferos/citologia
Embrião de Mamíferos/embriologia
Células-Tronco Hematopoéticas/citologia
Camundongos Endogâmicos C57BL
Camundongos Knockout
Camundongos Transgênicos
Microscopia Confocal
Fatores de Tempo
Saco Vitelino/embriologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02492-2


  3 / 15296 MEDLINE  
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[PMID]:29267285
[Au] Autor:Colombo DF; Burger L; Baubec T; Schübeler D
[Ad] Endereço:Friedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
[Ti] Título:Binding of high mobility group A proteins to the mammalian genome occurs as a function of AT-content.
[So] Source:PLoS Genet;13(12):e1007102, 2017 12.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Genomic location can inform on potential function and recruitment signals for chromatin-associated proteins. High mobility group (Hmg) proteins are of similar size as histones with Hmga1 and Hmga2 being particularly abundant in replicating normal tissues and in cancerous cells. While several roles for Hmga proteins have been proposed we lack a comprehensive description of their genomic location as a function of chromatin, DNA sequence and functional domains. Here we report such a characterization in mouse embryonic stem cells in which we introduce biotin-tagged constructs of wild-type and DNA-binding domain mutants. Comparative analysis of the genome-wide distribution of Hmga proteins reveals pervasive binding, a feature that critically depends on a functional DNA-binding domain and which is shared by both Hmga proteins. Assessment of the underlying queues instructive for this binding modality identifies AT richness, defined as high frequency of A or T bases, as the major criterion for local binding. Additionally, we show that other chromatin states such as those linked to cis-regulatory regions have little impact on Hmga binding both in stem and differentiated cells. As a consequence, Hmga proteins are preferentially found at AT-rich regions such as constitutively heterochromatic regions but are absent from enhancers and promoters arguing for a limited role in regulating individual genes. In line with this model, we show that genetic deletion of Hmga proteins in stem cells causes limited transcriptional effects and that binding is conserved in neuronal progenitors. Overall our comparative study describing the in vivo binding modality of Hmga1 and Hmga2 identifies the proteins' preference for AT-rich DNA genome-wide and argues against a suggested function of Hmga at regulatory regions. Instead we discover pervasive binding with enrichment at regions of higher AT content irrespective of local variation in chromatin modifications.
[Mh] Termos MeSH primário: Sequência Rica em At
Proteínas de Grupo de Alta Mobilidade/genética
Proteínas de Grupo de Alta Mobilidade/metabolismo
[Mh] Termos MeSH secundário: Animais
Composição de Bases
Sequência de Bases
Cromatina/genética
Cromatina/metabolismo
DNA/química
DNA/genética
DNA/metabolismo
Proteínas de Ligação a DNA/genética
Proteínas de Ligação a DNA/metabolismo
Células-Tronco Embrionárias/metabolismo
Histonas/genética
Camundongos
Camundongos Endogâmicos C57BL
Regiões Promotoras Genéticas
Ligação Proteica
Sequências Reguladoras de Ácido Nucleico
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chromatin); 0 (DNA-Binding Proteins); 0 (High Mobility Group Proteins); 0 (Histones); 9007-49-2 (DNA)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007102


  4 / 15296 MEDLINE  
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[PMID]:28457890
[Au] Autor:Saunders A; Li D; Faiola F; Huang X; Fidalgo M; Guallar D; Ding J; Yang F; Xu Y; Zhou H; Wang J
[Ad] Endereço:The Black Family Stem Cell Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; The Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA; Department of Cell, Developmental, and Regenerative Biology, Icahn School of Medicine
[Ti] Título:Context-Dependent Functions of NANOG Phosphorylation in Pluripotency and Reprogramming.
[So] Source:Stem Cell Reports;8(5):1115-1123, 2017 May 09.
[Is] ISSN:2213-6711
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The core pluripotency transcription factor NANOG is critical for embryonic stem cell (ESC) self-renewal and somatic cell reprogramming. Although NANOG is phosphorylated at multiple residues, the role of NANOG phosphorylation in ESC self-renewal is incompletely understood, and no information exists regarding its functions during reprogramming. Here we report our findings that NANOG phosphorylation is beneficial, although nonessential, for ESC self-renewal, and that loss of phosphorylation enhances NANOG activity in reprogramming. Mutation of serine 65 in NANOG to alanine (S65A) alone has the most significant impact on increasing NANOG reprogramming capacity. Mechanistically, we find that pluripotency regulators (ESRRB, OCT4, SALL4, DAX1, and TET1) are transcriptionally primed and preferentially associated with NANOG S65A at the protein level due to presumed structural alterations in the N-terminal domain of NANOG. These results demonstrate that a single phosphorylation site serves as a critical interface for controlling context-dependent NANOG functions in pluripotency and reprogramming.
[Mh] Termos MeSH primário: Reprogramação Celular
Células-Tronco Embrionárias/citologia
Células-Tronco Pluripotentes Induzidas/citologia
Mutação de Sentido Incorreto
Proteína Homeobox Nanog/metabolismo
Processamento de Proteína Pós-Traducional
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Células Cultivadas
Receptor Nuclear Órfão DAX-1/metabolismo
Proteínas de Ligação a DNA/metabolismo
Células-Tronco Embrionárias/metabolismo
Células-Tronco Pluripotentes Induzidas/metabolismo
Camundongos
Proteína Homeobox Nanog/química
Proteína Homeobox Nanog/genética
Fator 3 de Transcrição de Octâmero/metabolismo
Fosforilação
Domínios Proteicos
Proteínas Proto-Oncogênicas/metabolismo
Receptores Estrogênicos/metabolismo
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DAX-1 Orphan Nuclear Receptor); 0 (DNA-Binding Proteins); 0 (Esrrb protein, mouse); 0 (Nanog Homeobox Protein); 0 (Nanog protein, mouse); 0 (Nr0b1 protein, mouse); 0 (Octamer Transcription Factor-3); 0 (Pou5f1 protein, mouse); 0 (Proto-Oncogene Proteins); 0 (Receptors, Estrogen); 0 (Sall4 protein, mouse); 0 (TET1 protein, mouse); 0 (Transcription Factors)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


  5 / 15296 MEDLINE  
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[PMID]:28457886
[Au] Autor:Guo A; Huang S; Yu J; Wang H; Li H; Pei G; Shen L
[Ad] Endereço:State Key Laboratory of Cell Biology, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai 200031, China.
[Ti] Título:Single-Cell Dynamic Analysis of Mitosis in Haploid Embryonic Stem Cells Shows the Prolonged Metaphase and Its Association with Self-diploidization.
[So] Source:Stem Cell Reports;8(5):1124-1134, 2017 May 09.
[Is] ISSN:2213-6711
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The recent establishment of mammalian haploid embryonic stem cells (ESCs) provides new possibilities for genetic screening and for understanding genome evolution and function. However, the dynamics of mitosis in haploid ESCs is still unclear. Here, we report that the duration of mitosis in haploid ESCs, especially the metaphase, is significantly longer than that in diploid ESCs. Delaying mitosis by chemicals increased self-diploidization of haploid ESCs, while shortening mitosis stabilized haploid ESCs. Taken together, our study suggests that the delayed mitosis of haploid ESCs is associated with self-diploidization.
[Mh] Termos MeSH primário: Células-Tronco Embrionárias/citologia
Haploidia
Metáfase
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Diploide
Camundongos
Análise de Célula Única
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


  6 / 15296 MEDLINE  
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[PMID]:28467909
[Au] Autor:Bar S; Schachter M; Eldar-Geva T; Benvenisty N
[Ad] Endereço:The Azrieli Center for Stem Cells and Genetic Research, Department of Genetics, Silberman Institute of Life Sciences, The Hebrew University, Jerusalem 91904, Israel.
[Ti] Título:Large-Scale Analysis of Loss of Imprinting in Human Pluripotent Stem Cells.
[So] Source:Cell Rep;19(5):957-968, 2017 May 02.
[Is] ISSN:2211-1247
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The parent-specific monoallelic expression of imprinted genes is controlled by DNA methylation marks that are established differentially in the germline. Perturbation of these marks leads to loss of imprinting (LOI), which is associated with developmental disorders and malignancy and may also obstruct applications of human pluripotent stem cells (hPSCs). Previous studies of LOI in hPSCs were performed on relatively small numbers of cell lines, often leading to conflicting conclusions regarding imprinting stability. Here, we chart the landscape of LOI in hPSCs by applying a large-scale analysis of allele-specific RNA-seq data from more than 270 hPSC samples. We show that reprogrammed hPSCs acquire higher levels of LOI compared with embryonic stem cells and that LOI can pre-exist in their somatic cells of origin. Furthermore, different imprinted genes vary with respect to LOI incidence, surprisingly revealing that those controlled paternally are more prone to disruption. Our findings emphasize the importance of inspecting the imprinting status of hPSCs.
[Mh] Termos MeSH primário: Genoma Humano
Impressão Genômica
Células-Tronco Pluripotentes/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular
Metilação de DNA
Células-Tronco Embrionárias/metabolismo
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


  7 / 15296 MEDLINE  
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[PMID]:28468635
[Au] Autor:Maclary E; Hinten M; Harris C; Sethuraman S; Gayen S; Kalantry S
[Ad] Endereço:Department of Human Genetics, University of Michigan Medical School, Ann Arbor, MI, 48109-5618, USA.
[Ti] Título:PRC2 represses transcribed genes on the imprinted inactive X chromosome in mice.
[So] Source:Genome Biol;18(1):82, 2017 05 03.
[Is] ISSN:1474-760X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Polycomb repressive complex 2 (PRC2) catalyzes histone H3K27me3, which marks many transcriptionally silent genes throughout the mammalian genome. Although H3K27me3 is associated with silenced gene expression broadly, it remains unclear why some but not other PRC2 target genes require PRC2 and H3K27me3 for silencing. RESULTS: Here we define the transcriptional and chromatin features that predict which PRC2 target genes require PRC2/H3K27me3 for silencing by interrogating imprinted mouse X-chromosome inactivation. H3K27me3 is enriched at promoters of silenced genes across the inactive X chromosome. To abrogate PRC2 function, we delete the core PRC2 protein EED in F1 hybrid trophoblast stem cells (TSCs), which undergo imprinted inactivation of the paternally inherited X chromosome. Eed TSCs lack H3K27me3 and Xist lncRNA enrichment on the inactive X chromosome. Despite the absence of H3K27me3 and Xist RNA, only a subset of the inactivated X-linked genes is derepressed in Eed TSCs. Unexpectedly, in wild-type (WT) TSCs these genes are transcribed and are enriched for active chromatin hallmarks on the inactive-X, including RNA PolII, H3K27ac, and H3K36me3, but not the bivalent mark H3K4me2. By contrast, PRC2 targets that remain repressed in Eed TSCs are depleted for active chromatin characteristics in WT TSCs. CONCLUSIONS: A comparative analysis of transcriptional and chromatin features of inactive X-linked genes in WT and Eed TSCs suggests that PRC2 acts as a brake to prevent induction of transcribed genes on the inactive X chromosome, a mode of PRC2 function that may apply broadly.
[Mh] Termos MeSH primário: Impressão Genômica
Complexo Repressor Polycomb 2/metabolismo
Cromossomo X/genética
[Mh] Termos MeSH secundário: Animais
Cromatina/genética
Células-Tronco Embrionárias/metabolismo
Feminino
Inativação Gênica
Histonas/genética
Histonas/metabolismo
Masculino
Camundongos
Complexo Repressor Polycomb 2/genética
Trofoblastos/citologia
Inativação do Cromossomo X
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chromatin); 0 (Histones); EC 2.1.1.43 (Polycomb Repressive Complex 2)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180207
[Lr] Data última revisão:
180207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1186/s13059-017-1211-5


  8 / 15296 MEDLINE  
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[PMID]:29289608
[Au] Autor:Zeng W; Liu R; Zhang T; Zuo W; Ou Y; Tang Y; Xu H
[Ad] Endereço:State Key Laboratory of Silkworm Genome Biology, Southwest University, Chongqing 400715, China.
[Ti] Título:BmYki is transcribed into four functional splicing isoforms in the silk glands of the silkworm Bombyx mori.
[So] Source:Gene;646:39-46, 2018 Mar 10.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Yorkie (Yki), the Drosophila homolog of vertebrate yes-associated protein (YAP), is a key effector of the Hippo pathway, which modulates organ size via the transcriptional regulation of downstream targets involved in cell proliferation and survival. YAP has been shown to be expressed as multiple splicing isoforms in mammals, but thus far, no evidence of alternatively spliced Yki isoforms has been reported in insects. Here, we confirmed that the Yki protein of the silkworm Bombyx mori, BmYki, is transcribed in the silk gland into at least four splicing isoforms, named BmY1329, BmY1314, BmY1188, and BmY1173. Further analysis revealed that BmY1329 and BmY1314 each contain two WW domains, whereas BmY1188 and BmY1173 each contain only one WW domain. Each BmYki isoform functions in regulating expression of Yki target genes in cultured B. mori embryonic cells, and exhibits a few different effects on the expression of Yki targets. Interestingly, the expression of silk fibroin protein genes could also be influenced by each of the BmYki isoforms, suggesting that BmYki is involved in the regulation of silk protein-coding genes. This study provides novel insights into the role of BmYki. The contribution of each BmYki isoform to the modulation of gene expression will be of great interest for further study.
[Mh] Termos MeSH primário: Processamento Alternativo
Bombyx/genética
Transativadores/genética
Transativadores/metabolismo
[Mh] Termos MeSH secundário: Animais
Bombyx/crescimento & desenvolvimento
Bombyx/metabolismo
Células Cultivadas
Células-Tronco Embrionárias
Regulação da Expressão Gênica
Proteínas de Insetos/química
Proteínas de Insetos/genética
Proteínas de Insetos/metabolismo
Domínios Proteicos
Análise de Sequência de DNA
Seda/genética
Seda/metabolismo
Distribuição Tecidual
Transativadores/química
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Insect Proteins); 0 (Silk); 0 (Trans-Activators)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180101
[St] Status:MEDLINE


  9 / 15296 MEDLINE  
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[PMID]:29269485
[Au] Autor:Estarás C; Hsu HT; Huang L; Jones KA
[Ad] Endereço:Regulatory Biology Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA.
[Ti] Título:YAP repression of the gene controls hESC differentiation along the cardiac mesoderm lineage.
[So] Source:Genes Dev;31(22):2250-2263, 2017 11 15.
[Is] ISSN:1549-5477
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Activin/SMAD signaling in human embryonic stem cells (hESCs) ensures expression and stem cell pluripotency. In the presence of Wnt ligand, the Activin/SMAD transcription network switches to cooperate with Wnt/ß-catenin and induce mesendodermal (ME) differentiation genes. We show here that the Hippo effector YAP binds to the gene enhancer and prevents the gene from being induced by Activin in proliferating hESCs. ChIP-seq (chromatin immunoprecipitation [ChIP] combined with high-throughput sequencing) data show that YAP impairs SMAD recruitment and the accumulation of P-TEFb-associated RNA polymerase II (RNAPII) C-terminal domain (CTD)-Ser7 phosphorylation at the gene. CRISPR/ knockout of YAP in hESCs enables Activin to induce Wnt3 expression and stabilize ß-catenin, which then synergizes with Activin-induced SMADs to activate a subset of ME genes that is required to form cardiac mesoderm. Interestingly, exposure of YAP hESCs to Activin induces cardiac mesoderm markers ( and ) without activating Wnt-dependent cardiac inhibitor genes ( and ). Moreover, canonical Wnt target genes are up-regulated only modestly, if at all, under these conditions. Consequently, YAP-null hESCs exposed to Activin differentiate precisely into beating cardiomyocytes without further treatment. We conclude that YAP maintains hESC pluripotency by preventing expression in response to Activin, thereby blocking a direct route to embryonic cardiac mesoderm formation.
[Mh] Termos MeSH primário: Células-Tronco Embrionárias/metabolismo
Regulação da Expressão Gênica no Desenvolvimento
Miócitos Cardíacos/metabolismo
Proteínas Nucleares/fisiologia
Proteínas Repressoras/fisiologia
Fatores de Transcrição/fisiologia
Proteína Wnt3/genética
[Mh] Termos MeSH secundário: Ativinas/fisiologia
Fator de Transcrição CDX2/genética
Diferenciação Celular/genética
Linhagem da Célula
Células Cultivadas
Cromatina/metabolismo
Células-Tronco Embrionárias/citologia
Elementos Facilitadores Genéticos
Coração/embriologia
Seres Humanos
Mesoderma/citologia
Proteínas Nucleares/genética
Regiões Promotoras Genéticas
Proteínas Repressoras/genética
Transdução de Sinais
Proteínas Smad/antagonistas & inibidores
Elongação da Transcrição Genética
Fatores de Transcrição/genética
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CDX2 Transcription Factor); 0 (CDX2 protein, human); 0 (Chromatin); 0 (Nuclear Proteins); 0 (Repressor Proteins); 0 (Smad Proteins); 0 (Transcription Factors); 0 (WNT3 protein, human); 0 (Wnt3 Protein); 0 (YY1AP1 protein, human); 0 (beta Catenin); 104625-48-1 (Activins)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171223
[St] Status:MEDLINE
[do] DOI:10.1101/gad.307512.117


  10 / 15296 MEDLINE  
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[PMID]:29203199
[Au] Autor:Kar S; Patra SK
[Ad] Endereço:Epigenetics and Cancer Research Laboratory, Biochemistry and Molecular Biology Group, Department of Life Science, National Institute of Technology, Rourkela, Odisha 769008, India.
[Ti] Título:Overexpression of OCT4 induced by modulation of histone marks plays crucial role in breast cancer progression.
[So] Source:Gene;643:35-45, 2018 Feb 15.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:OCT4 is known as the gatekeeper of pluripotent embryonic state as it is responsible for maintenance of pluripotency via self-renewal of embryonic stem cells and acquisition of induced pluripotency via somatic cell reprogramming. OCT4 is responsible for oncogenic transformation by disrupting pre-scheduled differentiation programs and in general, favoring evolution of cancer cells into a more aggressive cancer stem cell phenotype. In this study, we have investigated in details, the epigenetic regulatory mechanisms responsible for over-expression and subsequent aberrant function of OCT4 in breast cancer. Expression of OCT4 in breast cancer tissues and cell lines was determined by qRT-PCR, Western blot, immunohistochemistry and immunocytochemistry followed by investigation of pro-tumorigenic properties such as cell proliferation, migration and apoptosis by gene knockdown and treatment with epigenetic modulators. Ectopic treatment of epigenetic modulators was done followed by MS-PCR and chromatin immunoprecipitation. OCT4 is over-expressed in both of the breast cancer cell lines; MCF7 and MDA-MB-231 and its inhibition resulted in drastic decrease in rate of cell proliferation, metastatic ability and induced apoptosis. After treatment with epigenetic modulators, general increase in expression of OCT4 was observed at both gene and protein levels; however, changes of promoter DNA methylation was not found to be significant during OCT4 over-expression. Active histone marks especially H3K4me3 and H3K9acS10p were enriched in the promoter region with very low levels of repressive marks H3K9me3 and H3K27me3 indicating that active histone modifications are the deciding factor in inducing over-expression of OCT4 during breast carcinogenesis. These findings could provide the basis on which epigenetic therapy, targeting reversible epigenetic modifications and their perpetuating enzymes, can be designed for effective treatment of aggressive breast cancer.
[Mh] Termos MeSH primário: Neoplasias da Mama/metabolismo
Fator 3 de Transcrição de Octâmero/biossíntese
[Mh] Termos MeSH secundário: Apoptose/fisiologia
Neoplasias da Mama/genética
Neoplasias da Mama/patologia
Diferenciação Celular/genética
Linhagem Celular Tumoral
Proliferação Celular/fisiologia
Metilação de DNA
Células-Tronco Embrionárias/metabolismo
Epigênese Genética
Feminino
Código das Histonas
Histonas/metabolismo
Seres Humanos
Células MCF-7
Células-Tronco Neoplásicas/metabolismo
Células-Tronco Neoplásicas/patologia
Fator 3 de Transcrição de Octâmero/genética
Fator 3 de Transcrição de Octâmero/metabolismo
Células-Tronco Pluripotentes/metabolismo
Regiões Promotoras Genéticas
Processamento de Proteína Pós-Traducional/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histones); 0 (Octamer Transcription Factor-3); 0 (POU5F1 protein, human)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180123
[Lr] Data última revisão:
180123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE



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