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[PMID]:29360449
[Au] Autor:Hua S; Liu C; Liu L; Wu D
[Ad] Endereço:Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China. Electronic address: huashengni0401@163.com.
[Ti] Título:miR-142-3p inhibits aerobic glycolysis and cell proliferation in hepatocellular carcinoma via targeting LDHA.
[So] Source:Biochem Biophys Res Commun;496(3):947-954, 2018 02 12.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cancer cells are addictively dependent on glycolysis even in an oxygen-rich condition. However, the mechanism underlying micro (mi)RNA regulation of aerobic glycolysis in cancer cells has not been fully understood. Here, we demonstrated that the expression of miR-142-3p was lower in hepatocellular carcinoma (HCC) as compared to adjacent non-tumor samples, which was confirmed in The Cancer Genome Atlas (TCGA) HCC cohorts and Gene Expression Omnibus (GEO) datasets. Function and pathway analysis showed that miR-142-3p was most relevent with metabolism. As predicted, the overexpression of miR-142-3p inhibited aerobic glycolysis and thus proliferation of HCC cells. Mechanistically, we identified lactate dehydrogenase A (LDHA), one of the important catalyticase for aerobic glycolysis, as the target of miR-142-3p. Exogenous expression of miR-142-3p reduced the protein levels of LDHA in both SK-Hep-1 and Huh7 cells. Dual luciferase report assays showed the expression of LDHA was directly modulated by miR-142-3p. miR-142-3p-induced deduction of aerobic glycolysis and proliferation were reversed by LDHA overexpression. Taken together, these results indicate that miR-142-3p could act as a tumor suppressor in HCC by targeting LDHA, suggesting new therapeutic targets for HCC treatment.
[Mh] Termos MeSH primário: Carcinoma Hepatocelular/metabolismo
Proliferação Celular
Regulação Neoplásica da Expressão Gênica/genética
Glucose/metabolismo
Lactato Desidrogenases/metabolismo
Neoplasias Hepáticas/metabolismo
MicroRNAs/metabolismo
[Mh] Termos MeSH secundário: Aerobiose
Carcinoma Hepatocelular/patologia
Glicólise
Seres Humanos
Neoplasias Hepáticas/patologia
Oxigênio/metabolismo
Ligação Proteica
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (MIRN142 microRNA, human); 0 (MicroRNAs); EC 1.1.- (Lactate Dehydrogenases); EC 1.1.1.28 (D-lactate dehydrogenase); IY9XDZ35W2 (Glucose); S88TT14065 (Oxygen)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180124
[St] Status:MEDLINE


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[PMID]:28467664
[Au] Autor:Gamella M; Privman M; Bakshi S; Melman A; Katz E
[Ad] Endereço:Department of Chemistry and Biomolecular Science, Clarkson University, Potsdam, NY, 13699-5810, USA.
[Ti] Título:DNA Release from Fe -Cross-Linked Alginate Films Triggered by Logically Processed Biomolecular Signals: Integration of Biomolecular Computing and Actuation.
[So] Source:Chemphyschem;18(13):1811-1821, 2017 Jul 05.
[Is] ISSN:1439-7641
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Signal-controlled release of DNA from Fe -cross-linked alginate hydrogel electrochemically deposited on an electrode surface was studied. The multiple input signals were logically processed with the help of the enzyme-biocatalyzed reactions. Boolean logic gates, OR, AND, INH, were realized with the biocatalytic reactions performed by the enzymes entrapped in the alginate film. Hydrogen peroxide produced by the enzymatic reactions resulted in the degradation of the alginate hydrogel and DNA release. The alginate degradation was facilitated by the formation of free radicals in the Fenton-type reaction catalyzed by iron cations cross-linking the alginate hydrogel. The studied approach is versatile and can be adapted to various chemical signals processed by various enzymes with differently implemented Boolean logic. This work illustrates a novel concept of functional integration of biomolecular computing and actuation.
[Mh] Termos MeSH primário: Alginatos/química
Computadores Moleculares
Reagentes para Ligações Cruzadas/química
DNA/metabolismo
Compostos Férricos/química
Lógica
[Mh] Termos MeSH secundário: Animais
Biocatálise
DNA/química
Esterases/química
Esterases/metabolismo
Glucose Oxidase/química
Glucose Oxidase/metabolismo
Ácido Glucurônico/química
Ácidos Hexurônicos/química
Peroxidase do Rábano Silvestre/química
Peroxidase do Rábano Silvestre/metabolismo
Lactato Desidrogenases/química
Lactato Desidrogenases/metabolismo
Oxigenases de Função Mista/química
Oxigenases de Função Mista/metabolismo
Nanopartículas/química
Nanopartículas/metabolismo
Dióxido de Silício/química
Dióxido de Silício/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alginates); 0 (Cross-Linking Reagents); 0 (Ferric Compounds); 0 (Hexuronic Acids); 7631-86-9 (Silicon Dioxide); 8A5D83Q4RW (Glucuronic Acid); 8C3Z4148WZ (alginic acid); 9007-49-2 (DNA); EC 1.- (Mixed Function Oxygenases); EC 1.1.- (Lactate Dehydrogenases); EC 1.1.3.4 (Glucose Oxidase); EC 1.11.1.- (Horseradish Peroxidase); EC 1.13.12.4 (lactate 2-monooxygenase); EC 3.1.- (Esterases)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1002/cphc.201700301


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[PMID]:28847921
[Au] Autor:Jiang T; Guo X; Yan J; Zhang Y; Wang Y; Zhang M; Sheng B; Ma C; Xu P; Gao C
[Ad] Endereço:State Key Laboratory of Microbial Technology, Shandong University, Jinan, People's Republic of China.
[Ti] Título:A Bacterial Multidomain NAD-Independent d-Lactate Dehydrogenase Utilizes Flavin Adenine Dinucleotide and Fe-S Clusters as Cofactors and Quinone as an Electron Acceptor for d-Lactate Oxidization.
[So] Source:J Bacteriol;199(22), 2017 Nov 15.
[Is] ISSN:1098-5530
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bacterial membrane-associated NAD-independent d-lactate dehydrogenase (Fe-S d-iLDH) oxidizes d-lactate into pyruvate. A sequence analysis of the enzyme reveals that it contains an Fe-S oxidoreductase domain in addition to a flavin adenine dinucleotide (FAD)-containing dehydrogenase domain, which differs from other typical d-iLDHs. Fe-S d-iLDH from KT2440 was purified as a His-tagged protein and characterized in detail. This monomeric enzyme exhibited activities with l-lactate and several d-2-hydroxyacids. Quinone was shown to be the preferred electron acceptor of the enzyme. The two domains of the enzyme were then heterologously expressed and purified separately. The Fe-S cluster-binding motifs predicted by sequence alignment were preliminarily verified by site-directed mutagenesis of the Fe-S oxidoreductase domain. The FAD-containing dehydrogenase domain retained 2-hydroxyacid-oxidizing activity, although it decreased compared to the full Fe-S d-iLDH. Compared to the intact enzyme, the FAD-containing dehydrogenase domain showed increased catalytic efficiency with cytochrome as the electron acceptor, but it completely lost the ability to use coenzyme Q Additionally, the FAD-containing dehydrogenase domain was no longer associated with the cell membrane, and it could not support the utilization of d-lactate as a carbon source. Based on the results obtained, we conclude that the Fe-S oxidoreductase domain functions as an electron transfer component to facilitate the utilization of quinone as an electron acceptor by Fe-S d-iLDH, and it helps the enzyme associate with the cell membrane. These functions make the Fe-S oxidoreductase domain crucial for the d-lactate utilization function of Fe-S d-iLDH. Lactate metabolism plays versatile roles in most domains of life. Lactate utilization processes depend on certain enzymes to oxidize lactate to pyruvate. In recent years, novel bacterial lactate-oxidizing enzymes have been continually reported, including the unique NAD-independent d-lactate dehydrogenase that contains an Fe-S oxidoreductase domain besides the typical flavin-containing domain (Fe-S d-iLDH). Although Fe-S d-iLDH is widely distributed among bacterial species, the investigation of it is insufficient. Fe-S d-iLDH from KT2440, which is the major d-lactate-oxidizing enzyme for the strain, might be a representative of this type of enzyme. A study of it will be helpful in understanding the detailed mechanisms underlying the lactate utilization processes.
[Mh] Termos MeSH primário: Flavina-Adenina Dinucleotídeo/metabolismo
Proteínas com Ferro-Enxofre/metabolismo
Lactato Desidrogenases/genética
Lactato Desidrogenases/metabolismo
Ácido Láctico/metabolismo
Quinonas/metabolismo
[Mh] Termos MeSH secundário: Proteínas de Bactérias/genética
Proteínas de Bactérias/metabolismo
Coenzimas
Citocromos c/metabolismo
Elétrons
Lactato Desidrogenases/isolamento & purificação
Mutagênese Sítio-Dirigida
NAD/metabolismo
Oxirredução
Pseudomonas putida/enzimologia
Ubiquinona/análogos & derivados
Ubiquinona/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bacterial Proteins); 0 (Coenzymes); 0 (Iron-Sulfur Proteins); 0 (Quinones); 0U46U6E8UK (NAD); 1339-63-5 (Ubiquinone); 146-14-5 (Flavin-Adenine Dinucleotide); 33X04XA5AT (Lactic Acid); 9007-43-6 (Cytochromes c); EC 1.1.- (Lactate Dehydrogenases); EC 1.1.1.28 (D-lactate dehydrogenase); EJ27X76M46 (coenzyme Q10)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170830
[St] Status:MEDLINE


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[PMID]:28841311
[Au] Autor:Stark T; Lieblein T; Pohland M; Kalden E; Freund P; Zangl R; Grewal R; Heilemann M; Eckert GP; Morgner N; Göbel MW
[Ti] Título:Peptidomimetics That Inhibit and Partially Reverse the Aggregation of Aß .
[So] Source:Biochemistry;56(36):4840-4849, 2017 Sep 12.
[Is] ISSN:1520-4995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The peptide sequence KLVFF resembles the hydrophobic core of the Aß peptide known to form amyloid plaques in Alzheimer's disease. Starting from its retro-inverso peptide, we have synthesized three generations of peptidomimetics. Step by step natural amino acids have been replaced by aromatic building blocks accessible from the Pd-catalyzed Catellani reaction. The final compound 18 is stable against proteolytic decay and largely prevents the aggregation of Aß over extended periods of time. The activity of the new inhibitors was tested first by fluorescence correlation spectroscopy. For closer examination of compound 18, additional techniques were also applied: laser-induced liquid bead ion desorption mass spectrometry, confocal laser scanning microscopy, thioflavin T fluorescence, and gel electrophoresis. Compound 18 not only retards the aggregation of chemically synthesized Aß but also can partially dissolve the oligomeric structures. Thioflavin binding mature fibrils, however, seem to resist the inhibitor.
[Mh] Termos MeSH primário: Peptídeos beta-Amiloides
Fragmentos de Peptídeos
Peptidomiméticos/química
Peptidomiméticos/farmacologia
[Mh] Termos MeSH secundário: Linhagem Celular
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Seres Humanos
Lactato Desidrogenases/genética
Lactato Desidrogenases/metabolismo
Estrutura Molecular
Fragmentos de Peptídeos/química
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Peptide Fragments); 0 (Peptidomimetics); 0 (amyloid beta-protein (1-42)); EC 1.1.- (Lactate Dehydrogenases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170826
[St] Status:MEDLINE
[do] DOI:10.1021/acs.biochem.7b00223


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[PMID]:28765498
[Au] Autor:Robinson CS; Singer ER; Piviani M; Rubio-Martinez LM
[Ad] Endereço:Department of Equine Clinical Science, Institute of Veterinary Science, University of Liverpool, Wirral, UK.
[Ti] Título:Are serum amyloid A or D-lactate useful to diagnose synovial contamination or sepsis in horses?
[So] Source:Vet Rec;181(16):425, 2017 Oct 21.
[Is] ISSN:2042-7670
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Synovial sepsis in horses is life threatening and accurate diagnosis allowing prompt treatment is warranted. This study assessed the diagnostic value of serum amyloid A (SAA) and D-lactate in blood and synovial fluid (SF) as diagnostic markers of synovial sepsis in horses and correlated them with total nucleated cell count (TNCC), percentage of neutrophils (%N) and total protein (TP) in SF. Blood and SF SAA and D-lactate concentrations were determined in a case-control observational study including 112 horses (38 with synovial contamination or sepsis (SCS), 66 with non-septic intra-synovial pathology (NSISP) and 8 controls). Blood and SF SAA were significantly higher in SCS than in NSISP and control horses. SAA values were similar in NSISP and control horses. SF SAA was moderately correlated with synovial TNCC, TP and blood SAA. Blood and SF SAA were 82.4 per cent and 80 per cent sensitive and 88.9 per cent and 73 per cent specific for diagnosis of SCS, with cut-off values of 60.7 and 1.14 µg/ml, respectively. Blood and SF D-lactate concentrations were not significantly different between groups. This study shows that blood and SF SAA concentrations can aid to distinguish SCS from non-septic synovial pathology; however, D-lactate was not useful.
[Mh] Termos MeSH primário: Doenças dos Cavalos/diagnóstico
Lactato Desidrogenases/sangue
Sepse/veterinária
Proteína Amiloide A Sérica/análise
Líquido Sinovial/química
[Mh] Termos MeSH secundário: Animais
Estudos de Casos e Controles
Feminino
Doenças dos Cavalos/sangue
Cavalos
Masculino
Sepse/sangue
Sepse/diagnóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Nm] Nome de substância:
0 (Serum Amyloid A Protein); EC 1.1.- (Lactate Dehydrogenases); EC 1.1.1.28 (D-lactate dehydrogenase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170803
[St] Status:MEDLINE
[do] DOI:10.1136/vr.104386


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[PMID]:28756228
[Au] Autor:Koukourakis M; Tsolou A; Pouliliou S; Lamprou I; Papadopoulou M; Ilemosoglou M; Kostoglou G; Ananiadou D; Sivridis E; Giatromanolaki A
[Ad] Endereço:Department of Radiotherapy / Oncology, Democritus University of Thrace, Alexandroupolis 68100, Greece. Electronic address: targ@her.forthnet.gr.
[Ti] Título:Blocking LDHA glycolytic pathway sensitizes glioblastoma cells to radiation and temozolomide.
[So] Source:Biochem Biophys Res Commun;491(4):932-938, 2017 Sep 30.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Up-regulation of lactate dehydrogenase LDHA, is a frequent event in human malignancies and relate to poor postoperative outcome. In the current study we examined the hypothesis that LDHA and anaerobic glycolysis, may contribute to the resistance of glioblastoma to radiotherapy and to temozolomide. METHODS AND MATERIALS: The expression of LDH5 isoenzyme (fully encoded by the LDHA gene) was assessed in human glioblastoma tissues. Experimental in vitro studies involved the T98 and U87 glioblastoma cell lines. Their sensitivity to radiotherapy and to temozolomide, following silencing of LDHA gene or following exposure to the LDHA chemical inhibitor 'oxamate' and to the glycolysis inhibitor '2-deoxy-d-glucose' (2DG), was studied. RESULTS: Glioblastoma tissues showed strong cytoplasmic and nuclear LDH5 expression in 0-90% (median 20%) of the neoplastic cells. T98 and U87 cell lines showed that blocking glycolysis, either with LDHA gene silencing or exposure to oxamate (30 mM) and blockage of glycolysis with 2DG (500 µM), results in enhanced radiation sensitivity, an effect that was more robust in the T98 radioresistant cell line. Furthermore, all three glycolysis targeting methods, significantly sensitized both cell lines to Temozolomide. CONCLUSIONS: The current study provides evidence that a large subgroup of human glioblastomas are highly glycolytic, and that inhibitors of glycolysis, like LDHA targeting agents, may prove of therapeutic importance by enhancing the efficacy of radiotherapy and temozolomide against this lethal disease.
[Mh] Termos MeSH primário: Dacarbazina/análogos & derivados
Glioblastoma/tratamento farmacológico
Glioblastoma/radioterapia
Glicólise/efeitos dos fármacos
Lactato Desidrogenases/antagonistas & inibidores
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Dacarbazina/farmacologia
Dacarbazina/uso terapêutico
Relação Dose-Resposta a Droga
Glioblastoma/metabolismo
Seres Humanos
Lactato Desidrogenases/metabolismo
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
7GR28W0FJI (Dacarbazine); EC 1.1.- (Lactate Dehydrogenases); EC 1.1.1.28 (D-lactate dehydrogenase); YF1K15M17Y (temozolomide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170731
[St] Status:MEDLINE


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[PMID]:28604752
[Au] Autor:Feng J; Yang H; Zhang Y; Wei H; Zhu Z; Zhu B; Yang M; Cao W; Wang L; Wu Z
[Ad] Endereço:Medical Oncology, The First Affiliated Hospital of Wannan Medical College, Wuhu, China.
[Ti] Título:Tumor cell-derived lactate induces TAZ-dependent upregulation of PD-L1 through GPR81 in human lung cancer cells.
[So] Source:Oncogene;36(42):5829-5839, 2017 Oct 19.
[Is] ISSN:1476-5594
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The clinical success of immunotherapy that inhibits the negative immune regulatory pathway programmed cell death protein 1/PD-1 ligand (PD-1/PD-L1) has initiated a new era in the treatment of metastatic cancer. PD-L1 expression is upregulated in many solid tumors including lung cancer and functions predominantly in lactate-enriched tumor microenvironments. Here, we provided evidence for PD-L1 induction in response to lactate stimulation in lung cancer cells. Lactate-induced PD-L1 induction was mediated by its receptor GPR81. The silencing of GPR81 signaling in lung cancer cells resulted in a decrease in PD-L1 protein levels and functional inactivation of PD-L1 promoter activity. In addition, GPR81-mediated upregulation of PD-L1 in glucose-stimulated lung cancer cells that recapitulates the enhanced glycolysis in vivo was dependent on lactate dehydrogenase A (LDHA). We also demonstrated that activation of GPR81 decreases intracellular cAMP levels and inhibits protein kinase A (PKA) activity, leading to activation of the transcriptional coactivator TAZ. Interaction of TAZ with the transcription factor TEAD was essential for TAZ activation of PD-L1 and induction of its expression. Furthermore, we found that lactate-induced activation of PD-L1 in tumor cells led to reduced production of interferon-γ and induction of apoptosis of cocultured Jurkat T-cell leukemia cells. Our findings reveal an unexpected role of lactate in contributing to tumor cell protection from cytotoxic T-cell targeting and establishes a direct connection between tumor cell metabolic reprograming and tumor evasion from the immune response.
[Mh] Termos MeSH primário: Antígeno B7-H1/metabolismo
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Ácido Láctico/metabolismo
Neoplasias Pulmonares/metabolismo
Receptores Acoplados a Proteínas-G/metabolismo
[Mh] Termos MeSH secundário: Apoptose
Antígeno B7-H1/genética
Linhagem Celular Tumoral
AMP Cíclico/metabolismo
Proteínas Quinases Dependentes de AMP Cíclico/genética
Proteínas Quinases Dependentes de AMP Cíclico/metabolismo
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Interferon gama/metabolismo
Peptídeos e Proteínas de Sinalização Intracelular/genética
Células Jurkat
Lactato Desidrogenases/genética
Lactato Desidrogenases/metabolismo
Neoplasias Pulmonares/patologia
Receptores Acoplados a Proteínas-G/genética
Transdução de Sinais
Linfócitos T Citotóxicos/imunologia
Ativação Transcricional
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (B7-H1 Antigen); 0 (CD274 protein, human); 0 (GPR81 protein, human); 0 (Intracellular Signaling Peptides and Proteins); 0 (Receptors, G-Protein-Coupled); 0 (WWTR1 protein, human); 33X04XA5AT (Lactic Acid); 82115-62-6 (Interferon-gamma); E0399OZS9N (Cyclic AMP); EC 1.1.- (Lactate Dehydrogenases); EC 1.1.1.28 (D-lactate dehydrogenase); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170613
[St] Status:MEDLINE
[do] DOI:10.1038/onc.2017.188


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[PMID]:28508704
[Au] Autor:He D; Ma J; Long K; Wang X; Li X; Jiang A; Li M
[Ad] Endereço:a Institute of Animal Genetics & Breeding, College of Animal Science & Technology , Sichuan Agricultural University , Wen'jiang , China.
[Ti] Título:Differential expression of genes related to glucose metabolism in domesticated pigs and wild boar.
[So] Source:Biosci Biotechnol Biochem;81(8):1478-1483, 2017 Aug.
[Is] ISSN:1347-6947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Glucose metabolism is a basic biological process that shows substantial variation within and between species. Using pig as a model organism, we investigated differences in glucose metabolic genes in seven tissues from domesticated pigs (Rongchang pig and Tibetan pig, meanwhile, the Tibetan pig just as a special case of the domesticated pig under plateau condition) and wild boar. We found large differences in the expression of genes involved in multiple aspects of glucose metabolism, including genes associated with glucose transport, gluconeogenesis, and glycolysis. In addition, we identified microRNAs (miRNAs) that may be involved in the divergence of glucose metabolism in pig. A combined analysis of mRNA and miRNA expression indicated that some miRNA:mRNA pairs showed ab facto function in it. Our results provide a valuable resource for further determination of miRNA regulatory roles in pig glucose metabolism and reveal the divergence of glucose metabolism in pigs under domestication.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica
Glucose/metabolismo
Músculo Esquelético/metabolismo
Sus scrofa/genética
Suínos/genética
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/genética
Proteínas Quinases Ativadas por AMP/metabolismo
Animais
Transporte Biológico
Domesticação
Perfilação da Expressão Gênica
Gluconeogênese/genética
Transportador de Glucose Tipo 1/genética
Transportador de Glucose Tipo 1/metabolismo
Glucosefosfato Desidrogenase/genética
Glucosefosfato Desidrogenase/metabolismo
Glicólise/genética
Hexoquinase/genética
Hexoquinase/metabolismo
Lactato Desidrogenases/genética
Lactato Desidrogenases/metabolismo
MicroRNAs/genética
MicroRNAs/metabolismo
Especificidade de Órgãos
Fosfofrutoquinase-1 Muscular/genética
Fosfofrutoquinase-1 Muscular/metabolismo
Proteínas Proto-Oncogênicas c-akt/genética
Proteínas Proto-Oncogênicas c-akt/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Fator de Transcrição STAT3/genética
Fator de Transcrição STAT3/metabolismo
Especificidade da Espécie
Sus scrofa/metabolismo
Suínos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glucose Transporter Type 1); 0 (MicroRNAs); 0 (RNA, Messenger); 0 (STAT3 Transcription Factor); EC 1.1.- (Lactate Dehydrogenases); EC 1.1.1.28 (D-lactate dehydrogenase); EC 1.1.1.49 (Glucosephosphate Dehydrogenase); EC 2.7.1.- (Phosphofructokinase-1, Muscle Type); EC 2.7.1.1 (Hexokinase); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.31 (AMP-Activated Protein Kinases); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170517
[St] Status:MEDLINE
[do] DOI:10.1080/09168451.2017.1322893


  9 / 458 MEDLINE  
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[PMID]:28445027
[Au] Autor:Varga MJ; Dzierlenga MW; Schwartz SD
[Ad] Endereço:Department of Chemistry and Biochemistry, University of Arizona , 1306 East University Boulevard, Tucson, Arizona 85721, United States.
[Ti] Título:Structurally Linked Dynamics in Lactate Dehydrogenases of Evolutionarily Distinct Species.
[So] Source:Biochemistry;56(19):2488-2496, 2017 May 16.
[Is] ISSN:1520-4995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We present new findings about how primary and secondary structure affects the role of fast protein motions in the reaction coordinates of enzymatic reactions. Using transition path sampling and committor distribution analysis, we examined the difference in the role of these fast protein motions in the reaction coordinate of lactate dehydrogenases (LDHs) of Apicomplexa organisms Plasmodium falciparum and Cryptosporidium parvum. Having evolved separately from a common malate dehydrogenase ancestor, the two enzymes exhibit several important structural differences, notably a five-amino acid insertion in the active site loop of P. falciparum LDH. We find that these active site differences between the two organisms' LDHs likely cause a decrease in the contribution of the previously determined LDH rate-promoting vibration to the reaction coordinate of P. falciparum LDH compared to that of C. parvum LDH, specifically in the coupling of the rate-promoting vibration and the hydride transfer. This effect, while subtle, directly shows how changes in structure near the active site of LDH alter catalytically important motions. Insights provided by studying these alterations would prove to be useful in identifying LDH inhibitors that specifically target the isozymes of these parasitic organisms.
[Mh] Termos MeSH primário: Cryptosporidium parvum/enzimologia
Lactato Desidrogenases/metabolismo
Modelos Moleculares
Plasmodium falciparum/enzimologia
Proteínas de Protozoários/metabolismo
[Mh] Termos MeSH secundário: Biocatálise
Domínio Catalítico
Biologia Computacional
Bases de Dados de Proteínas
Evolução Molecular
Ligações de Hidrogênio
Isoenzimas/química
Isoenzimas/genética
Isoenzimas/metabolismo
Lactato Desidrogenases/química
Lactato Desidrogenases/genética
Simulação de Dinâmica Molecular
Mutagênese Insercional
Conformação Proteica
Proteínas de Protozoários/química
Proteínas de Protozoários/genética
Teoria Quântica
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Isoenzymes); 0 (Protozoan Proteins); EC 1.1.- (Lactate Dehydrogenases)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170714
[Lr] Data última revisão:
170714
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170427
[St] Status:MEDLINE
[do] DOI:10.1021/acs.biochem.7b00245


  10 / 458 MEDLINE  
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[PMID]:28282895
[Au] Autor:Pipicz M; Kocsis GF; Sárváry-Arantes L; Bencsik P; Varga ZV; Ferdinandy P; Csont T
[Ad] Endereço:Department of Biochemistry, Faculty of Medicine, University of Szeged, Dóm tér. 9., H-6720 Szeged, Hungary. pipicz.marton@med.u-szeged.hu.
[Ti] Título:Low-Dose Endotoxin Induces Late Preconditioning, Increases Peroxynitrite Formation, and Activates STAT3 in the Rat Heart.
[So] Source:Molecules;22(3), 2017 Mar 08.
[Is] ISSN:1420-3049
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Administration of low-dose endotoxin (lipopolysaccharide, LPS) 24 h before a lethal ischemia induces pharmacological late preconditioning. The exact mechanism of this phenomenon is not clear. Here we aimed to investigate whether low-dose LPS exerts late effects on peroxynitrite formation and activation of Akt, Erk, and STAT3 in the heart. Male Wistar rats were injected with LPS (S. typhimurium; 0.5 mg/kg i.p.) or saline. Twenty-four hours later, hearts were isolated, perfused for 10 min, and then used for biochemical analyses. LPS pretreatment enhanced cardiac formation of the peroxynitrite marker 3-nitrotyrosine. LPS pretreatment also increased cardiac levels of the peroxynitrite precursor nitric oxide (NO) and superoxide. The activities of Ca2+-independent NO synthase and xanthine oxidoreductase increased in LPS-pretreated hearts. LPS pretreatment resulted in significantly enhanced phosphorylation of STAT3 and non-significantly increased phosphorylation of Akt without affecting the activation of Erk. In separate experiments, isolated working hearts were subjected to 30 min global ischemia and 20 min reperfusion. LPS pretreatment significantly improved ischemia-reperfusion-induced deterioration of cardiac function. We conclude that LPS pretreatment enhances cardiac peroxynitrite formation and activates STAT3 24 h later, which may contribute to LPS-induced late preconditioning.
[Mh] Termos MeSH primário: Endotoxinas/administração & dosagem
Precondicionamento Isquêmico Miocárdico
Isquemia Miocárdica/metabolismo
Ácido Peroxinitroso/biossíntese
Fator de Transcrição STAT3/metabolismo
[Mh] Termos MeSH secundário: Animais
Lactato Desidrogenases/metabolismo
Lipopolissacarídeos/administração & dosagem
Masculino
Óxido Nítrico/metabolismo
Óxido Nítrico Sintase/metabolismo
Oxirredução
Ratos
Tirosina/análogos & derivados
Tirosina/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endotoxins); 0 (Lipopolysaccharides); 0 (STAT3 Transcription Factor); 14691-52-2 (Peroxynitrous Acid); 31C4KY9ESH (Nitric Oxide); 3604-79-3 (3-nitrotyrosine); 42HK56048U (Tyrosine); EC 1.1.- (Lactate Dehydrogenases); EC 1.14.13.39 (Nitric Oxide Synthase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170518
[Lr] Data última revisão:
170518
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170312
[St] Status:MEDLINE



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