Base de dados : MEDLINE
Pesquisa : G02.111.570.080.689.330.700 [Categoria DeCS]
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  1 / 8048 MEDLINE  
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[PMID]:29253128
[Au] Autor:Mohácsik P; Erdélyi F; Baranyi M; Botz B; Szabó G; Tóth M; Haltrich I; Helyes Z; Sperlágh B; Tóth Z; Sinkó R; Lechan RM; Bianco AC; Fekete C; Gereben B
[Ad] Endereço:Department of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary.
[Ti] Título:A Transgenic Mouse Model for Detection of Tissue-Specific Thyroid Hormone Action.
[So] Source:Endocrinology;159(2):1159-1171, 2018 02 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thyroid hormone (TH) is present in the systemic circulation and thus should affect all cells similarly in the body. However, tissues have a complex machinery that allows tissue-specific optimization of local TH action that calls for the assessment of TH action in a tissue-specific manner. Here, we report the creation of a TH action indicator (THAI) mouse model to study tissue-specific TH action. The model uses a firefly luciferase reporter readout in the context of an intact transcriptional apparatus and all elements of TH metabolism and transport and signaling. The THAI mouse allows the assessment of the changes of TH signaling in tissue samples or in live animals using bioluminescence, both in hypothyroidism and hyperthyroidism. Beyond pharmacologically manipulated TH levels, the THAI mouse is sufficiently sensitive to detect deiodinase-mediated changes of TH action in the interscapular brown adipose tissue (BAT) that preserves thermal homeostasis during cold stress. The model revealed that in contrast to the cold-induced changes of TH action in the BAT, the TH action in this tissue, at room temperature, is independent of noradrenergic signaling. Our data demonstrate that the THAI mouse can also be used to test TH receptor isoform-specific TH action. Thus, THAI mouse constitutes a unique model to study tissue-specific TH action within a physiological/pathophysiological context and test the performance of thyromimetics. In conclusion, THAI mouse provides an in vivo model to assess a high degree of tissue specificity of TH signaling, allowing alteration of tissue function in health and disease, independently of changes in circulating levels of TH.
[Mh] Termos MeSH primário: Genes Reporter
Elementos de Resposta
Hormônios Tireóideos/farmacologia
Hormônios Tireóideos/fisiologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Feminino
Regulação da Expressão Gênica
Células HEK293
Seres Humanos
Hipertireoidismo/genética
Hipertireoidismo/metabolismo
Hipotireoidismo/genética
Hipotireoidismo/metabolismo
Iodeto Peroxidase/genética
Iodeto Peroxidase/metabolismo
Masculino
Camundongos
Camundongos Transgênicos
Modelos Animais
Especificidade de Órgãos/efeitos dos fármacos
Especificidade de Órgãos/genética
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Thyroid Hormones); EC 1.11.1.8 (Iodide Peroxidase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180215
[Lr] Data última revisão:
180215
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00582


  2 / 8048 MEDLINE  
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[PMID]:28458340
[Au] Autor:Kume T
[Ad] Endereço:Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University.
[Ti] Título:Therapeutic Potential of the Activators of the Nuclear Factor Erythroid 2-Related Factor 2-Antioxidant Response Element Pathway in Brain Disorders.
[So] Source:Biol Pharm Bull;40(5):553-556, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Oxidative stress is recognized as an important mediator of brain disorders. Nevertheless, there are few antioxidants approved for brain diseases. There are two types of mechanisms as antioxidant systems in vivo, antioxidants and antioxidant enzymes. Antioxidants are consumed by the reaction with reactive oxygen species. Thus, it is important to maintain high concentrations at the requisite site. On the other hand, antioxidant capacity is maintained for around a half-day to one day once antioxidant enzymes are induced. Therefore, low molecular-weight compounds that could induce antioxidant enzymes are considered to be suitable for the treatment and prevention of brain diseases. The nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) pathway is known as a system for inducing these antioxidant enzymes. Here, the potential for low molecular-weight compounds capable of activating the Nrf2-ARE pathway to become therapeutic agents for brain diseases is discussed.
[Mh] Termos MeSH primário: Antioxidantes/metabolismo
Encefalopatias/tratamento farmacológico
Fator 2 Relacionado a NF-E2/agonistas
Elementos de Resposta/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Encefalopatias/genética
Seres Humanos
Fator 2 Relacionado a NF-E2/genética
Transdução de Sinais/efeitos dos fármacos
Transdução de Sinais/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antioxidants); 0 (NF-E2-Related Factor 2); 0 (NFE2L2 protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b17-00091


  3 / 8048 MEDLINE  
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[PMID]:29273554
[Au] Autor:Shuwen H; Qing Z; Yan Z; Xi Y
[Ad] Endereço:Department of Medical Oncology, Huzhou Central Hospital, Huzhou, Zhejiang Province, China.
[Ti] Título:Competitive endogenous RNA in colorectal cancer: A systematic review.
[So] Source:Gene;645:157-162, 2018 Mar 01.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Colorectal cancer is one of the most common malignant tumours. Competitive endogenous RNA (ceRNA) networks have been hypothesized, in which various RNAs regulate each other's expression using microRNA response elements (MREs). Recent evidence has highlighted the crucial regulatory roles of ceRNA networks in colorectal cancer. In this review, we summarize the present research methods as well as the currently known ceRNA competitors and targets in colorectal cancer. In addition, we discuss the significance of ceRNA and shortcomings of current studies of colorectal cancer.
[Mh] Termos MeSH primário: Neoplasias Colorretais/genética
Pseudogenes/genética
RNA Longo não Codificante/genética
RNA/genética
[Mh] Termos MeSH secundário: Regulação Neoplásica da Expressão Gênica
Redes Reguladoras de Genes
Seres Humanos
MicroRNAs/genética
Elementos de Resposta
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (MicroRNAs); 0 (RNA, Long Noncoding); 0 (RNA, circular); 63231-63-0 (RNA)
[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:171224
[St] Status:MEDLINE


  4 / 8048 MEDLINE  
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[PMID]:29283230
[Ti] Título:Canonical and Noncanonical Mechanisms of Glucocorticoid Stress Hormones Action.
[So] Source:Usp Fiziol Nauk;47(3):59-69, 2016 Jul-Sep.
[Is] ISSN:0301-1798
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Hormones of stress, glucocorticoids, regulate numerous physiological processes and functions. These hormonal effects involve diverse mechanisms of action. Glucocorticoid receptors (GRs) are transcription factors which regulate gene expression by canonical mechanism of the hormone action through interaction with specific nucleotide sequence (GRE) in the regulatory region of the gene. The effects of the canonical mechanism develop for several hours. Non-genomic rapid effects of the hormone emerged in seconds- minuets and supposed to be associated with yet not identified receptor in the plasma membrane. In addition to these slow and rapid hormonal actions, one more slow non-canonical mechanism of glucocorticoid action become increasingly evident. This mechanism is based on protein-protein interactions of GRs with other transcription factors. The main modern concepts of canonical, non-canonical and membrane mechanisms of hormone action are discussed in the review.
[Mh] Termos MeSH primário: Membrana Celular/metabolismo
Células Eucarióticas/metabolismo
Glucocorticoides/metabolismo
NF-kappa B/metabolismo
Receptores de Glucocorticoides/metabolismo
Fator de Transcrição AP-1/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Eucarióticas/citologia
Regulação da Expressão Gênica
Glucocorticoides/genética
Seres Humanos
NF-kappa B/genética
Ligação Proteica
Mapeamento de Interação de Proteínas
Receptores de Glucocorticoides/genética
Elementos de Resposta
Transdução de Sinais
Estresse Fisiológico
Fatores de Tempo
Fator de Transcrição AP-1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Glucocorticoids); 0 (NF-kappa B); 0 (Receptors, Glucocorticoid); 0 (Transcription Factor AP-1)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171229
[St] Status:MEDLINE


  5 / 8048 MEDLINE  
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[PMID]:28747434
[Au] Autor:Sallon C; Callebaut I; Boulay I; Fontaine J; Logeart-Avramoglou D; Henriquet C; Pugnière M; Cayla X; Monget P; Harichaux G; Labas V; Canepa S; Taragnat C
[Ad] Endereço:From the Unité Physiologie de la Reproduction et des Comportements, UMR85, Institut National de la Recherche Agronomique, CNRS, Institut Français du Cheval et de l'Equitation, Université de Tours, F-37380 Nouzilly, France.
[Ti] Título:Thrombospondin-1 (TSP-1), a new bone morphogenetic protein-2 and -4 (BMP-2/4) antagonist identified in pituitary cells.
[So] Source:J Biol Chem;292(37):15352-15368, 2017 09 15.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bone morphogenetic proteins (BMPs) regulate diverse cellular responses during embryogenesis and in adulthood including cell differentiation, proliferation, and death in various tissues. In the adult pituitary, BMPs participate in the control of hormone secretion and cell proliferation, suggesting a potential endocrine/paracrine role for BMPs, but some of the mechanisms are unclear. Here, using a bioactivity test based on embryonic cells (C3H10T1/2) transfected with a BMP-responsive element, we sought to determine whether pituitary cells secrete BMPs or BMP antagonists. Interestingly, we found that pituitary-conditioned medium contains a factor that inhibits action of BMP-2 and -4. Combining surface plasmon resonance and high-resolution mass spectrometry helped pinpoint this factor as thrombospondin-1 (TSP-1). Surface plasmon resonance and co-immunoprecipitation confirmed that recombinant human TSP-1 can bind BMP-2 and -4 and antagonize their effects on C3H10T1/2 cells. Moreover, TSP-1 inhibited the action of serum BMPs. We also report that the von Willebrand type C domain of TSP-1 is likely responsible for this BMP-2/4-binding activity, an assertion based on sequence similarity that TSP-1 shares with the von Willebrand type C domain of Crossveinless 2 (CV-2), a BMP antagonist and member of the chordin family. In summary, we identified for the first time TSP-1 as a BMP-2/-4 antagonist and presented a structural basis for the physical interaction between TSP-1 and BMP-4. We propose that TSP-1 could regulate bioavailability of BMPs, either produced locally or reaching the pituitary via blood circulation. In conclusion, our findings provide new insights into the involvement of TSP-1 in the BMP-2/-4 mechanisms of action.
[Mh] Termos MeSH primário: Proteína Morfogenética Óssea 2/antagonistas & inibidores
Proteína Morfogenética Óssea 4/antagonistas & inibidores
Modelos Moleculares
Hipófise/secreção
Elementos de Resposta
Trombospondina 1/secreção
[Mh] Termos MeSH secundário: Animais
Animais Endogâmicos
Proteína Morfogenética Óssea 2/sangue
Proteína Morfogenética Óssea 2/genética
Proteína Morfogenética Óssea 2/metabolismo
Proteína Morfogenética Óssea 4/sangue
Proteína Morfogenética Óssea 4/genética
Proteína Morfogenética Óssea 4/metabolismo
Linhagem Celular
Células Cultivadas
Biologia Computacional
Feminino
Genes Reporter
Seres Humanos
Camundongos
Hipófise/citologia
Hipófise/metabolismo
Domínios e Motivos de Interação entre Proteínas
Proteínas Recombinantes de Fusão/química
Proteínas Recombinantes de Fusão/isolamento & purificação
Proteínas Recombinantes de Fusão/metabolismo
Proteínas Recombinantes/química
Proteínas Recombinantes/metabolismo
Homologia de Sequência de Aminoácidos
Carneiro Doméstico
Trombospondina 1/química
Trombospondina 1/isolamento & purificação
Trombospondina 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (BMP2 protein, human); 0 (BMP4 protein, human); 0 (Bone Morphogenetic Protein 2); 0 (Bone Morphogenetic Protein 4); 0 (Recombinant Fusion Proteins); 0 (Recombinant Proteins); 0 (Thrombospondin 1); 0 (thrombospondin-1, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171230
[Lr] Data última revisão:
171230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.736207


  6 / 8048 MEDLINE  
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[PMID]:27777301
[Au] Autor:Liu X; Cai X; Hu B; Mei Z; Zhang D; Ouyang G; Wang J; Zhang W; Xiao W
[Ad] Endereço:From the Key Laboratory of Aquatic Biodiversity and Conservation and.
[Ti] Título:Forkhead Transcription Factor 3a (FOXO3a) Modulates Hypoxia Signaling via Up-regulation of the von Hippel-Lindau Gene (VHL).
[So] Source:J Biol Chem;291(49):25692-25705, 2016 Dec 02.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:FOXO3a, a member of the forkhead homeobox type O (FOXO) family of transcriptional factors, regulates cell survival in response to DNA damage, caloric restriction, and oxidative stress. The von Hippel-Lindau (VHL) tumor suppressor gene encodes a component of the E3 ubiquitin ligase complex that mediates hypoxia-inducible factor α degradation under aerobic conditions, thus acting as one of the key regulators of hypoxia signaling. However, whether FOXO3a impacts cellular hypoxia stress remains unknown. Here we show that FOXO3a directly binds to the VHL promoter and up-regulates VHL expression. Using a zebrafish model, we confirmed the up-regulation of vhl by foxo3b, an ortholog of mammalian FOXO3a Furthermore, by employing the clustered regularly interspaced short palindromic repeats (CRISPR)-associated RNA-guided endonuclease Cas9 (CRISPR/Cas9) technology, we deleted foxo3b in zebrafish and determined that expression of hypoxia-inducible genes was affected under hypoxia. Moreover, foxo3b-null zebrafish exhibited impaired acute hypoxic tolerance, resulting in death. In conclusion, our findings suggest that, by modulating hypoxia-inducible factor activity via up-regulation of VHL, FOXO3a (foxo3b) plays an important role in survival in response to hypoxic stress.
[Mh] Termos MeSH primário: Proteína Forkhead Box O3/metabolismo
Elementos de Resposta
Transdução de Sinais
Proteínas Supressoras de Tumor/biossíntese
Regulação para Cima
Proteína Supressora de Tumor Von Hippel-Lindau/biossíntese
Proteínas de Peixe-Zebra/biossíntese
Peixe-Zebra/metabolismo
[Mh] Termos MeSH secundário: Animais
Hipóxia Celular
Proteína Forkhead Box O3/genética
Células HEK293
Seres Humanos
Proteínas Supressoras de Tumor/genética
Proteína Supressora de Tumor Von Hippel-Lindau/genética
Peixe-Zebra/genética
Proteínas de Peixe-Zebra/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FOXO3 protein, human); 0 (Forkhead Box Protein O3); 0 (Tumor Suppressor Proteins); 0 (Vhl protein, zebrafish); 0 (Zebrafish Proteins); EC 2.3.2.27 (Von Hippel-Lindau Tumor Suppressor Protein); EC 6.3.2.- (VHL protein, human)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171202
[Lr] Data última revisão:
171202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


  7 / 8048 MEDLINE  
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[PMID]:29045464
[Au] Autor:Rajagopalan D; Pandey AK; Xiuzhen MC; Lee KK; Hora S; Zhang Y; Chua BH; Kwok HS; Bhatia SS; Deng LW; Tenen DG; Kappei D; Jha S
[Ad] Endereço:Cancer Science Institute of Singapore, National University of Singapore, Singapore.
[Ti] Título:TIP60 represses telomerase expression by inhibiting Sp1 binding to the TERT promoter.
[So] Source:PLoS Pathog;13(10):e1006681, 2017 Oct.
[Is] ISSN:1553-7374
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:HIV1-TAT interactive protein (TIP60) is a haploinsufficient tumor suppressor. However, the potential mechanisms endowing its tumor suppressor ability remain incompletely understood. It plays a vital role in virus-induced cancers where TIP60 down-regulates the expression of human papillomavirus (HPV) oncoprotein E6 which in turn destabilizes TIP60. This intrigued us to identify the role of TIP60, in the context of a viral infection, where it is targeted by oncoproteins. Through an array of molecular biology techniques such as Chromatin immunoprecipitation, expression analysis and mass spectrometry, we establish the hitherto unknown role of TIP60 in repressing the expression of the catalytic subunit of the human telomerase complex, TERT, a key driver for immortalization. TIP60 acetylates Sp1 at K639, thus inhibiting Sp1 binding to the TERT promoter. We identified that TIP60-mediated growth suppression of HPV-induced cervical cancer is mediated in part due to TERT repression through Sp1 acetylation. In summary, our study has identified a novel substrate for TIP60 catalytic activity and a unique repressive mechanism acting at the TERT promoter in virus-induced malignancies.
[Mh] Termos MeSH primário: Regulação Enzimológica da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Histona Acetiltransferases/metabolismo
Proteínas de Neoplasias/metabolismo
Elementos de Resposta
Fator de Transcrição Sp1/metabolismo
Telomerase/biossíntese
Neoplasias do Colo do Útero/metabolismo
[Mh] Termos MeSH secundário: Feminino
Células HeLa
Histona Acetiltransferases/genética
Seres Humanos
Lisina Acetiltransferase 5
Proteínas de Neoplasias/genética
Fator de Transcrição Sp1/genética
Telomerase/genética
Neoplasias do Colo do Útero/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Neoplasm Proteins); 0 (Sp1 Transcription Factor); 0 (Sp1 protein, human); EC 2.3.1.48 (Histone Acetyltransferases); EC 2.3.1.48 (KAT5 protein, human); EC 2.3.1.48 (Lysine Acetyltransferase 5); EC 2.7.7.49 (TERT protein, human); EC 2.7.7.49 (Telomerase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171019
[St] Status:MEDLINE
[do] DOI:10.1371/journal.ppat.1006681


  8 / 8048 MEDLINE  
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[PMID]:29023469
[Au] Autor:Choi SH; Severson E; Pear WS; Liu XS; Aster JC; Blacklow SC
[Ad] Endereço:Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA, United States of America.
[Ti] Título:The common oncogenomic program of NOTCH1 and NOTCH3 signaling in T-cell acute lymphoblastic leukemia.
[So] Source:PLoS One;12(10):e0185762, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Notch is a major oncogenic driver in T cell acute lymphoblastic leukemia (T-ALL), in part because it binds to an enhancer that increases expression of MYC. Here, we exploit the capacity of activated NOTCH1 and NOTCH3 to induce T-ALL, despite substantial divergence in their intracellular regions, as a means to elucidate a broad, common Notch-dependent oncogenomic program through systematic comparison of the transcriptomes and Notch-bound genomic regulatory elements of NOTCH1- and NOTCH3-dependent T-ALL cells. ChIP-seq studies show a high concordance of functional NOTCH1 and NOTCH3 genomic binding sites that are enriched in binding motifs for RBPJ, the transcription factor that recruits activated Notch to DNA. The interchangeability of NOTCH1 and NOTCH3 was confirmed by rescue of NOTCH1-dependent T-ALL cells with activated NOTCH3 and vice versa. Despite remarkable overall similarity, there are nuanced differences in chromatin landscapes near critical common Notch target genes, most notably at a Notch-dependent enhancer that regulates MYC, which correlates with responsiveness to Notch pathway inhibitors. Overall, a common oncogenomic program driven by binding of either Notch is sufficient to maintain T-ALL cell growth, whereas cell-context specific differences appear to influence the response of T-ALL cells to Notch inhibition.
[Mh] Termos MeSH primário: Leucemia-Linfoma Linfoblástico de Células T Precursoras/metabolismo
Receptor Notch1/metabolismo
Receptor Notch3/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Regulação Leucêmica da Expressão Gênica
Seres Humanos
Proteína de Ligação a Sequências Sinal de Recombinação J de Imunoglobina/biossíntese
Proteína de Ligação a Sequências Sinal de Recombinação J de Imunoglobina/genética
Leucemia-Linfoma Linfoblástico de Células T Precursoras/genética
Proteínas Proto-Oncogênicas c-myc/biossíntese
Proteínas Proto-Oncogênicas c-myc/genética
Receptor Notch1/genética
Receptor Notch3/genética
Elementos de Resposta
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Immunoglobulin J Recombination Signal Sequence-Binding Protein); 0 (MYC protein, human); 0 (NOTCH1 protein, human); 0 (NOTCH3 protein, human); 0 (Proto-Oncogene Proteins c-myc); 0 (RBPJ protein, human); 0 (Receptor, Notch1); 0 (Receptor, Notch3)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171022
[Lr] Data última revisão:
171022
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171013
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185762


  9 / 8048 MEDLINE  
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[PMID]:28912063
[Au] Autor:Liu L; Song Y; Xu J; Li D; Li G; An L
[Ad] Endereço:Ministry of Education Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, Lanzhou 730000, China.
[Ti] Título:Differential expression by chromatin modifications of alcohol dehydrogenase 1 of Chorispora bungeana in cold stress.
[So] Source:Gene;636:1-16, 2017 Dec 15.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Epigenetic modifications regulate plant genes to cope with a variety of environmental stresses. Chorispora bungeana is an alpine subnival plant with strong tolerance to multiple abiotic stresses, especially cold stress. In this study, we characterized the alcohol dehydrogenase 1 gene from Chorispora bungeana, CbADH1, that is up-regulated in cold conditions. Overexpression of CbADH1 in Arabidopsis thaliana improved cold tolerance, as indicated by a decreased lethal temperature (LT50). Chromatin immunoprecipitation assays showed that histone H3 is removed from the promoter region and the middle-coding region of the gene. H3K9 acetylation and H3K4 trimethylation increased throughout the gene and in the proximal promoter region, respectively. Moreover, increased Ser5P and Ser2P polymerase II accumulation further indicated changes in the transcription initiation and elongation of CbADH1 were due to the cold stress. Taken together, our results suggested that CbADH1 is highly expressed during cold stress, and is regulated by epigenetic modifications. This study expands our understanding of the regulation of gene expression by epigenetic modifications in response to environmental cues.
[Mh] Termos MeSH primário: Álcool Desidrogenase/genética
Brassicaceae/enzimologia
Resposta ao Choque Frio/genética
Proteínas de Plantas/genética
[Mh] Termos MeSH secundário: Álcool Desidrogenase/química
Álcool Desidrogenase/metabolismo
Sequência de Aminoácidos
Arabidopsis/genética
Brassicaceae/genética
Cromatina/metabolismo
Clonagem Molecular
Sequência Conservada
Histonas/metabolismo
Folhas de Planta/enzimologia
Proteínas de Plantas/química
Proteínas de Plantas/metabolismo
RNA Polimerase II/metabolismo
Elementos de Resposta
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chromatin); 0 (Histones); 0 (Plant Proteins); EC 1.1.1.1 (Alcohol Dehydrogenase); EC 2.7.7.- (RNA Polymerase II)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE


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[PMID]:28825728
[Au] Autor:Xiao J; Jin R; Yu X; Shen M; Wagner JD; Pai A; Song C; Zhuang M; Klasfeld S; He C; Santos AM; Helliwell C; Pruneda-Paz JL; Kay SA; Lin X; Cui S; Garcia MF; Clarenz O; Goodrich J; Zhang X; Austin RS; Bonasio R; Wagner D
[Ad] Endereço:Department of Biology, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
[Ti] Título:Cis and trans determinants of epigenetic silencing by Polycomb repressive complex 2 in Arabidopsis.
[So] Source:Nat Genet;49(10):1546-1552, 2017 Oct.
[Is] ISSN:1546-1718
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Disruption of gene silencing by Polycomb protein complexes leads to homeotic transformations and altered developmental-phase identity in plants. Here we define short genomic fragments, known as Polycomb response elements (PREs), that direct Polycomb repressive complex 2 (PRC2) placement at developmental genes regulated by silencing in Arabidopsis thaliana. We identify transcription factor families that bind to these PREs, colocalize with PRC2 on chromatin, physically interact with and recruit PRC2, and are required for PRC2-mediated gene silencing in vivo. Two of the cis sequence motifs enriched in the PREs are cognate binding sites for the identified transcription factors and are necessary and sufficient for PRE activity. Thus PRC2 recruitment in Arabidopsis relies in large part on binding of trans-acting factors to cis-localized DNA sequence motifs.
[Mh] Termos MeSH primário: Proteínas de Arabidopsis/fisiologia
Arabidopsis/genética
Repressão Epigenética/genética
Regulação da Expressão Gênica de Plantas
Inativação Gênica
Complexo Repressor Polycomb 2/fisiologia
Proteínas do Grupo Polycomb/fisiologia
Elementos de Resposta/genética
[Mh] Termos MeSH secundário: Motivos de Aminoácidos
Arabidopsis/metabolismo
Proteínas de Arabidopsis/biossíntese
Proteínas de Arabidopsis/genética
Sítios de Ligação
DNA de Plantas/genética
DNA de Plantas/metabolismo
Flores/crescimento & desenvolvimento
Ontologia Genética
Ensaios de Triagem em Larga Escala
Família Multigênica
Folhas de Planta/ultraestrutura
Plantas Geneticamente Modificadas
Ligação Proteica
Mapeamento de Interação de Proteínas
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arabidopsis Proteins); 0 (DNA, Plant); 0 (Polycomb-Group Proteins); 0 (Transcription Factors); EC 2.1.1.43 (Polycomb Repressive Complex 2)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170822
[St] Status:MEDLINE
[do] DOI:10.1038/ng.3937



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