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  1 / 8048 MEDLINE  
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PMID:29253128
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
Dirección:Department of Endocrine Neurobiology, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary.
Título:A Transgenic Mouse Model for Detection of Tissue-Specific Thyroid Hormone Action.
Fuente:Endocrinology; 159(2):1159-1171, 2018 02 01.
ISSN:1945-7170
País de publicación:United States
Idioma:eng
Resumen: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.
Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nombre de substancia:0 (Thyroid Hormones); EC 1.11.1.8 (Iodide Peroxidase)


  2 / 8048 MEDLINE  
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PMID:28458340
Autor:Kume T
Dirección:Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyoto University.
Título:Therapeutic Potential of the Activators of the Nuclear Factor Erythroid 2-Related Factor 2-Antioxidant Response Element Pathway in Brain Disorders.
Fuente:Biol Pharm Bull; 40(5):553-556, 2017.
ISSN:1347-5215
País de publicación:Japan
Idioma:eng
Resumen: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.
Tipo de publicación:JOURNAL ARTICLE; REVIEW
Nombre de substancia:0 (Antioxidants); 0 (NF-E2-Related Factor 2); 0 (NFE2L2 protein, human)


  3 / 8048 MEDLINE  
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PMID:29273554
Autor:Shuwen H; Qing Z; Yan Z; Xi Y
Dirección:Department of Medical Oncology, Huzhou Central Hospital, Huzhou, Zhejiang Province, China.
Título:Competitive endogenous RNA in colorectal cancer: A systematic review.
Fuente:Gene; 645:157-162, 2018 Mar 01.
ISSN:1879-0038
País de publicación:Netherlands
Idioma:eng
Resumen: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.
Tipo de publicación:JOURNAL ARTICLE; REVIEW
Nombre de substancia:0 (MicroRNAs); 0 (RNA, Long Noncoding); 0 (RNA, circular); 63231-63-0 (RNA)


  4 / 8048 MEDLINE  
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PMID:29283230
Título:Canonical and Noncanonical Mechanisms of Glucocorticoid Stress Hormones Action.
Fuente:Usp Fiziol Nauk; 47(3):59-69, 2016 Jul-Sep.
ISSN:0301-1798
País de publicación:Russia (Federation)
Idioma:rus
Resumen: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.
Tipo de publicación:JOURNAL ARTICLE; REVIEW
Nombre de substancia:0 (Glucocorticoids); 0 (NF-kappa B); 0 (Receptors, Glucocorticoid); 0 (Transcription Factor AP-1)


  5 / 8048 MEDLINE  
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PMID:28747434
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
Dirección: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.
Título:Thrombospondin-1 (TSP-1), a new bone morphogenetic protein-2 and -4 (BMP-2/4) antagonist identified in pituitary cells.
Fuente:J Biol Chem; 292(37):15352-15368, 2017 09 15.
ISSN:1083-351X
País de publicación:United States
Idioma:eng
Resumen: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.
Tipo de publicación:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
Nombre de substancia: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)


  6 / 8048 MEDLINE  
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PMID:27777301
Autor:Liu X; Cai X; Hu B; Mei Z; Zhang D; Ouyang G; Wang J; Zhang W; Xiao W
Dirección:From the Key Laboratory of Aquatic Biodiversity and Conservation and.
Título:Forkhead Transcription Factor 3a (FOXO3a) Modulates Hypoxia Signaling via Up-regulation of the von Hippel-Lindau Gene (VHL).
Fuente:J Biol Chem; 291(49):25692-25705, 2016 Dec 02.
ISSN:1083-351X
País de publicación:United States
Idioma:eng
Resumen: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.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia: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)


  7 / 8048 MEDLINE  
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PMID:29045464
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
Dirección:Cancer Science Institute of Singapore, National University of Singapore, Singapore.
Título:TIP60 represses telomerase expression by inhibiting Sp1 binding to the TERT promoter.
Fuente:PLoS Pathog; 13(10):e1006681, 2017 Oct.
ISSN:1553-7374
País de publicación:United States
Idioma:eng
Resumen: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.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia: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)


  8 / 8048 MEDLINE  
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PMID:29023469
Autor:Choi SH; Severson E; Pear WS; Liu XS; Aster JC; Blacklow SC
Dirección:Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA, United States of America.
Título:The common oncogenomic program of NOTCH1 and NOTCH3 signaling in T-cell acute lymphoblastic leukemia.
Fuente:PLoS One; 12(10):e0185762, 2017.
ISSN:1932-6203
País de publicación:United States
Idioma:eng
Resumen: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.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia: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)


  9 / 8048 MEDLINE  
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PMID:28912063
Autor:Liu L; Song Y; Xu J; Li D; Li G; An L
Dirección:Ministry of Education Key Laboratory of Cell Activities and Stress Adaptations, School of Life Sciences, Lanzhou University, Lanzhou 730000, China.
Título:Differential expression by chromatin modifications of alcohol dehydrogenase 1 of Chorispora bungeana in cold stress.
Fuente:Gene; 636:1-16, 2017 Dec 15.
ISSN:1879-0038
País de publicación:Netherlands
Idioma:eng
Resumen: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.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (Chromatin); 0 (Histones); 0 (Plant Proteins); EC 1.1.1.1 (Alcohol Dehydrogenase); EC 2.7.7.- (RNA Polymerase II)


  10 / 8048 MEDLINE  
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PMID:28825728
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
Dirección:Department of Biology, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Título:Cis and trans determinants of epigenetic silencing by Polycomb repressive complex 2 in Arabidopsis.
Fuente:Nat Genet; 49(10):1546-1552, 2017 Oct.
ISSN:1546-1718
País de publicación:United States
Idioma:eng
Resumen: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.
Tipo de publicación:JOURNAL ARTICLE
Nombre de substancia:0 (Arabidopsis Proteins); 0 (DNA, Plant); 0 (Polycomb-Group Proteins); 0 (Transcription Factors); EC 2.1.1.43 (Polycomb Repressive Complex 2)



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