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Pesquisa : G05.308 [Categoria DeCS]
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[PMID]:29414693
[Au] Autor:Andreev DE; Dmitriev SE; Loughran G; Terenin IM; Baranov PV; Shatsky IN
[Ad] Endereço:Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, Moscow, Russia. Electronic address: cycloheximide@yandex.ru.
[Ti] Título:Translation control of mRNAs encoding mammalian translation initiation factors.
[So] Source:Gene;651:174-182, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Eukaryotic cells evolved highly complex and accurate protein synthesis machinery that is finely tuned by various signaling pathways. Dysregulation of translation is a hallmark of many diseases, including cancer, and thus pharmacological approaches to modulate translation become very promising. While there has been much progress in our understanding of mammalian mRNA-specific translation control, surprisingly, relatively little is known about whether and how the protein components of the translation machinery shape translation of their own mRNAs. Here we analyze mammalian mRNAs encoding components of the translation initiation machinery for potential regulatory features such as 5'TOP motifs, TISU motifs, poor start codon nucleotide context and upstream open reading frames.
[Mh] Termos MeSH primário: Fatores de Iniciação em Eucariotos/genética
Regulação da Expressão Gênica
RNA Mensageiro/metabolismo
[Mh] Termos MeSH secundário: Regiões 5' não Traduzidas
Animais
Seres Humanos
Mamíferos
Biossíntese de Proteínas
Sequência de Oligopirimidina na Região 5' Terminal do RNA
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (5' Untranslated Regions); 0 (Eukaryotic Initiation Factors); 0 (RNA, Messenger)
[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:180208
[St] Status:MEDLINE


  2 / 212690 MEDLINE  
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[PMID]:29389946
[Au] Autor:Okhovat MA; Ziari K; Ranjbaran R; Nikouyan N
[Ad] Endereço:Diagnostic Laboratory Sciences and Technology Research Center, School of Paramedical Sciences, Shiraz University of Medical Sciences, Shiraz, Iran.
[Ti] Título:The effect of histone deacetylase inhibitors on AHSP expression.
[So] Source:PLoS One;13(2):e0189267, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Alpha-hemoglobin stabilizing protein (AHSP) is a molecular chaperone that can reduce the damage caused by excess free α-globin to erythroid cells in patients with impaired ß-globin chain synthesis. We assessed the effect of sodium phenylbutyrate and sodium valproate, two histone deacetylase inhibitors (HDIs) that are being studied for the treatment of hemoglobinopathies, on the expression of AHSP, BCL11A (all isoforms), γ-globin genes (HBG1/2), and some related transcription factors including GATA1, NFE2, EKLF, KLF4, and STAT3. For this purpose, the K562 cell line was cultured for 2, 4, and 6 days in the presence and absence of sodium phenylbutyrate and sodium valproate. Relative real-time qRT-PCR analysis of mRNA levels was performed to determine the effects of the two compounds on gene expression. Expression of all target mRNAs increased significantly (p < 0.05), except for the expression of BCL11A, which was down-regulated (p < 0.05) in the cells treated with both compounds relative to the levels measured for untreated cells. The findings indicated that sodium valproate had a more considerable effect than sodium phenylbutyrate (p < 0.0005) on BCL11A repression and the up-regulation of other studied genes. γ-Globin and AHSP gene expression continuously increased during the culture period in the treated cells, with the highest gene expression observed for 1 mM sodium valproate after 6 days. Both compounds repressed the expression of BCL11A (-XL, -L, -S) and up-regulated GATA1, NFE2, EKLF, KLF4, STAT3, AHSP, and γ-globin genes expression. Moreover, sodium valproate showed a stronger effect on repressing BCL11A and escalating the expression of other target genes. The findings of this in vitro experiment could be considered in selecting drugs for clinical use in patients with ß-hemoglobinopathies.
[Mh] Termos MeSH primário: Proteínas Sanguíneas/metabolismo
Inibidores de Histona Desacetilases/farmacologia
Chaperonas Moleculares/metabolismo
[Mh] Termos MeSH secundário: Regulação da Expressão Gênica/efeitos dos fármacos
Hemoglobinopatias/tratamento farmacológico
Hemoglobinopatias/genética
Inibidores de Histona Desacetilases/uso terapêutico
Seres Humanos
Células K562
Fenilbutiratos/farmacologia
Reação em Cadeia da Polimerase em Tempo Real
Ácido Valproico/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AHSP protein, human); 0 (Blood Proteins); 0 (Histone Deacetylase Inhibitors); 0 (Molecular Chaperones); 0 (Phenylbutyrates); 614OI1Z5WI (Valproic Acid); 7WY7YBI87E (4-phenylbutyric acid)
[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:180202
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189267


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[PMID]:29382572
[Au] Autor:Lv C; Mo C; Liu H; Wu C; Li Z; Li J; Wang Y
[Ad] Endereço:Key Laboratory of Bio-resources and Eco-environment of Ministry of Education, College of Life Sciences, Sichuan University, Chengdu 610065, PR China.
[Ti] Título:Dopamine D2-like receptors (DRD2 and DRD4) in chickens: Tissue distribution, functional analysis, and their involvement in dopamine inhibition of pituitary prolactin expression.
[So] Source:Gene;651:33-43, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Dopamine (DA) D2-like (and D1-like) receptors are suggested to mediate the dopamine actions in the anterior pituitary and/or CNS of birds. However, the information regarding the structure, functionality, and expression of avian D2-like receptors have not been fully characterized. In this study, we cloned two D2-like receptors (cDRD2, cDRD4) from chicken brain using RACE PCR. The cloned cDRD4 is a 378-amino acid receptor, which shows 57% amino acid (a.a.) identity with mouse DRD4. As in mammals, two cDRD2 isoforms, cDRD2L (long isoform, 437 a.a.) and cDRD2S (short isoform, 408 a.a.), which differ in their third intracellular loop, were identified in chickens. Using cell-based luciferase reporter assays or Western blot, we demonstrated that cDRD4, cDRD2L and cDRD2S could be activated by dopamine and quinpirole (a D2-like receptor agonist) dose-dependently, and their activation inhibits cAMP signaling pathway and stimulates MAPK/ERK signaling cascade, indicating that they are functional receptors capable of mediating dopamine actions. Quantitative real-time PCR revealed that cDRD2 and cDRD4 are widely expressed in chicken tissues with abundant expression noted in anterior pituitary, and their expressions are likely controlled by their promoters near exon 1, as demonstrated by dual-luciferase reporter assays in DF-1 cells. In accordance with cDRD2/cDRD4 expression in the pituitary, DA or quinpirole could partially inhibit vasoactive intestinal peptide-induced prolactin expression in cultured chick pituitary cells. Together, our data proves the functionality of DRD2 and DRD4 in birds and aids to uncover the conserved roles of DA/D2-like receptor system in vertebrates, such as its action on the pituitary.
[Mh] Termos MeSH primário: Galinhas/metabolismo
Dopamina/metabolismo
Hipófise/metabolismo
Prolactina/biossíntese
Receptores de Dopamina D2/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Galinhas/genética
Clonagem Molecular
DNA Complementar
Feminino
Regulação da Expressão Gênica
Células HEK293
Seres Humanos
Masculino
Prolactina/antagonistas & inibidores
Regiões Promotoras Genéticas
Receptores de Dopamina D2/genética
Receptores de Dopamina D2/fisiologia
Transdução de Sinais
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (Receptors, Dopamine D2); 9002-62-4 (Prolactin); VTD58H1Z2X (Dopamine)
[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:180201
[St] Status:MEDLINE


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[PMID]:29380441
[Au] Autor:Waugh CA; Arukwe A; Jaspers VLB
[Ad] Endereço:Environmental Toxicology, Department of Biology, Faculty of Natural Sciences, Norwegian University of Science and Technology, Trondheim, Norway.
[Ti] Título:Deregulation of microRNA-155 and its transcription factor NF-kB by polychlorinated biphenyls during viral infections.
[So] Source:APMIS;126(3):234-240, 2018 Mar.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Polychlorinated biphenyls (PCBs), and similar environmental contaminants, have been linked to virus outbreaks and increased viral induced mortality since the 1970s. Yet the mechanisms behind this increased susceptibility remain elusive. It has recently been illustrated that the innate immune viral detection system is tightly regulated by small non-coding RNAs, including microRNAs (miRNAs). For virus infections miRNA-155 expression is an important host response against infection, and deregulation of this miRNA is closely associated with adverse outcomes. Thus, we designed a targeted in vitro study using primary chicken fibroblasts, first exposed to a mixture of PCBs (Arochlor-1250) before being stimulated with a synthetic RNA virus (poly I:C), to determine if PCBs have the potential to deregulate miRNA-155. In this paper, we provide the first data for the deregulation of miRNA-155 when a host is exposed to a mixture of PCBs before a virus infection. Thus, we provide important evidence that PCBs can be involved in the deregulation of important miRNA pathways involved in the immune system; thereby demonstrating novel insights into the mechanism of PCB toxicity on the immune system.
[Mh] Termos MeSH primário: Imunidade Inata/genética
MicroRNAs/genética
NF-kappa B/genética
Poli I-C/farmacologia
Bifenilos Policlorados/química
Vírus/imunologia
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Embrião de Galinha
Galinhas/genética
Galinhas/imunologia
Regulação da Expressão Gênica/imunologia
Seres Humanos
Viroses/genética
Viroses/imunologia
Viroses/virologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN155 microRNA, human); 0 (MicroRNAs); 0 (NF-kappa B); DFC2HB4I0K (Polychlorinated Biphenyls); O84C90HH2L (Poly I-C)
[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:180131
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12811


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[PMID]:29351307
[Au] Autor:Merentie M; Rissanen R; Lottonen-Raikaslehto L; Huusko J; Gurzeler E; Turunen MP; Holappa L; Mäkinen P; Ylä-Herttuala S
[Ad] Endereço:A. I. Virtanen Institute for Molecular Sciences, Faculty of Health Sciences, University of Eastern Finland, Kuopio, Finland.
[Ti] Título:Doxycycline modulates VEGF-A expression: Failure of doxycycline-inducible lentivirus shRNA vector to knockdown VEGF-A expression in transgenic mice.
[So] Source:PLoS One;13(1):e0190981, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vascular endothelial growth factor-A (VEGF-A) is the master regulator of angiogenesis, vascular permeability and growth. However, its role in mature blood vessels is still not well understood. To better understand the role of VEGF-A in the adult vasculature, we generated a VEGF-A knockdown mouse model carrying a doxycycline (dox)-regulatable short hairpin RNA (shRNA) transgene, which silences VEGF-A. The aim was to find the critical level of VEGF-A reduction for vascular well-being in vivo. In vitro, the dox-inducible lentiviral shRNA vector decreased VEGF-A expression efficiently and dose-dependently in mouse endothelial cells and cardiomyocytes. In the generated transgenic mice plasma VEGF-A levels decreased shortly after the dox treatment but returned back to normal after two weeks. VEGF-A expression decreased shortly after the dox treatment only in some tissues. Surprisingly, increasing the dox exposure time and dose led to elevated VEGF-A expression in some tissues of both wildtype and knockdown mice, suggesting that dox itself has an effect on VEGF-A expression. When the effect of dox on VEGF-A levels was further tested in naïve/non-transduced cells, the dox administration led to a decreased VEGF-A expression in endothelial cells but to an increased expression in cardiomyocytes. In conclusion, the VEGF-A knockdown was achieved in a dox-regulatable fashion with a VEGF-A shRNA vector in vitro, but not in the knockdown mouse model in vivo. Dox itself was found to regulate VEGF-A expression explaining the unexpected results in mice. The effect of dox on VEGF-A levels might at least partly explain its previously reported beneficial effects on myocardial and brain ischemia. Also, this effect on VEGF-A should be taken into account in all studies using dox-regulated vectors.
[Mh] Termos MeSH primário: Doxiciclina/farmacologia
Regulação da Expressão Gênica/efeitos dos fármacos
Técnicas de Silenciamento de Genes
Lentivirus/genética
RNA Interferente Pequeno/genética
Fator A de Crescimento do Endotélio Vascular/genética
[Mh] Termos MeSH secundário: Animais
Vetores Genéticos
Camundongos
Camundongos Transgênicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA, Small Interfering); 0 (Vascular Endothelial Growth Factor A); N12000U13O (Doxycycline)
[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:180120
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190981


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[PMID]:29337061
[Au] Autor:Li Q; Qin Z; Nie F; Bi H; Zhao R; Pan B; Ma J; Xie X
[Ad] Endereço:Department of Plastic and Reconstructive Surgery, Peking University Third Hospital, Beijing, 100191, China.
[Ti] Título:Metabolic reprogramming in keloid fibroblasts: Aerobic glycolysis and a novel therapeutic strategy.
[So] Source:Biochem Biophys Res Commun;496(2):641-647, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Keloids, tumor-like fibroproliferative cutaneous lesions, were reported in metabolic disturbance. However, the metabolic character remains unclear. The purpose of this study is to determine if glycolytic reprogramming is important for the pathogenesis of keloids and to assess the inhibition potential of glycolysis in keloid treatment. An intracellular metabolic profile assay was used to compare metabolic phenotypes between normal skin fibroblasts and keloid fibroblasts (NFs and KFs). Our data indicated that KFs underwent reprogramming of their metabolic phonotype from oxidative phosphorylation to aerobic glycolysis (Warburg effect) with augmented glycolysis and glycolytic capacity. Both gene and protein assays showed that the expression of glycolytic enzymes was upregulated in KFs compared to NFs. Our data showed higher glucose influx and lactate production in KFs compared to NFs. Furthermore, the proliferation of KFs was suppressed in a dose-dependent and time-dependent manner after inhibition of glycolysis with 2-deoxy-glucose (2-DG). Taken together, these findings suggested that keloids underwent a reprogrammed metabolic phenotype of aerobic glycolysis. This was essential for keloid hyperplasia, and glycolytic inhibitors might provide a potential treatment for keloids.
[Mh] Termos MeSH primário: Fibroblastos/patologia
Queloide/patologia
[Mh] Termos MeSH secundário: Proliferação Celular/efeitos dos fármacos
Células Cultivadas
Desoxiglucose/farmacologia
Fibroblastos/efeitos dos fármacos
Fibroblastos/metabolismo
Regulação da Expressão Gênica
Glucose/metabolismo
Glicólise/efeitos dos fármacos
Seres Humanos
Queloide/tratamento farmacológico
Queloide/genética
Queloide/metabolismo
Ácido Láctico/metabolismo
Consumo de Oxigênio
Pele/metabolismo
Pele/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
33X04XA5AT (Lactic Acid); 9G2MP84A8W (Deoxyglucose); IY9XDZ35W2 (Glucose)
[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:180117
[St] Status:MEDLINE


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[PMID]:29214789
[Au] Autor:Kim CW; Han JH; Wu L; Choi JY
[Ad] Endereço:Department of Otorhinolaryngology, Hallym University College of Medicine, Seoul, Korea.
[Ti] Título:microRNA-183 is Essential for Hair Cell Regeneration after Neomycin Injury in Zebrafish.
[So] Source:Yonsei Med J;59(1):141-147, 2018 Jan.
[Is] ISSN:1976-2437
[Cp] País de publicação:Korea (South)
[La] Idioma:eng
[Ab] Resumo:PURPOSE: microRNAs (miRNAs) are non-coding RNAs composed of 20 to 22 nucleotides that regulate development and differentiation in various organs by silencing specific RNAs and regulating gene expression. In the present study, we show that the microRNA (miR)-183 cluster is upregulated during hair cell regeneration and that its inhibition reduces hair cell regeneration following neomycin-induced ototoxicity in zebrafish. MATERIALS AND METHODS: miRNA expression patterns after neomycin exposure were analyzed using microarray chips. Quantitative polymerase chain reaction was performed to validate miR-183 cluster expression patterns following neomycin exposure (500 µM for 2 h). After injection of an antisense morpholino (MO) to miR-183 (MO-183) immediately after fertilization, hair cell regeneration after neomycin exposure in neuromast cells was evaluated by fluorescent staining (YO-PRO1). The MO-183 effect also was assessed in transgenic zebrafish larvae expressing green fluorescent protein (GFP) in inner ear hair cells. RESULTS: Microarray analysis clearly showed that the miR-183 cluster (miR-96, miR-182, and miR-183) was upregulated after neomycin treatment. We also confirmed upregulated expression of the miR-183 cluster during hair cell regeneration after neomycin-induced ototoxicity. miR-183 inhibition using MO-183 reduced hair cell regeneration in both wild-type and GFP transgenic zebrafish larvae. CONCLUSION: Our work demonstrates that the miR-183 cluster is essential for the regeneration of hair cells following ototoxic injury in zebrafish larvae. Therefore, regulation of the miR-183 cluster can be a novel target for stimulation of hair cell regeneration.
[Mh] Termos MeSH primário: Células Ciliadas Auditivas/fisiologia
MicroRNAs/metabolismo
Regeneração/genética
Peixe-Zebra/genética
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Contagem de Células
Perfilação da Expressão Gênica
Regulação da Expressão Gênica/efeitos dos fármacos
Técnicas de Silenciamento de Genes
Proteínas de Fluorescência Verde/metabolismo
Células Ciliadas Auditivas/efeitos dos fármacos
Larva/efeitos dos fármacos
Larva/genética
MicroRNAs/genética
Morfolinos/farmacologia
Neomicina/toxicidade
Regeneração/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MIRN183 microRNA, zebrafish); 0 (MicroRNAs); 0 (Morpholinos); 1404-04-2 (Neomycin); 147336-22-9 (Green Fluorescent Proteins)
[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:171208
[St] Status:MEDLINE
[do] DOI:10.3349/ymj.2018.59.1.141


  8 / 212690 MEDLINE  
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[PMID]:29202686
[Au] Autor:Feldmeyer B; Elsner D; Alleman A; Foitzik S
[Ad] Endereço:Senckenberg Biodiversity and Climate Research Centre (BiK-F), Molecular Ecology, Senckenberganlage 25, 60325, Frankfurt am Main, Germany. barbara.feldmeyer@senckenberg.de.
[Ti] Título:Species-specific genes under selection characterize the co-evolution of slavemaker and host lifestyles.
[So] Source:BMC Evol Biol;17(1):237, 2017 Dec 04.
[Is] ISSN:1471-2148
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The transition to a parasitic lifestyle entails comprehensive changes to the selective regime. In parasites, genes encoding for traits that facilitate host detection, exploitation and transmission should be under selection. Slavemaking ants are social parasites that exploit the altruistic behaviour of their hosts by stealing heterospecific host brood during raids, which afterwards serve as slaves in slavemaker nests. Here we search for evidence of selection in the transcriptomes of three slavemaker species and three closely related hosts. We expected selection on genes underlying recognition and raiding or defense behaviour. Analyses of selective forces in species with a slavemaker or host lifestyle allowed investigation into whether or not repeated instances of slavemaker evolution share the same genetic basis. To investigate the genetic basis of host-slavemaker co-evolution, we created orthologous clusters from transcriptome sequences of six Temnothorax ant species - three slavemakers and three hosts - to identify genes with signatures of selection. We further tested for functional enrichment in selected genes from slavemakers and hosts respectively and investigated which pathways the according genes belong to. RESULTS: Our phylogenetic analysis, based on more than 5000 ortholog sequences, revealed sister species status for two slavemakers as well as two hosts, contradicting a previous phylogeny based on mtDNA. We identified 309 genes with signs of positive selection on branches leading to slavemakers and 161 leading to hosts. Among these were genes potentially involved in cuticular hydrocarbon synthesis, thus species recognition, and circadian clock functionality possibly explaining the different activity patterns of slavemakers and hosts. There was little overlap of genes with signatures of positive selection among species, which are involved in numerous different functions and different pathways. CONCLUSIONS: We identified different genes, functions and pathways under positive selection in each species. These results point to species-specific adaptations rather than convergent trajectories during the evolution of the slavemaker and host lifestyles suggesting that the evolution of parasitism, even in closely related species, may be achieved in diverse ways.
[Mh] Termos MeSH primário: Formigas/genética
Formigas/parasitologia
Comportamento Animal
Evolução Biológica
Interações Hospedeiro-Parasita/genética
Seleção Genética
[Mh] Termos MeSH secundário: Animais
Regulação da Expressão Gênica
Funções Verossimilhança
Filogenia
Especificidade da Espécie
[Pt] Tipo de publicação:JOURNAL ARTICLE
[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:171206
[St] Status:MEDLINE
[do] DOI:10.1186/s12862-017-1078-9


  9 / 212690 MEDLINE  
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[PMID]:28466892
[Au] Autor:Bondí R; Longo F; Messina M; D'Angelo F; Visca P; Leoni L; Rampioni G
[Ad] Endereço:Department of Science, University Roma Tre, Rome, Italy. giordano.rampioni@uniroma3.it.
[Ti] Título:The multi-output incoherent feedforward loop constituted by the transcriptional regulators LasR and RsaL confers robustness to a subset of quorum sensing genes in Pseudomonas aeruginosa.
[So] Source:Mol Biosyst;13(6):1080-1089, 2017 Jun 01.
[Is] ISSN:1742-2051
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Quorum sensing (QS) is an intercellular communication system which controls virulence-related phenotypes in the human pathogen Pseudomonas aeruginosa. LasR is the QS receptor protein which responds to the signal molecule N-(3-oxododecanoyl)homoserine lactone (3OC -HSL) and promotes signal production by increasing the transcription of the 3OC -HSL synthase gene, lasI. LasR also activates the expression of other genes, including rsaL, coding for the RsaL protein which acts as a transcriptional repressor of lasI. Direct gene activation and RsaL-mediated gene repression, both exerted by LasR on the expression of the output gene lasI, generate a regulatory network motif known as the type 1 incoherent feedforward loop (IFFL-1) that governs 3OC -HSL production. In addition to lasI, RsaL directly represses a set of LasR-activated genes; hence, the IFFL-1 generated by LasR and RsaL is a multi-output IFFL-1. Here we demonstrate that the multi-output IFFL-1 constituted by LasR and RsaL confers robustness with respect to fluctuations in the levels of LasR to the phenotypes controlled by both these transcriptional regulators (e.g. 3OC -HSL synthesis and pyocyanin production). In contrast, other virulence-related phenotypes controlled by LasR but not by RsaL (e.g. elastase and protease production) are sensitive to changes in LasR levels. Overall, the multi-output IFFL-1 generated by LasR and RsaL splits the QS regulon into two distinct sub-regulons with different robustness with respect to LasR fluctuations. This emerging regulatory property enhances the phenotypic plasticity of P. aeruginosa, thus contributing to its adaptation to changing environments.
[Mh] Termos MeSH primário: Proteínas de Bactérias/metabolismo
Pseudomonas aeruginosa/metabolismo
Pseudomonas aeruginosa/fisiologia
Percepção de Quorum
Proteínas Repressoras/metabolismo
Transativadores/metabolismo
[Mh] Termos MeSH secundário: 4-Butirolactona/análogos & derivados
4-Butirolactona/metabolismo
Proteínas de Bactérias/genética
Regulação da Expressão Gênica
Homosserina/análogos & derivados
Homosserina/metabolismo
Proteínas Repressoras/genética
Transativadores/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (LasR protein, Pseudomonas aeruginosa); 0 (N-(3-oxododecanoyl)homoserine lactone); 0 (Repressor Proteins); 0 (Trans-Activators); 0 (rsaL protein, Pseudomonas aeruginosa); 1192-20-7 (homoserine lactone); 6KA95X0IVO (Homoserine); OL659KIY4X (4-Butyrolactone)
[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:170504
[St] Status:MEDLINE
[do] DOI:10.1039/c7mb00040e


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[PMID]:28457941
[Au] Autor:Menazza S; Sun J; Appachi S; Chambliss KL; Kim SH; Aponte A; Khan S; Katzenellenbogen JA; Katzenellenbogen BS; Shaul PW; Murphy E
[Ad] Endereço:Systems Biology Center, National Heart Lung and Blood Institute, NIH, Bethesda, MD, United States.
[Ti] Título:Non-nuclear estrogen receptor alpha activation in endothelium reduces cardiac ischemia-reperfusion injury in mice.
[So] Source:J Mol Cell Cardiol;107:41-51, 2017 Jun.
[Is] ISSN:1095-8584
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Steroid hormone receptors including estrogen receptors (ER) classically function as ligand-regulated transcription factors. However, estrogens also elicit cellular effects through binding to extra-nuclear ER (ERα, ERß, and G protein-coupled ER or GPER) that are coupled to kinases. How extra-nuclear ER actions impact cardiac ischemia-reperfusion (I/R) injury is unknown. We treated ovariectomized wild-type female mice with estradiol or an estrogen-dendrimer conjugate (EDC), which selectively activates extra-nuclear ER, or vehicle interventions for two weeks. I/R injury was then evaluated in isolated Langendorff perfused hearts. Two weeks of treatment with estradiol significantly decreased infarct size and improved post-ischemic contractile function. Similarly, EDC treatment significantly decreased infarct size and increased post-ischemic functional recovery compared to vehicle-treated hearts. EDC also caused an increase in myocardial protein S-nitrosylation, consistent with previous studies showing a role for this post-translational modification in cardioprotection. In further support of a role for S-nitrosylation, inhibition of nitric oxide synthase, but not soluble guanylyl cyclase blocked the EDC mediated protection. The administration of ICI182,780, which is an agonist of G-protein coupled estrogen receptor (GPER) and an antagonist of ERα and ERß, did not result in protection; however, ICI182,780 significantly blocked EDC-mediated cardioprotection, indicating participation of ERα and/or ERß. In studies determining the specific ER subtype and cellular target involved, EDC decreased infarct size and improved functional recovery in mice lacking ERα in cardiomyocytes. In contrast, protection was lost in mice deficient in endothelial cell ERα. Thus, extra-nuclear ERα activation in endothelium reduces cardiac I/R injury in mice, and this likely entails increased protein S-nitrosylation. Since EDC does not stimulate uterine growth, in the clinical setting EDC-like compounds may provide myocardial protection without undesired uterotrophic and cancer-promoting effects.
[Mh] Termos MeSH primário: Receptor alfa de Estrogênio/genética
Receptor beta de Estrogênio/genética
Isquemia/genética
Traumatismo por Reperfusão/genética
[Mh] Termos MeSH secundário: Animais
Endotélio/metabolismo
Endotélio/patologia
Receptor alfa de Estrogênio/antagonistas & inibidores
Receptor beta de Estrogênio/antagonistas & inibidores
Estrogênios/genética
Estrogênios/metabolismo
Feminino
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Isquemia/metabolismo
Isquemia/patologia
Camundongos
Ovariectomia
Processamento de Proteína Pós-Traducional/efeitos dos fármacos
Receptores Estrogênicos/antagonistas & inibidores
Receptores Acoplados a Proteínas-G/antagonistas & inibidores
Traumatismo por Reperfusão/metabolismo
Traumatismo por Reperfusão/patologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Estrogen Receptor alpha); 0 (Estrogen Receptor beta); 0 (Estrogens); 0 (GPR30 protein, mouse); 0 (Receptors, Estrogen); 0 (Receptors, G-Protein-Coupled)
[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:170502
[St] Status:MEDLINE



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