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[PMID]:28632756
[Au] Autor:Hall JA; McElwee MK; Freedman JH
[Ad] Endereço:Biomolecular Screening Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, United States of America.
[Ti] Título:Identification of ATF-7 and the insulin signaling pathway in the regulation of metallothionein in C. elegans suggests roles in aging and reactive oxygen species.
[So] Source:PLoS One;12(6):e0177432, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It has been proposed that aging results from the lifelong accumulation of intracellular damage via reactions with reactive oxygen species (ROS). Metallothioneins are conserved cysteine-rich proteins that function as efficient ROS scavengers and may affect longevity. To better understand mechanisms controlling metallothionein expression, the regulatory factors and pathways that controlled cadmium-inducible transcription of the C. elegans metallothionein gene, mtl-1, were identified. The transcription factor ATF-7 was identified in both ethylmethanesulfonate mutagenesis and candidate gene screens. PMK-1 and members of the insulin signaling pathway, PDK-1 and AKT-1/2, were also identified as mtl-1 regulators. Genetic and previous results support a model for the regulation of cadmium-inducible mtl-1 transcription based on the derepression of the constitutively active transcription factor ELT-2. In addition, knockdown of the mammalian homologs of PDK1 and ATF7 in HEK293 cells resulted in changes in metallothionein expression, suggesting that this pathway was evolutionarily conserved. The insulin signaling pathway is known to influence the aging process; however, various factors responsible for affecting the aging phenotype are unknown. Identification of portions of the insulin signaling pathway as regulators of metallothionein expression supports the hypothesis that longevity is affected by the expression of this efficient ROS scavenger.
[Mh] Termos MeSH primário: Fatores Ativadores da Transcrição/metabolismo
Proteínas de Caenorhabditis elegans/metabolismo
Caenorhabditis elegans/metabolismo
Regulação da Expressão Gênica
Insulina/metabolismo
Longevidade/genética
Metalotioneína/genética
Espécies Reativas de Oxigênio/metabolismo
[Mh] Termos MeSH secundário: Fatores Ativadores da Transcrição/genética
Animais
Animais Geneticamente Modificados
Caenorhabditis elegans/genética
Caenorhabditis elegans/crescimento & desenvolvimento
Proteínas de Caenorhabditis elegans/genética
Células HEK293
Seres Humanos
Mutagênese
Fosforilação
Proteínas Serina-Treonina Quinases/genética
Proteínas Serina-Treonina Quinases/metabolismo
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATF-7 protein, C elegans); 0 (ATF7 protein, human); 0 (Activating Transcription Factors); 0 (Caenorhabditis elegans Proteins); 0 (Insulin); 0 (Reactive Oxygen Species); 9038-94-2 (Metallothionein); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.2 (pyruvate dehydrogenase (acetyl-transferring) kinase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0177432


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[PMID]:28396503
[Au] Autor:Yamada S; Okamura M; Oda A; Murakami H; Ohta K; Yamada T
[Ad] Endereço:Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, 153-8902, Japan.
[Ti] Título:Correlation of Meiotic DSB Formation and Transcription Initiation Around Fission Yeast Recombination Hotspots.
[So] Source:Genetics;206(2):801-809, 2017 Jun.
[Is] ISSN:1943-2631
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Meiotic homologous recombination, a critical event for ensuring faithful chromosome segregation and creating genetic diversity, is initiated by programmed DNA double-strand breaks (DSBs) formed at recombination hotspots. Meiotic DSB formation is likely to be influenced by other DNA-templated processes including transcription, but how DSB formation and transcription interact with each other has not been understood well. In this study, we used fission yeast to investigate a possible interplay of these two events. A group of hotspots in fission yeast are associated with sequences similar to the cyclic AMP response element and activated by the ATF/CREB family transcription factor dimer Atf1-Pcr1. We first focused on one of those hotspots, , and Atf1. Our results showed that multiple transcripts, shorter than the full-length messenger RNA, emanate from a region surrounding the hotspot. Interestingly, we found that the previously known recombination-activation region of Atf1 is also a transactivation domain, whose deletion affected DSB formation and short transcript production at These results point to a possibility that the two events may be related to each other at In fact, comparison of published maps of meiotic transcripts and hotspots suggested that hotspots are very often located close to meiotically transcribed regions. These observations therefore propose that meiotic DSB formation in fission yeast may be connected to transcription of surrounding regions.
[Mh] Termos MeSH primário: Fator 1 Ativador da Transcrição/genética
Fatores Ativadores da Transcrição/genética
Quebras de DNA de Cadeia Dupla
Fosfoproteínas/genética
Recombinação Genética
Proteínas de Schizosaccharomyces pombe/genética
Schizosaccharomyces/genética
[Mh] Termos MeSH secundário: Proteína de Ligação ao Elemento de Resposta ao AMP Cíclico
Recombinação Homóloga/genética
Meiose/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Activating Transcription Factor 1); 0 (Activating Transcription Factors); 0 (Cyclic AMP Response Element-Binding Protein); 0 (Pcr1 protein, S pombe); 0 (Phosphoproteins); 0 (Schizosaccharomyces pombe Proteins); 0 (atf1 protein, S pombe)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170412
[St] Status:MEDLINE
[do] DOI:10.1534/genetics.116.197954


  3 / 386 MEDLINE  
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[PMID]:28242759
[Au] Autor:Nikonorova IA; Al-Baghdadi RJT; Mirek ET; Wang Y; Goudie MP; Wetstein BB; Dixon JL; Hine C; Mitchell JR; Adams CM; Wek RC; Anthony TG
[Ad] Endereço:From the Department of Nutritional Sciences, and.
[Ti] Título:Obesity challenges the hepatoprotective function of the integrated stress response to asparaginase exposure in mice.
[So] Source:J Biol Chem;292(16):6786-6798, 2017 Apr 21.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Obesity increases risk for liver toxicity by the anti-leukemic agent asparaginase, but the mechanism is unknown. Asparaginase activates the integrated stress response (ISR) via sensing amino acid depletion by the eukaryotic initiation factor 2 (eIF2) kinase GCN2. The goal of this work was to discern the impact of obesity, alone alongside genetic disruption of the ISR, on mechanisms of liver protection during chronic asparaginase exposure in mice. Following diet-induced obesity, biochemical analysis of livers revealed that asparaginase provoked hepatic steatosis that coincided with activation of another eIF2 kinase PKR-like endoplasmic reticulum kinase (PERK), a major ISR transducer to ER stress. Genetic loss of intensified hepatic PERK activation to asparaginase, yet surprisingly, mRNA levels of key ISR gene targets such as and failed to increase. Instead, mechanistic target of rapamycin complex 1 (mTORC1) signal transduction was unleashed, and this coincided with liver dysfunction reflected by a failure to maintain hydrogen sulfide production or apolipoprotein B100 (ApoB100) expression. In contrast, obese mice lacking hepatic activating transcription factor 4 ( ) showed an exaggerated ISR and greater loss of endogenous hydrogen sulfide but normal inhibition of mTORC1 and maintenance of ApoB100 during asparaginase exposure. In both genetic mouse models, expression and phosphorylation of Sestrin2, an ATF4 gene target, was increased by asparaginase, suggesting mTORC1 inhibition during asparaginase exposure is not driven via eIF2-ATF4-Sestrin2. In conclusion, obesity promotes a maladaptive ISR during asparaginase exposure. GCN2 functions to repress mTORC1 activity and maintain ApoB100 protein levels independently of expression, whereas hydrogen sulfide production is promoted via GCN2-ATF4 pathway.
[Mh] Termos MeSH primário: Asparaginase/metabolismo
Fígado Gorduroso/metabolismo
Fígado/patologia
Obesidade/metabolismo
[Mh] Termos MeSH secundário: Fator 4 Ativador da Transcrição/genética
Fatores Ativadores da Transcrição/metabolismo
Animais
Apolipoproteína B-100/metabolismo
Proteínas de Ciclo Celular/metabolismo
Modelos Animais de Doenças
Fator de Iniciação 2 em Eucariotos/metabolismo
Fígado Gorduroso/patologia
Deleção de Genes
Glutationa/química
Sulfeto de Hidrogênio/química
Fígado/efeitos dos fármacos
Fígado/metabolismo
Alvo Mecanístico do Complexo 1 de Rapamicina
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Obesos
Camundongos Transgênicos
Complexos Multiproteicos/metabolismo
Proteínas Nucleares/genética
Proteínas Serina-Treonina Quinases/genética
Serina-Treonina Quinases TOR/metabolismo
eIF-2 Quinase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Activating Transcription Factors); 0 (Apolipoprotein B-100); 0 (Atf4 protein, mouse); 0 (Atf5 protein, mouse); 0 (Cell Cycle Proteins); 0 (Eukaryotic Initiation Factor-2); 0 (Multiprotein Complexes); 0 (Nuclear Proteins); 0 (TRB3 protein, mouse); 0 (sestrin 2 protein, mouse); 145891-90-3 (Activating Transcription Factor 4); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.11.1 (Eif2ak4 protein, mouse); EC 2.7.11.1 (Mechanistic Target of Rapamycin Complex 1); EC 2.7.11.1 (PERK kinase); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (eIF-2 Kinase); EC 3.5.1.1 (Asparaginase); GAN16C9B8O (Glutathione); YY9FVM7NSN (Hydrogen Sulfide)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170301
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M116.768408


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[PMID]:28143980
[Au] Autor:Pohlers S; Martin R; Krüger T; Hellwig D; Hänel F; Kniemeyer O; Saluz HP; Van Dijck P; Ernst JF; Brakhage A; Mühlschlegel FA; Kurzai O
[Ad] Endereço:Septomics Research Center, Leibniz Institute for Natural Product Research and Infection Biology-Hans Knöll Institute (HKI), Jena, Germany.
[Ti] Título:Lipid Signaling via Pkh1/2 Regulates Fungal CO2 Sensing through the Kinase Sch9.
[So] Source:MBio;8(1), 2017 Jan 31.
[Is] ISSN:2150-7511
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Adaptation to alternating CO concentrations is crucial for all organisms. Carbonic anhydrases-metalloenzymes that have been found in all domains of life-enable fixation of scarce CO by accelerating its conversion to bicarbonate and ensure maintenance of cellular metabolism. In fungi and other eukaryotes, the carbonic anhydrase Nce103 has been shown to be essential for growth in air (~0.04% CO ). Expression of NCE103 is regulated in response to CO availability. In Saccharomyces cerevisiae, NCE103 is activated by the transcription factor ScCst6, and in Candida albicans and Candida glabrata, it is activated by its homologues CaRca1 and CgRca1, respectively. To identify the kinase controlling Cst6/Rca1, we screened an S. cerevisiae kinase/phosphatase mutant library for the ability to regulate NCE103 in a CO -dependent manner. We identified ScSch9 as a potential ScCst6-specific kinase, as the sch9Δ mutant strain showed deregulated NCE103 expression on the RNA and protein levels. Immunoprecipitation revealed the binding capabilities of both proteins, and detection of ScCst6 phosphorylation by ScSch9 in vitro confirmed Sch9 as the Cst6 kinase. We could show that CO -dependent activation of Sch9, which is part of a kinase cascade, is mediated by lipid/Pkh1/2 signaling but not TORC1. Finally, we tested conservation of the identified regulatory cascade in the pathogenic yeast species C. albicans and C. glabrata Deletion of SCH9 homologues of both species impaired CO -dependent regulation of NCE103 expression, which indicates a conservation of the CO adaptation mechanism among yeasts. Thus, Sch9 is a Cst6/Rca1 kinase that links CO adaptation to lipid signaling via Pkh1/2 in fungi. IMPORTANCE: All living organisms have to cope with alternating CO concentrations as CO levels range from very low in the atmosphere (0.04%) to high (5% and more) in other niches, including the human body. In fungi, CO is sensed via two pathways. The first regulates virulence in pathogenic yeast by direct activation of adenylyl cyclase. The second pathway, although playing a fundamental role in fungal metabolism, is much less understood. Here the transcription factor Cst6/Rca1 controls carbon homeostasis by regulating carbonic anhydrase expression. Upstream signaling in this pathway remains elusive. We identify Sch9 as the kinase controlling Cst6/Rca1 activity in yeast and demonstrate that this pathway is conserved in pathogenic yeast species, which highlights identified key players as potential pharmacological targets. Furthermore, we provide a direct link between adaptation to changing CO conditions and lipid/Pkh1/2 signaling in yeast, thus establishing a new signaling cascade central to metabolic adaptation.
[Mh] Termos MeSH primário: Proteínas Quinases Dependentes de 3-Fosfoinositídeo/metabolismo
Dióxido de Carbono/metabolismo
Metabolismo dos Lipídeos
Proteínas Serina-Treonina Quinases/metabolismo
Proteínas de Saccharomyces cerevisiae/metabolismo
Saccharomyces cerevisiae/fisiologia
Transdução de Sinais
[Mh] Termos MeSH secundário: Fatores Ativadores da Transcrição/metabolismo
Adenosina Trifosfatases/metabolismo
Candida albicans/genética
Candida glabrata/genética
Anidrases Carbônicas/metabolismo
Deleção de Genes
Regulação Fúngica da Expressão Gênica
Metaloendopeptidases/metabolismo
Proteínas Mitocondriais/metabolismo
Proteínas Serina-Treonina Quinases/genética
Saccharomyces cerevisiae/genética
Saccharomyces cerevisiae/metabolismo
Proteínas de Saccharomyces cerevisiae/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Activating Transcription Factors); 0 (CST6 protein, S cerevisiae); 0 (Mitochondrial Proteins); 0 (Saccharomyces cerevisiae Proteins); 142M471B3J (Carbon Dioxide); EC 2.7.11.1 (3-Phosphoinositide-Dependent Protein Kinases); EC 2.7.11.1 (PKH1 protein, S cerevisiae); EC 2.7.11.1 (PKH2 protein, S cerevisiae); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (SCH9 protein, S cerevisiae); EC 3.4.24.- (Metalloendopeptidases); EC 3.6.1.- (Adenosine Triphosphatases); EC 3.6.1.- (YTA12 protein, S cerevisiae); EC 4.2.1.1 (Carbonic Anhydrases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170202
[St] Status:MEDLINE


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[PMID]:27714816
[Au] Autor:Wang X; Hu M; Xing F; Wang M; Wang B; Qian D
[Ad] Endereço:Department of Microbiology, Qingdao University Medical College, Qingdao, Shandong, P.R. China.
[Ti] Título:Human cytomegalovirus infection promotes the stemness of U251 glioma cells.
[So] Source:J Med Virol;89(5):878-886, 2017 May.
[Is] ISSN:1096-9071
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glioblastoma (GBM) are the most common and aggressive tumors of human brain. Recent studies showed that human cytomegalovirus (HCMV) can induce malignant transformation of tumor cells to maintain stemness. Transcription factor 5 (ATF5) is an anti-apoptotic protein that is highly expressed in malignant glioma. The aim of this study is to investigate the effect of HCMV infection on the stem cell makers of U251 cells. U251 cells were infected by AD169 HCMV strain (MOI = 1). The expression of stem cell makers (CD133, NES, Notch1) in infected U251 cells were compared with the expression in uninfected U251 cell to see the difference between them. Then, the changes of cell proliferation activity and the expression level of Notch intracellular domain (NICD), Notch1, ATF5, and IE protein were detected in the infected cells, and the expressions of Notch1 and NICD were increased. Cell proliferation assay showed that HCMV infection significantly increased the proliferation. These cells could form tumor spheres in non-adherent conditions. Consistent with these findings, the effect of silencing ATF5 on the proliferation of HCMV-infected U251 cells was also examined. The result shows that short interfering RNA-mediated ATF5 downregulation inhibited this process. These findings imply that HCMV infection may regulate ATF5 signaling pathway to increase cell malignant traits and maintain stemness. J. Med. Virol. 89:878-886, 2017. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Antígeno AC133/análise
Transformação Celular Viral
Citomegalovirus/crescimento & desenvolvimento
Nestina/análise
Neuroglia/virologia
Receptor Notch1/análise
[Mh] Termos MeSH secundário: Fatores Ativadores da Transcrição/análise
Linhagem Celular Tumoral
Proliferação Celular
Perfilação da Expressão Gênica
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AC133 Antigen); 0 (ATF5 protein, human); 0 (Activating Transcription Factors); 0 (NES protein, human); 0 (NOTCH1 protein, human); 0 (Nestin); 0 (PROM1 protein, human); 0 (Receptor, Notch1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161008
[St] Status:MEDLINE
[do] DOI:10.1002/jmv.24708


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[PMID]:27802171
[Au] Autor:Obier N; Cauchy P; Assi SA; Gilmour J; Lie-A-Ling M; Lichtinger M; Hoogenkamp M; Noailles L; Cockerill PN; Lacaud G; Kouskoff V; Bonifer C
[Ad] Endereço:Institute of Biomedical Research, College of Medicine and Dentistry, University of Birmingham, Birmingham B15 2TT, UK.
[Ti] Título:Cooperative binding of AP-1 and TEAD4 modulates the balance between vascular smooth muscle and hemogenic cell fate.
[So] Source:Development;143(23):4324-4340, 2016 12 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The transmission of extracellular signals into the nucleus involves inducible transcription factors, but how different signalling pathways act in a cell type-specific fashion is poorly understood. Here, we studied the regulatory role of the AP-1 transcription factor family in blood development using embryonic stem cell differentiation coupled with genome-wide transcription factor binding and gene expression analyses. AP-1 factors respond to MAP kinase signalling and comprise dimers of FOS, ATF and JUN proteins. To examine genes regulated by AP-1 and to examine how it interacts with other inducible transcription factors, we abrogated its global DNA-binding activity using a dominant-negative FOS peptide. We show that FOS and JUN bind to and activate a specific set of vascular genes and that AP-1 inhibition shifts the balance between smooth muscle and hematopoietic differentiation towards blood. Furthermore, AP-1 is required for de novo binding of TEAD4, a transcription factor connected to Hippo signalling. Our bottom-up approach demonstrates that AP-1- and TEAD4-associated cis-regulatory elements form hubs for multiple signalling-responsive transcription factors and define the cistrome that regulates vascular and hematopoietic development by extrinsic signals.
[Mh] Termos MeSH primário: Diferenciação Celular/fisiologia
Proteínas de Ligação a DNA/metabolismo
Células-Tronco Embrionárias/citologia
Proteínas Musculares/metabolismo
Músculo Liso Vascular/citologia
Fator de Transcrição AP-1/metabolismo
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Fatores Ativadores da Transcrição/metabolismo
Animais
Sítios de Ligação/genética
Linhagem Celular
Proteínas de Ligação a DNA/genética
Expressão Gênica/genética
Perfilação da Expressão Gênica
Camundongos
Músculo Liso Vascular/metabolismo
Ligação Proteica
Proteínas Proto-Oncogênicas c-fos/metabolismo
Proteínas Proto-Oncogênicas c-jun/metabolismo
Transdução de Sinais/fisiologia
Fator de Transcrição AP-1/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Activating Transcription Factors); 0 (DNA-Binding Proteins); 0 (Muscle Proteins); 0 (Proto-Oncogene Proteins c-fos); 0 (Proto-Oncogene Proteins c-jun); 0 (Tead4 protein, mouse); 0 (Transcription Factor AP-1); 0 (Transcription Factors)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161102
[St] Status:MEDLINE


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[PMID]:27693377
[Au] Autor:Solon-Biet SM; Cogger VC; Pulpitel T; Heblinski M; Wahl D; McMahon AC; Warren A; Durrant-Whyte J; Walters KA; Krycer JR; Ponton F; Gokarn R; Wali JA; Ruohonen K; Conigrave AD; James DE; Raubenheimer D; Morrison CD; Le Couteur DG; Simpson SJ
[Ad] Endereço:Charles Perkins Centre, University of Sydney, Sydney 2006, Australia; Ageing and Alzheimers Institute, Centre for Education and Research on Ageing, ANZAC Research Institute, Concord Hospital, University of Sydney, Sydney 2139, Australia; School of Life and Environmental Sciences, University of Sydne
[Ti] Título:Defining the Nutritional and Metabolic Context of FGF21 Using the Geometric Framework.
[So] Source:Cell Metab;24(4):555-565, 2016 Oct 11.
[Is] ISSN:1932-7420
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Fibroblast growth factor 21 (FGF21) is the first known endocrine signal activated by protein restriction. Although FGF21 is robustly elevated in low-protein environments, increased FGF21 is also seen in various other contexts such as fasting, overfeeding, ketogenic diets, and high-carbohydrate diets, leaving its nutritional context and physiological role unresolved and controversial. Here, we use the Geometric Framework, a nutritional modeling platform, to help reconcile these apparently conflicting findings in mice confined to one of 25 diets that varied in protein, carbohydrate, and fat content. We show that FGF21 was elevated under low protein intakes and maximally when low protein was coupled with high carbohydrate intakes. Our results explain how elevation of FGF21 occurs both under starvation and hyperphagia, and show that the metabolic outcomes associated with elevated FGF21 depend on the nutritional context, differing according to whether the animal is in a state of under- or overfeeding.
[Mh] Termos MeSH primário: Fenômenos Fisiológicos da Nutrição Animal
Fatores de Crescimento de Fibroblastos/metabolismo
[Mh] Termos MeSH secundário: Fatores Ativadores da Transcrição/genética
Fatores Ativadores da Transcrição/metabolismo
Animais
Apetite
Proteínas na Dieta/metabolismo
Metabolismo Energético
Feminino
Fatores de Crescimento de Fibroblastos/sangue
Regulação da Expressão Gênica
Glucose/metabolismo
Fator de Crescimento Insulin-Like I/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Modelos Biológicos
Fenótipo
Proteína Desacopladora 1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Activating Transcription Factors); 0 (Atf5 protein, mouse); 0 (Dietary Proteins); 0 (Uncoupling Protein 1); 0 (fibroblast growth factor 21); 62031-54-3 (Fibroblast Growth Factors); 67763-96-6 (Insulin-Like Growth Factor I); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170626
[Lr] Data última revisão:
170626
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161004
[St] Status:MEDLINE


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[PMID]:27545884
[Au] Autor:Chikka MR; Anbalagan C; Dvorak K; Dombeck K; Prahlad V
[Ad] Endereço:Department of Biology, Aging Mind and Brain Initiative, 143 Biology Building East, 338 BBE, University of Iowa, Iowa City, IA 52242, USA.
[Ti] Título:The Mitochondria-Regulated Immune Pathway Activated in the C. elegans Intestine Is Neuroprotective.
[So] Source:Cell Rep;16(9):2399-414, 2016 Aug 30.
[Is] ISSN:2211-1247
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Immunological mediators that originate outside the nervous system can affect neuronal health. However, their roles in neurodegeneration remain largely unknown. Here, we show that the p38MAPK-mediated immune pathway activated in intestinal cells of Caenorhabditis elegans upon mitochondrial dysfunction protects neurons in a cell-non-autonomous fashion. Specifically, mitochondrial complex I dysfunction induced by rotenone activates the p38MAPK/CREB/ATF-7-dependent innate immune response pathway in intestinal cells of C. elegans. Activation of p38MAPK in the gut is neuroprotective. Enhancing the p38MAPK-mediated immune pathway in intestinal cells alone suppresses rotenone-induced dopaminergic neuron loss, while downregulating it in the intestine exacerbates neurodegeneration. The p38MAPK/ATF-7 immune pathway modulates autophagy and requires autophagy and the PTEN-induced putative kinase PINK-1 for conferring neuroprotection. Thus, mitochondrial damage induces the clearance of mitochondria by the immune pathway, protecting the organism from the toxic effects of mitochondrial dysfunction. We propose that mitochondria are subject to constant surveillance by innate immune mechanisms.
[Mh] Termos MeSH primário: Fatores Ativadores da Transcrição/genética
Proteínas de Caenorhabditis elegans/genética
Caenorhabditis elegans/imunologia
Neurônios Dopaminérgicos/imunologia
Complexo I de Transporte de Elétrons/genética
Mitocôndrias/imunologia
Proteínas Quinases p38 Ativadas por Mitógeno/genética
[Mh] Termos MeSH secundário: Fatores Ativadores da Transcrição/imunologia
Animais
Caenorhabditis elegans/efeitos dos fármacos
Caenorhabditis elegans/genética
Proteínas de Caenorhabditis elegans/imunologia
Dopamina/metabolismo
Neurônios Dopaminérgicos/efeitos dos fármacos
Neurônios Dopaminérgicos/patologia
Complexo I de Transporte de Elétrons/deficiência
Complexo I de Transporte de Elétrons/imunologia
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/imunologia
Células Epiteliais/patologia
Trato Gastrointestinal/efeitos dos fármacos
Trato Gastrointestinal/imunologia
Trato Gastrointestinal/patologia
Regulação da Expressão Gênica
Imunidade Inata
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/patologia
Degradação Mitocondrial/efeitos dos fármacos
Degradação Mitocondrial/genética
Degeneração Neural/induzido quimicamente
Degeneração Neural/genética
Degeneração Neural/imunologia
Rotenona/toxicidade
Transdução de Sinais
Proteínas Quinases p38 Ativadas por Mitógeno/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATF-7 protein, C elegans); 0 (Activating Transcription Factors); 0 (Caenorhabditis elegans Proteins); 03L9OT429T (Rotenone); EC 1.6.5.3 (Electron Transport Complex I); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases); VTD58H1Z2X (Dopamine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160823
[St] Status:MEDLINE


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[PMID]:27498002
[Au] Autor:Liu Y; Maekawa T; Yoshida K; Furuse T; Kaneda H; Wakana S; Ishii S
[Ad] Endereço:Laboratory of Molecular Genetics, RIKEN Tsukuba Institute, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan; Department of Molecular Genetics and Ph.D. Program in Human Biology, School of Integrative and Global Majors, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8575, Japan.
[Ti] Título:ATF7 ablation prevents diet-induced obesity and insulin resistance.
[So] Source:Biochem Biophys Res Commun;478(2):696-702, 2016 09 16.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The activating transcription factor (ATF)2 family of transcription factors regulates a variety of metabolic processes, including adipogenesis and adaptive thermogenesis. ATF7 is a member of the ATF2 family, and mediates epigenetic changes induced by environmental stresses, such as social isolation and pathogen infection. However, the metabolic role of ATF7 remains unknown. The aim of the present study is to examine the role of ATF7 in metabolism using ATF7-dificeint mice. Atf7(-/-) mice exhibited lower body weight and resisted diet-induced obesity. Serum triglycerides, resistin, and adipose tissue mass were all significantly lower in ATF7-deficient mice. Fasting glucose levels and glucose tolerance were unaltered, but systemic insulin sensitivity was increased, by ablation of ATF7. Indirect calorimetry revealed that oxygen consumption by Atf7(-/-) mice was comparable to that of wild-type littermates on a standard chow diet, but increased energy expenditure was observed in Atf7(-/-) mice on a high-fat diet. Hence, ATF7 ablation may impair the development and function of adipose tissue and result in elevated energy expenditure in response to high-fat-feeding obesity and insulin resistance, indicating that ATF7 is a potential therapeutic target for diet-induced obesity and insulin resistance.
[Mh] Termos MeSH primário: Fatores Ativadores da Transcrição/deficiência
Adipogenia/genética
Resistência à Insulina
Obesidade/genética
Obesidade/prevenção & controle
Fatores de Transcrição/deficiência
[Mh] Termos MeSH secundário: Fatores Ativadores da Transcrição/genética
Adipócitos/citologia
Adipócitos/metabolismo
Tecido Adiposo Branco/citologia
Tecido Adiposo Branco/metabolismo
Animais
Glicemia/metabolismo
Dieta Hiperlipídica
Metabolismo Energético/genética
Expressão Gênica
Insulina/sangue
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Obesidade/etiologia
Obesidade/patologia
Consumo de Oxigênio/genética
Resistina/genética
Resistina/metabolismo
Fatores de Transcrição/genética
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ATF7 protein, mouse); 0 (Activating Transcription Factors); 0 (Blood Glucose); 0 (Insulin); 0 (Resistin); 0 (Retn protein, mouse); 0 (Transcription Factors); 0 (Triglycerides)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171127
[Lr] Data última revisão:
171127
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160808
[St] Status:MEDLINE


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[PMID]:27287286
[Ti] Título:Chromatin-Bound MDM2 Plays a p53-Independent Role in Tumor Metabolism.
[So] Source:Cancer Discov;6(7):693, 2016 Jul.
[Is] ISSN:2159-8290
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:MDM2 regulates genes involved in serine metabolism and redox homeostasis in a p53-independent manner.
[Mh] Termos MeSH primário: Cromatina/metabolismo
Metabolismo Energético
Neoplasias/metabolismo
Proteínas Proto-Oncogênicas c-mdm2/metabolismo
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Fatores Ativadores da Transcrição/metabolismo
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Neoplasias/genética
Oxirredução
[Pt] Tipo de publicação:EDITORIAL; LETTER
[Nm] Nome de substância:
0 (Activating Transcription Factors); 0 (Chromatin); 0 (Tumor Suppressor Protein p53); EC 2.3.2.27 (Proto-Oncogene Proteins c-mdm2)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160612
[St] Status:MEDLINE
[do] DOI:10.1158/2159-8290.CD-RW2016-108



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