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Pesquisa : A11.872.700.250.875 [Categoria DeCS]
Referências encontradas : 568 [refinar]
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[PMID]:29434199
[Au] Autor:Hayashi T; Ozaki H; Sasagawa Y; Umeda M; Danno H; Nikaido I
[Ad] Endereço:Bioinformatics Research Unit, Advanced Center for Computing and Communication, RIKEN, 2-1 Hirosawa Wako, Saitama, 351-0198, Japan.
[Ti] Título:Single-cell full-length total RNA sequencing uncovers dynamics of recursive splicing and enhancer RNAs.
[So] Source:Nat Commun;9(1):619, 2018 02 12.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Total RNA sequencing has been used to reveal poly(A) and non-poly(A) RNA expression, RNA processing and enhancer activity. To date, no method for full-length total RNA sequencing of single cells has been developed despite the potential of this technology for single-cell biology. Here we describe random displacement amplification sequencing (RamDA-seq), the first full-length total RNA-sequencing method for single cells. Compared with other methods, RamDA-seq shows high sensitivity to non-poly(A) RNA and near-complete full-length transcript coverage. Using RamDA-seq with differentiation time course samples of mouse embryonic stem cells, we reveal hundreds of dynamically regulated non-poly(A) transcripts, including histone transcripts and long noncoding RNA Neat1. Moreover, RamDA-seq profiles recursive splicing in >300-kb introns. RamDA-seq also detects enhancer RNAs and their cell type-specific activity in single cells. Taken together, we demonstrate that RamDA-seq could help investigate the dynamics of gene expression, RNA-processing events and transcriptional regulation in single cells.
[Mh] Termos MeSH primário: Sequenciamento de Nucleotídeos em Larga Escala/métodos
Células-Tronco Embrionárias Murinas/metabolismo
Processamento de RNA
RNA Longo não Codificante/genética
RNA Mensageiro/genética
Análise de Célula Única/métodos
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Diferenciação Celular
Elementos Facilitadores Genéticos
Éxons
Histonas/genética
Histonas/metabolismo
Íntrons
Camundongos
Células-Tronco Embrionárias Murinas/citologia
RNA Longo não Codificante/metabolismo
RNA Mensageiro/metabolismo
Análise de Sequência de RNA
Transcrição Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Histones); 0 (NEAT1 long non-coding RNA, mouse); 0 (RNA, Long Noncoding); 0 (RNA, Messenger)
[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:180214
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-018-02866-0


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[PMID]:29207259
[Au] Autor:Chen X; Wang R; Liu X; Wu Y; Zhou T; Yang Y; Perez A; Chen YC; Hu L; Chadarevian JP; Assadieskandar A; Zhang C; Ying QL
[Ad] Endereço:Eli and Edythe Broad Center for Regenerative Medicine and Stem Cell Research at USC, Department of Stem Cell Biology and Regenerative Medicine, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
[Ti] Título:A Chemical-Genetic Approach Reveals the Distinct Roles of GSK3α and GSK3ß in Regulating Embryonic Stem Cell Fate.
[So] Source:Dev Cell;43(5):563-576.e4, 2017 Dec 04.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glycogen synthase kinase 3 (GSK3) plays a central role in diverse cellular processes. GSK3 has two mammalian isozymes, GSK3α and GSK3ß, whose functions remain ill-defined because of a lack of inhibitors that can distinguish between the two highly homologous isozymes. Here, we show that GSK3α and GSK3ß can be selectively inhibited in mouse embryonic stem cells (ESCs) using a chemical-genetic approach. Selective inhibition of GSK3ß is sufficient to maintain mouse ESC self-renewal, whereas GSK3α inhibition promotes mouse ESC differentiation toward neural lineages. Genome-wide transcriptional analysis reveals that GSK3α and GSK3ß have distinct sets of downstream targets. Furthermore, selective inhibition of individual GSK3 isozymes yields distinct phenotypes from gene deletion, highlighting the power of the chemical-genetic approach in dissecting kinase catalytic functions from the protein's scaffolding functions. Our study opens new avenues for defining GSK3 isozyme-specific functions in various cellular processes.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Linhagem da Célula
Glicogênio Sintase Quinase 3 beta/genética
Quinase 3 da Glicogênio Sintase/genética
Células-Tronco Embrionárias Murinas/citologia
[Mh] Termos MeSH secundário: Animais
Estudo de Associação Genômica Ampla/métodos
Camundongos
Camundongos Knockout
Fosforilação
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta); EC 2.7.11.26 (Glycogen Synthase Kinase 3); EC 2.7.11.26 (glycogen synthase kinase 3 alpha)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE


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[PMID]:28457889
[Au] Autor:Sim YJ; Kim MS; Nayfeh A; Yun YJ; Kim SJ; Park KT; Kim CH; Kim KS
[Ad] Endereço:Department of Biomedical Science, Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul 04763, Republic of Korea.
[Ti] Título:2i Maintains a Naive Ground State in ESCs through Two Distinct Epigenetic Mechanisms.
[So] Source:Stem Cell Reports;8(5):1312-1328, 2017 May 09.
[Is] ISSN:2213-6711
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mouse embryonic stem cells (ESCs) are maintained in serum with leukemia inhibitory factor (LIF) to maintain self-renewal and pluripotency. Recently, a 2i culture method was reported using a combination of MEK inhibition (MEKi) and GSK3 inhibition (GSK3i) with LIF to maintain ESCs in a naive ground state. How 2i maintains a ground state of ESCs remains elusive. Here we show that MEKi and GSK3i maintain the ESC ground state by downregulating global DNA methylation through two distinct mechanisms. MEK1 phosphorylates JMJD2C for ubiquitin-mediated protein degradation. Therefore, MEKi increased JMJD2C protein levels but decreased DNMT3 expression. JMJD2C promotes TET1 activity to increase 5-hydroxymethylcytosine (5hmC) levels. GSK3i suppressed DNMT3 expression, thereby decreasing DNA methylation without affecting 5hmC levels. Furthermore, 2i increased PRDM14 expression to inhibit DNMT3A/B protein expression by promoting G9a-mediated DNMT3A/B protein degradation. Collectively, 2i allows ESCs to maintain a naive ground state through JMJD2C-dependent TET1 activation and PRDM14/G9a-mediated DNMT3A/B protein degradation.
[Mh] Termos MeSH primário: Epigênese Genética
Quinase 3 da Glicogênio Sintase/antagonistas & inibidores
Células-Tronco Pluripotentes Induzidas/metabolismo
MAP Quinase Quinase 1/antagonistas & inibidores
Células-Tronco Embrionárias Murinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
DNA (Citosina-5-)-Metiltransferases/genética
DNA (Citosina-5-)-Metiltransferases/metabolismo
Metilação de DNA
Quinase 3 da Glicogênio Sintase/metabolismo
Células-Tronco Pluripotentes Induzidas/citologia
Histona Desmetilases com o Domínio Jumonji/metabolismo
MAP Quinase Quinase 1/metabolismo
Camundongos
Células-Tronco Embrionárias Murinas/citologia
Inibidores de Proteínas Quinases/farmacologia
Proteólise
Fatores de Transcrição/genética
Fatores de Transcrição/metabolismo
Ubiquitinação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Prdm14 protein, mouse); 0 (Protein Kinase Inhibitors); 0 (Transcription Factors); EC 1.14.11.- (Jmjd2c protein, mouse); EC 1.14.11.- (Jumonji Domain-Containing Histone Demethylases); EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferases); EC 2.7.11.26 (Glycogen Synthase Kinase 3); EC 2.7.12.2 (MAP Kinase Kinase 1)
[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


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[PMID]:29337257
[Au] Autor:Dimopoulou M; Verhoef A; Gomes CA; van Dongen CW; Rietjens IMCM; Piersma AH; van Ravenzwaay B
[Ad] Endereço:Division of Toxicology, Wageningen University, The Netherlands; National Institute of Public Health and the Environment (RIVM), Bilthoven, The Netherlands. Electronic address: myrto.dimopoulou@wur.nl.
[Ti] Título:A comparison of the embryonic stem cell test and whole embryo culture assay combined with the BeWo placental passage model for predicting the embryotoxicity of azoles.
[So] Source:Toxicol Lett;286:10-21, 2018 Apr.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:In the present study, we show the value of combining toxico-dynamic and -kinetic in vitro approaches for embryotoxicity testing of azoles. Both the whole embryo culture (WEC) and the embryonic stem cells test (EST) predicted the in vivo potency ranking of twelve tested azoles with moderate accuracy. Combining these results with relative placental transfer rates (Papp values) as determined in the BeWo cell culture model, increased the predictability of both WEC and EST, with R values increasing from 0.51 to 0.87 and from 0.35 to 0.60, respectively. The comparison of these in vitro systems correlated well (R = 0.67), correctly identifying the in vivo strong and weak embryotoxicants. Evaluating also specific gene responses related with the retinoic acid and sterol biosynthesis pathways, which represent the toxicological and fungicidal mode of action of azoles respectively in the WEC and EST, we observed that the differential regulation of Dhrs3 and Msmo1 reached higher magnitudes in both systems compared to Cyp26a1 and Cyp51. Establishing sensitive biomarkers across the in vitro systems for studying the underlying mechanism of action of chemicals, such as azoles, is valuable for comparing alternative in vitro models and for improving insight in the mechanism of developmental toxicity of chemicals.
[Mh] Termos MeSH primário: Azóis/toxicidade
Bioensaio
Embrião de Mamíferos/efeitos dos fármacos
Células-Tronco Embrionárias Murinas/efeitos dos fármacos
Placenta/efeitos dos fármacos
Teratogênios/toxicidade
Testes de Toxicidade/métodos
[Mh] Termos MeSH secundário: Oxirredutases do Álcool/genética
Oxirredutases do Álcool/metabolismo
Animais
Transporte Biológico
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular
Relação Dose-Resposta a Droga
Técnicas de Cultura Embrionária
Embrião de Mamíferos/metabolismo
Embrião de Mamíferos/patologia
Feminino
Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Seres Humanos
Cinética
Camundongos
Oxigenases de Função Mista/genética
Oxigenases de Função Mista/metabolismo
Células-Tronco Embrionárias Murinas/metabolismo
Células-Tronco Embrionárias Murinas/patologia
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/metabolismo
Miócitos Cardíacos/patologia
Placenta/metabolismo
Placenta/patologia
Gravidez
Reprodutibilidade dos Testes
Ácido Retinoico 4 Hidroxilase/genética
Ácido Retinoico 4 Hidroxilase/metabolismo
Medição de Risco
Esterol 14-Desmetilase/genética
Esterol 14-Desmetilase/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Azoles); 0 (Teratogens); EC 1.- (Mixed Function Oxygenases); EC 1.1.- (Alcohol Oxidoreductases); EC 1.1.1.71 (DHRS3 protein, mouse); EC 1.14.13.70 (Cyp51 protein, mouse); EC 1.14.13.70 (Sterol 14-Demethylase); EC 1.14.13.72 (methylsterol monooxygenase); EC 1.14.14.1 (Cyp26a1 protein, mouse); EC 1.14.14.1 (Retinoic Acid 4-Hydroxylase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE


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[PMID]:28461660
[Au] Autor:Nichols J; Jones K
[Ti] Título:Derivation of Mouse Embryonic Stem (ES) Cell Lines Using Small-Molecule Inhibitors of Erk and Gsk3 Signaling (2i).
[So] Source:Cold Spring Harb Protoc;2017(5):pdb.prot094086, 2017 May 01.
[Is] ISSN:1559-6095
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The efficiency of embryonic stem (ES) cell derivation is very high if embryos are incubated, from the eight-cell stage, in the presence of the two inhibitors of signaling via the Erk and Gsk3 pathways (PD0325901 and CHIR99021, respectively, known as "2i"). The success rate may vary, depending on the quality of the embryos and the speed with which they are processed, but it is not unusual to obtain ES cell lines from all embryos allocated to the study, even from the least permissive strains. Furthermore, ES cells can be efficiently obtained from any complex genetic mouse model or for in vitro analysis and additional genetic manipulation in any background of choice.
[Mh] Termos MeSH primário: MAP Quinases Reguladas por Sinal Extracelular/antagonistas & inibidores
Quinase 3 da Glicogênio Sintase/antagonistas & inibidores
Células-Tronco Embrionárias Murinas/citologia
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Benzamidas/farmacologia
Processos de Crescimento Celular
Linhagem Celular
Meios de Cultura
Difenilamina/análogos & derivados
Difenilamina/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Camundongos
Piridinas/farmacologia
Pirimidinas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzamides); 0 (Chir 99021); 0 (Culture Media); 0 (PD 0325901); 0 (Pyridines); 0 (Pyrimidines); 9N3CBB0BIQ (Diphenylamine); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 2.7.11.26 (Glycogen Synthase Kinase 3)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1101/pdb.prot094086


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[PMID]:29179218
[Au] Autor:Wang L; Cui Y; Liu Q; Song Y; Hu Q; Tang M; Hescheler J; Xi J
[Ad] Endereço:Department of Physiology and Chinese-German Stem Cell Center, School of Basic Medicine, Huazhong University of Science and Technology, The Key Laboratory for Drug Target Researches and Pharmacodynamic Evaluation of Hubei Province, Wuhan, China.
[Ti] Título:Puerarin Enhances Ca2+ Reuptake and Ca2+ Content of Sarcoplasmic Reticulum in Murine Embryonic Stem Cell-Derived Cardiomyocytes via Upregulation of SERCA2a.
[So] Source:Cell Physiol Biochem;44(3):1199-1212, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: The embryonic stem cell-derived cardiomyocytes (ES-CMs) serve as potential sources for cardiac regenerative therapy. However, the immature sarcoplasmic reticulum (SR) function of ES-CMs prevents its application. In this report, we examined the effect of puerarin, an isoflavone compound, on SR function of murine ES-CMs. METHODS: Murine ES-CMs were harvested by embryoid body-based differentiation method. Confocal calcium imaging and whole-cell patch clamps were performed to assess the function of SR. The mRNA expression levels of SR-related genes were examined by quantitative PCR. The protein expression of sarcoplasmic reticulum calcium-ATPase 2a (SERCA2a) was evaluated by immunofluorescent and western blot. RESULTS: Long-term application of puerarin promotes basic properties of spontaneous calcium transient with increased amplitude, decay velocity, and decreased duration. Puerarin fails to alter ICa,L but increases the Ca2+ content of SR. Puerarin-treated ES-CMs have intact SR Ca2+ cycling with more SR Ca2+ reuptake. Long-term application of puerarin asynchronously upregulates the mRNA and protein expression of SERCA2a, as well as the transcripts of calsequestrin and triadin in developing ES-CMs. Application of puerarin during the stage of post-cardiac differentiation upregulates dose-dependently the transcripts of SERCA2a, phospholamban and tridin which can be reversed by the inhibitors of the PI3K/Akt and MAPK/ERK signaling pathways, but shows no effect on the protein expression of SERCA2a. CONCLUSION: This study demonstrates that long-term puerarin treatment enhances Ca2+ reuptake and Ca2+ content via upregulation of SERCA2a.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Isoflavonas/farmacologia
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/metabolismo
Regulação para Cima/efeitos dos fármacos
Vasodilatadores/farmacologia
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Androstadienos/farmacologia
Animais
Benzamidas/farmacologia
Proteínas de Ligação ao Cálcio/metabolismo
Calsequestrina/genética
Calsequestrina/metabolismo
Proteínas de Transporte/genética
Proteínas de Transporte/metabolismo
Diferenciação Celular/efeitos dos fármacos
Difenilamina/análogos & derivados
Difenilamina/farmacologia
Camundongos
Microscopia Confocal
Células-Tronco Embrionárias Murinas/citologia
Proteínas Musculares/genética
Proteínas Musculares/metabolismo
Miócitos Cardíacos/citologia
Miócitos Cardíacos/metabolismo
Técnicas de Patch-Clamp
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Retículo Sarcoplasmático/metabolismo
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/antagonistas & inibidores
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/genética
Transdução de Sinais/efeitos dos fármacos
Tapsigargina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Androstadienes); 0 (Benzamides); 0 (Calcium-Binding Proteins); 0 (Calsequestrin); 0 (Carrier Proteins); 0 (Isoflavones); 0 (Muscle Proteins); 0 (PD 0325901); 0 (Vasodilator Agents); 0 (phospholamban); 0 (triadin); 67526-95-8 (Thapsigargin); 9N3CBB0BIQ (Diphenylamine); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.6.3.8 (Sarcoplasmic Reticulum Calcium-Transporting ATPases); SY7Q814VUP (Calcium); XVA4O219QW (wortmannin); Z9W8997416 (puerarin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1159/000485450


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[PMID]:27770834
[Au] Autor:Rao Y; Cui J; Yin L; Liu W; Liu W; Sun M; Yan X; Wang L; Chen F
[Ad] Endereço:Laboratory of Tissue Engineering, College of Life Sciences, Northwest University, Taibai North Rd 229, Xi'an, Shaanxi Province, 710069, People's Republic of China.
[Ti] Título:Preclinical study of mouse pluripotent parthenogenetic embryonic stem cell derivatives for the construction of tissue-engineered skin equivalent.
[So] Source:Stem Cell Res Ther;7(1):156, 2016 10 22.
[Is] ISSN:1757-6512
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Embryonic stem cell (ESC) derivatives hold great promise for the construction of tissue-engineered skin equivalents (TESE). However, harvesting of ESCs destroys viable embryos and may lead to political and ethical concerns over their application. In the current study, we directed mouse parthenogenetic embryonic stem cells (pESCs) to differentiate into fibroblasts, constructed TESE, and evaluated its function in vivo. METHODS: The stemness marker expression and the pluripotent differentiation ability of pESCs were tested. After embryoid body (EB) formation and adherence culture, mesenchymal stem cells (MSCs) were enriched and directed to differentiate into fibroblastic lineage. Characteristics of derived fibroblasts were assessed by quantitative real-time PCR and ELISA. Functional ability of the constructed TESE was tested by a mouse skin defects repair model. RESULTS: Mouse pESCs expressed stemness marker and could form teratoma containing three germ layers. MSCs could be enriched from outgrowths of EBs and directed to differentiate into fibroblastic lineage. These cells express a high level of growth factors including FGF, EGF, VEGF, TGF, PDGF, and IGF1, similar to those of ESC-derived fibroblasts and mouse fibroblasts. Seeded into collagen gels, the fibroblasts derived from pESCs could form TESE. Mouse skin defects could be successfully repaired 15 days after transplantation of TESE constructed by fibroblasts derived from pESCs. CONCLUSIONS: pESCs could be induced to differentiate into fibroblastic lineage, which could be applied to the construction of TESE and skin defect repair. Particularly, pESC derivatives avoid the limitations of political and ethical concerns, and provide a promising source for regenerative medicine.
[Mh] Termos MeSH primário: Células-Tronco Embrionárias Murinas/citologia
Partenogênese/fisiologia
Pele/citologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/fisiologia
Linhagem da Célula/fisiologia
Corpos Embrioides/citologia
Corpos Embrioides/metabolismo
Fibroblastos/citologia
Fibroblastos/metabolismo
Camadas Germinativas/citologia
Camadas Germinativas/metabolismo
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Células-Tronco Embrionárias Murinas/metabolismo
Medicina Regenerativa/métodos
Pele/metabolismo
Engenharia Tecidual/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Intercellular Signaling Peptides and Proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:27773674
[Au] Autor:Rafiee MR; Girardot C; Sigismondo G; Krijgsveld J
[Ad] Endereço:German Cancer Research Center (DKFZ), Im Neuenheimer Feld 581, 69120 Heidelberg, Germany; Excellence Cluster CellNetworks, Heidelberg University, 69120 Heidelberg, Germany; European Molecular Biology Laboratory (EMBL), Genome Biology Unit, Meyerhofstrasse 1, 69117 Heidelberg, Germany.
[Ti] Título:Expanding the Circuitry of Pluripotency by Selective Isolation of Chromatin-Associated Proteins.
[So] Source:Mol Cell;64(3):624-635, 2016 Nov 03.
[Is] ISSN:1097-4164
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Maintenance of pluripotency is regulated by a network of transcription factors coordinated by Oct4, Sox2, and Nanog (OSN), yet a systematic investigation of the composition and dynamics of the OSN protein network specifically on chromatin is still missing. Here we have developed a method combining ChIP with selective isolation of chromatin-associated proteins (SICAP) followed by mass spectrometry to identify chromatin-bound partners of a protein of interest. ChIP-SICAP in mouse embryonic stem cells (ESCs) identified over 400 proteins associating with OSN, including several whose interaction depends on the pluripotent state. Trim24, a previously unrecognized protein in the network, converges with OSN on multiple enhancers and suppresses the expression of developmental genes while activating cell cycle genes. Consistently, Trim24 significantly improved efficiency of cellular reprogramming, demonstrating its direct functionality in establishing pluripotency. Collectively, ChIP-SICAP provides a powerful tool to decode chromatin protein composition, further enhanced by its integrative capacity to perform ChIP-seq.
[Mh] Termos MeSH primário: Cromatina/química
Células-Tronco Embrionárias Murinas/metabolismo
Proteína Homeobox Nanog/genética
Proteínas Nucleares/genética
Fator 3 de Transcrição de Octâmero/genética
Células-Tronco Pluripotentes/metabolismo
Fatores de Transcrição SOXB1/genética
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação
Diferenciação Celular
Reprogramação Celular
Cromatina/metabolismo
Imunoprecipitação da Cromatina/métodos
Perfilação da Expressão Gênica
Regulação da Expressão Gênica
Marcação por Isótopo
Espectrometria de Massas/métodos
Camundongos
Células-Tronco Embrionárias Murinas/citologia
Proteína Homeobox Nanog/metabolismo
Proteínas Nucleares/metabolismo
Fator 3 de Transcrição de Octâmero/metabolismo
Células-Tronco Pluripotentes/citologia
Ligação Proteica
Fatores de Transcrição SOXB1/metabolismo
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chromatin); 0 (Nanog Homeobox Protein); 0 (Nanog protein, mouse); 0 (Nuclear Proteins); 0 (Octamer Transcription Factor-3); 0 (Pou5f1 protein, mouse); 0 (SOXB1 Transcription Factors); 0 (Sox2 protein, mouse); 0 (Transcription Factors); 0 (transcriptional intermediary factor 1)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180114
[Lr] Data última revisão:
180114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161105
[St] Status:MEDLINE


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[PMID]:28455373
[Au] Autor:Matsuda K; Mikami T; Oki S; Iida H; Andrabi M; Boss JM; Yamaguchi K; Shigenobu S; Kondoh H
[Ad] Endereço:Graduate School of Frontier Biosciences, Osaka University, Yamadaoka 1-3, Suita, Osaka 565-0871, Japan.
[Ti] Título:ChIP-seq analysis of genomic binding regions of five major transcription factors highlights a central role for ZIC2 in the mouse epiblast stem cell gene regulatory network.
[So] Source:Development;144(11):1948-1958, 2017 06 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:To obtain insight into the transcription factor (TF)-dependent regulation of epiblast stem cells (EpiSCs), we performed ChIP-seq analysis of the genomic binding regions of five major TFs. Analysis of biotinylated ZIC2, OTX2, SOX2, POU5F1 and POU3F1 binding in EpiSCs identified several new features. (1) Megabase-scale genomic domains rich in ZIC2 peaks and genes alternate with those rich in POU3F1 but sparse in genes, reflecting the clustering of regulatory regions that act at short and long-range, which involve binding of ZIC2 and POU3F1, respectively. (2) The enhancers bound by ZIC2 and OTX2 prominently regulate TF genes in EpiSCs. (3) The binding sites for SOX2 and POU5F1 in mouse embryonic stem cells (ESCs) and EpiSCs are divergent, reflecting the shift in the major acting TFs from SOX2/POU5F1 in ESCs to OTX2/ZIC2 in EpiSCs. (4) This shift in the major acting TFs appears to be primed by binding of ZIC2 in ESCs at relevant genomic positions that later function as enhancers following the disengagement of SOX2/POU5F1 from major regulatory functions and subsequent binding by OTX2. These new insights into EpiSC gene regulatory networks gained from this study are highly relevant to early stage embryogenesis.
[Mh] Termos MeSH primário: Imunoprecipitação da Cromatina
Regulação da Expressão Gênica no Desenvolvimento
Redes Reguladoras de Genes
Camadas Germinativas/citologia
Células-Tronco Embrionárias Murinas/metabolismo
Análise de Sequência de RNA
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Animais
Sítios de Ligação/genética
Biotinilação
Genoma
Camadas Germinativas/metabolismo
Seres Humanos
Camundongos
Células-Tronco Embrionárias Murinas/citologia
Fator 3 de Transcrição de Octâmero/metabolismo
Fatores de Transcrição Otx/metabolismo
Ligação Proteica
Fatores de Transcrição SOXB1/metabolismo
Fatores de Transcrição/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Octamer Transcription Factor-3); 0 (Otx Transcription Factors); 0 (Otx2 protein, mouse); 0 (Pou5f1 protein, mouse); 0 (SOXB1 Transcription Factors); 0 (Transcription Factors); 0 (Zic2 protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.1242/dev.143479


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[PMID]:28468752
[Au] Autor:Zhou F; Xie F; Jin K; Zhang Z; Clerici M; Gao R; van Dinther M; Sixma TK; Huang H; Zhang L; Ten Dijke P
[Ad] Endereço:Life Sciences Institute and Innovation Center for Cell Signaling Network, Zhejiang University, Hangzhou, China.
[Ti] Título:USP4 inhibits SMAD4 monoubiquitination and promotes activin and BMP signaling.
[So] Source:EMBO J;36(11):1623-1639, 2017 06 01.
[Is] ISSN:1460-2075
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:SMAD4 is a common intracellular effector for TGF-ß family cytokines, but the mechanism by which its activity is dynamically regulated is unclear. We demonstrated that ubiquitin-specific protease (USP) 4 strongly induces activin/BMP signaling by removing the inhibitory monoubiquitination from SMAD4. This modification was triggered by the recruitment of the E3 ligase, SMURF2, to SMAD4 following ligand-induced regulatory (R)-SMAD-SMAD4 complex formation. Whereas the interaction of the negative regulator c-SKI inhibits SMAD4 monoubiquitination, the ligand stimulates the recruitment of SMURF2 to the c-SKI-SMAD2 complex and triggers c-SKI ubiquitination and degradation. Thus, SMURF2 has a role in termination and initiation of TGF-ß family signaling. An increase in monoubiquitinated SMAD4 in USP4-depleted mouse embryonic stem cells (mESCs) decreased both the BMP- and activin-induced changes in the embryonic stem cell fate. USP4 sustained SMAD4 activity during activin- and BMP-mediated morphogenic events in early zebrafish embryos. Moreover, zebrafish depleted of USP4 exhibited defective cell migration and slower coordinated cell movement known as epiboly, both of which could be rescued by SMAD4. Therefore, USP4 is a critical determinant of SMAD4 activity.
[Mh] Termos MeSH primário: Receptores de Proteínas Morfogenéticas Ósseas/metabolismo
Subunidades beta de Inibinas/metabolismo
Processamento de Proteína Pós-Traducional
Proteínas Proto-Oncogênicas/metabolismo
Transdução de Sinais
Proteína Smad4/metabolismo
Ubiquitina Tiolesterase/metabolismo
Ubiquitinação
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Movimento Celular
Células Cultivadas
Seres Humanos
Camundongos
Células-Tronco Embrionárias Murinas/fisiologia
Ubiquitina-Proteína Ligases/metabolismo
Proteases Específicas de Ubiquitina
Peixe-Zebra/embriologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins); 0 (Smad4 Protein); 0 (Smad4 protein, mouse); 0 (inhibin beta A subunit); 93443-12-0 (Inhibin-beta Subunits); EC 2.3.2.26 (Smurf2 protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.11.30 (Bone Morphogenetic Protein Receptors); EC 3.1.2.15 (Usp4 protein, mouse); EC 3.4.19.12 (Ubiquitin Thiolesterase); EC 3.4.19.12 (Ubiquitin-Specific Proteases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:180106
[Lr] Data última revisão:
180106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.15252/embj.201695372



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