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[PMID]:28470848
[Au] Autor:Camprubi E; Jordan SF; Vasiliadou R; Lane N
[Ad] Endereço:Department of Genetics, Evolution and Environment, University College London, London, UK.
[Ti] Título:Iron catalysis at the origin of life.
[So] Source:IUBMB Life;69(6):373-381, 2017 06.
[Is] ISSN:1521-6551
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Iron-sulphur proteins are ancient and drive fundamental processes in cells, notably electron transfer and CO fixation. Iron-sulphur minerals with equivalent structures could have played a key role in the origin of life. However, the 'iron-sulphur world' hypothesis has had a mixed reception, with questions raised especially about the feasibility of a pyrites-pulled reverse Krebs cycle. Phylogenetics suggests that the earliest cells drove carbon and energy metabolism via the acetyl CoA pathway, which is also replete in Fe(Ni)S proteins. Deep differences between bacteria and archaea in this pathway obscure the ancestral state. These differences make sense if early cells depended on natural proton gradients in alkaline hydrothermal vents. If so, the acetyl CoA pathway diverged with the origins of active ion pumping, and ancestral CO fixation might have been equivalent to methanogens, which depend on a membrane-bound NiFe hydrogenase, energy converting hydrogenase. This uses the proton-motive force to reduce ferredoxin, thence CO . The mechanism suggests that pH could modulate reduction potential at the active site of the enzyme, facilitating the difficult reduction of CO by H . This mechanism could be generalised under abiotic conditions so that steep pH differences across semi-conducting Fe(Ni)S barriers drives not just the first steps of CO fixation to C1 and C2 organics such as CO, CH SH and CH COSH, but a series of similar carbonylation and hydrogenation reactions to form longer chain carboxylic acids such as pyruvate, oxaloacetate and α-ketoglutarate, as in the incomplete reverse Krebs cycle found in methanogens. We suggest that the closure of a complete reverse Krebs cycle, by regenerating acetyl CoA directly, displaced the acetyl CoA pathway from many modern groups. A later reliance on acetyl CoA and ATP eliminated the need for the proton-motive force to drive most steps of the reverse Krebs cycle. © 2017 IUBMB Life, 69(6):373-381, 2017.
[Mh] Termos MeSH primário: Acetilcoenzima A/química
Ferredoxinas/química
Proteínas com Ferro-Enxofre/química
Ferro/química
Origem da Vida
[Mh] Termos MeSH secundário: Acetilcoenzima A/metabolismo
Archaea/química
Archaea/metabolismo
Bactérias/química
Bactérias/metabolismo
Ciclo do Carbono
Dióxido de Carbono/química
Dióxido de Carbono/metabolismo
Catálise
Ciclo do Ácido Cítrico
Ferredoxinas/metabolismo
Concentração de Íons de Hidrogênio
Fontes Hidrotermais
Ferro/metabolismo
Proteínas com Ferro-Enxofre/metabolismo
Ácidos Cetoglutáricos/química
Ácidos Cetoglutáricos/metabolismo
Ácido Oxaloacético/química
Ácido Oxaloacético/metabolismo
Prótons
Ácido Pirúvico/química
Ácido Pirúvico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ferredoxins); 0 (Iron-Sulfur Proteins); 0 (Ketoglutaric Acids); 0 (Protons); 142M471B3J (Carbon Dioxide); 2F399MM81J (Oxaloacetic Acid); 72-89-9 (Acetyl Coenzyme A); 8558G7RUTR (Pyruvic Acid); 8ID597Z82X (alpha-ketoglutaric acid); E1UOL152H7 (Iron)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1002/iub.1632


  2 / 4127 MEDLINE  
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[PMID]:29199988
[Au] Autor:Mydy LS; Mashhadi Z; Knight TW; Fenske T; Hagemann T; Hoppe RW; Han L; Miller TR; Schwabacher AW; Silvaggi NR
[Ad] Endereço:Department of Chemistry and Biochemistry, University of Wisconsin-Milwaukee, Milwaukee, WI 53211, USA.
[Ti] Título:Swit_4259, an acetoacetate decarboxylase-like enzyme from Sphingomonas wittichii RW1.
[So] Source:Acta Crystallogr F Struct Biol Commun;73(Pt 12):672-681, 2017 Dec 01.
[Is] ISSN:2053-230X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The Gram-negative bacterium Sphingomonas wittichii RW1 is notable for its ability to metabolize a variety of aromatic hydrocarbons. Not surprisingly, the S. wittichii genome contains a number of putative aromatic hydrocarbon-degrading gene clusters. One of these includes an enzyme of unknown function, Swit_4259, which belongs to the acetoacetate decarboxylase-like superfamily (ADCSF). Here, it is reported that Swit_4259 is a small (28.8 kDa) tetrameric ADCSF enzyme that, unlike the prototypical members of the superfamily, does not have acetoacetate decarboxylase activity. Structural characterization shows that the tertiary structure of Swit_4259 is nearly identical to that of the true decarboxylases, but there are important differences in the fine structure of the Swit_4259 active site that lead to a divergence in function. In addition, it is shown that while it is a poor substrate, Swit_4259 can catalyze the hydration of 2-oxo-hex-3-enedioate to yield 2-oxo-4-hydroxyhexanedioate. It is also demonstrated that Swit_4259 has pyruvate aldolase-dehydratase activity, a feature that is common to all of the family V ADCSF enzymes studied to date. The enzymatic activity, together with the genomic context, suggests that Swit_4259 may be a hydratase with a role in the metabolism of an as-yet-unknown hydrocarbon. These data have implications for engineering bioremediation pathways to degrade specific pollutants, as well as structure-function relationships within the ADCSF in general.
[Mh] Termos MeSH primário: Proteínas de Bactérias/química
Proteínas de Bactérias/metabolismo
Carboxiliases/química
Sphingomonas/enzimologia
[Mh] Termos MeSH secundário: Acetoacetatos/química
Acetoacetatos/metabolismo
Proteínas de Bactérias/genética
Carboxiliases/genética
Carboxiliases/metabolismo
Domínio Catalítico
Cristalografia por Raios X
Ácidos Cetoglutáricos/metabolismo
Espectroscopia de Ressonância Magnética
Modelos Moleculares
Conformação Proteica
Ácido Pirúvico/química
Ácido Pirúvico/metabolismo
Espectrometria de Massas por Ionização por Electrospray
Especificidade por Substrato
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetoacetates); 0 (Bacterial Proteins); 0 (Ketoglutaric Acids); 4ZI204Y1MC (acetoacetic acid); 8558G7RUTR (Pyruvic Acid); 8ID597Z82X (alpha-ketoglutaric acid); EC 4.1.1.- (Carboxy-Lyases); EC 4.1.1.4 (acetoacetate decarboxylase)
[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:171205
[St] Status:MEDLINE
[do] DOI:10.1107/S2053230X17015862


  3 / 4127 MEDLINE  
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[PMID]:29173237
[Au] Autor:Robertson RC; Seira Oriach C; Murphy K; Moloney GM; Cryan JF; Dinan TG; Ross RP; Stanton C
[Ad] Endereço:1School of Microbiology,University College Cork,Cork,Republic of Ireland.
[Ti] Título:Deficiency of essential dietary n-3 PUFA disrupts the caecal microbiome and metabolome in mice.
[So] Source:Br J Nutr;118(11):959-970, 2017 Dec.
[Is] ISSN:1475-2662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:n-3 PUFA are lipids that play crucial roles in immune-regulation, cardio-protection and neurodevelopment. However, little is known about the role that these essential dietary fats play in modulating caecal microbiota composition and the subsequent production of functional metabolites. To investigate this, female C57BL/6 mice were assigned to one of three diets (control (CON), n-3 supplemented (n3+) or n-3 deficient (n3-)) during gestation, following which their male offspring were continued on the same diets for 12 weeks. Caecal content of mothers and offspring were collected for 16S sequencing and metabolic phenotyping. n3- male offspring displayed significantly less % fat mass than n3+ and CON. n-3 Status also induced a number of changes to gut microbiota composition such that n3- offspring had greater abundance of Tenericutes, Anaeroplasma and Coriobacteriaceae. Metabolomics analysis revealed an increase in caecal metabolites involved in energy metabolism in n3+ including α-ketoglutaric acid, malic acid and fumaric acid. n3- animals displayed significantly reduced acetate, butyrate and total caecal SCFA production. These results demonstrate that dietary n-3 PUFA regulate gut microbiota homoeostasis whereby n-3 deficiency may induce a state of disturbance. Further studies are warranted to examine whether these microbial and metabolic disturbances are causally related to changes in metabolic health outcomes.
[Mh] Termos MeSH primário: Fenômenos Fisiológicos da Nutrição Animal
Ceco/microbiologia
Ácidos Graxos Ômega-3/deficiência
Microbioma Gastrointestinal
[Mh] Termos MeSH secundário: Animais
Composição Corporal
DNA Bacteriano/isolamento & purificação
Dieta
Suplementos Nutricionais
Ácidos Graxos/metabolismo
Ácidos Graxos Ômega-3/sangue
Feminino
Fumaratos/metabolismo
Ácidos Cetoglutáricos/metabolismo
Malatos/metabolismo
Masculino
Metaboloma
Metabolômica
Camundongos
Camundongos Endogâmicos C57BL
RNA Ribossômico 16S/isolamento & purificação
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Bacterial); 0 (Fatty Acids); 0 (Fatty Acids, Omega-3); 0 (Fumarates); 0 (Ketoglutaric Acids); 0 (Malates); 0 (RNA, Ribosomal, 16S); 817L1N4CKP (malic acid); 88XHZ13131 (fumaric acid); 8ID597Z82X (alpha-ketoglutaric acid)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171218
[Lr] Data última revisão:
171218
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1017/S0007114517002999


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[PMID]:28063221
[Au] Autor:Sahebkar A; Sancho E; Abelló D; Camps J; Joven J
[Ad] Endereço:Mashhad University of Medical Sciences, Biotechnology Research Center, Mashhad, Iran.
[Ti] Título:Novel circulating biomarkers for non-alcoholic fatty liver disease: A systematic review.
[So] Source:J Cell Physiol;233(2):849-855, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Currently, a liver biopsy remains the only reliable way to precisely diagnose non-alcoholic fatty liver disease (NAFLD) and establish the severity of liver injury, presence of fibrosis, and architecture remodeling. However, the cost and the intrinsic invasive procedure of a liver biopsy rules it out as a gold standard diagnostic test, and the imaging test are not the best choice due to the price, and currently is being refined. The lack of a biomarker of NAFLD pushes to develop this new line of research. The aim of the present systematic review is to clarify and update all the NAFLD biomarkers described in the literature until recently. We highlight α-ketoglutarate and CK18-F as currently the best potential biomarker of NAFLD. However, due to methodological differences, we propose the implementation of international, multicenter, multiethnic studies with larger population size, and biopsy proven NAFLD diagnosis to analyze and compare α-ketoglutarate and CK18-F as potential biomarkers of the silent evolution of NAFLD.
[Mh] Termos MeSH primário: Queratina-18/sangue
Ácidos Cetoglutáricos/sangue
Fígado/metabolismo
Hepatopatia Gordurosa não Alcoólica/sangue
[Mh] Termos MeSH secundário: Animais
Biomarcadores/sangue
Biópsia
Seres Humanos
Fígado/patologia
Hepatopatia Gordurosa não Alcoólica/diagnóstico
Valor Preditivo dos Testes
Prognóstico
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (KRT18 protein, human); 0 (Keratin-18); 0 (Ketoglutaric Acids); 8ID597Z82X (alpha-ketoglutaric acid)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170108
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25779


  5 / 4127 MEDLINE  
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[PMID]:28874460
[Au] Autor:Martin-Lorenzo M; Martinez PJ; Baldan-Martin M; Ruiz-Hurtado G; Prado JC; Segura J; de la Cuesta F; Barderas MG; Vivanco F; Ruilope LM; Alvarez-Llamas G
[Ad] Endereço:From the Department of Immunology, IIS-Fundacion Jimenez Diaz, REDinREN, Madrid, Spain (M.M.-L., P.J.M., F.V., G.A.-L.); Department of Vascular Physiopathology, Hospital Nacional de Paraplejicos SESCAM, Toledo, Spain (M.B.-M., M.G.B.); Hypertension Unit, Instituto de Investigación imas12, Hospital U
[Ti] Título:Citric Acid Metabolism in Resistant Hypertension: Underlying Mechanisms and Metabolic Prediction of Treatment Response.
[So] Source:Hypertension;70(5):1049-1056, 2017 Nov.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Resistant hypertension (RH) affects 9% to 12% of hypertensive adults. Prolonged exposure to suboptimal blood pressure control results in end-organ damage and cardiovascular risk. Spironolactone is the most effective drug for treatment, but not all patients respond and side effects are not negligible. Little is known on the mechanisms responsible for RH. We aimed to identify metabolic alterations in urine. In addition, a potential capacity of metabolites to predict response to spironolactone was investigated. Urine was collected from 29 patients with RH and from a group of 13 subjects with pseudo-RH. For patients, samples were collected before and after spironolactone administration and were classified in responders (n=19) and nonresponders (n=10). Nuclear magnetic resonance was applied to identify altered metabolites and pathways. Metabolites were confirmed by liquid chromatography-mass spectrometry. Citric acid cycle was the pathway most significantly altered ( <0.0001). Metabolic concentrations were quantified and ranged from ng/mL malate to µg/mL citrate. Citrate and oxaloacetate increased in RH versus pseudoresistant. Together with α-ketoglutarate and malate, they were able to discriminate between responders and nonresponders, being the 4 metabolites increased in nonresponders. Combined as a prediction panel, they showed receiver operating characteristiccurve with area under the curve of 0.96. We show that citric acid cycle and deregulation of reactive oxygen species homeostasis control continue its activation after hypertension was developed. A metabolic panel showing alteration before spironolactone treatment and predicting future response of patients is shown. These molecular indicators will contribute optimizing the rate of control of RH patients with spironolactone.
[Mh] Termos MeSH primário: Ácido Cítrico
Resistência a Medicamentos/fisiologia
Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos
Hipertensão
Espironolactona
[Mh] Termos MeSH secundário: Idoso
Anti-Hipertensivos/administração & dosagem
Anti-Hipertensivos/efeitos adversos
Anti-Hipertensivos/farmacocinética
Cromatografia Líquida/métodos
Ácido Cítrico/análise
Ácido Cítrico/metabolismo
Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/diagnóstico
Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/urina
Feminino
Seres Humanos
Hipertensão/tratamento farmacológico
Hipertensão/epidemiologia
Hipertensão/metabolismo
Ácidos Cetoglutáricos/análise
Ácidos Cetoglutáricos/metabolismo
Masculino
Meia-Idade
Valor Preditivo dos Testes
Prognóstico
Espanha/epidemiologia
Espironolactona/administração & dosagem
Espironolactona/efeitos adversos
Espironolactona/farmacocinética
Urinálise/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Ketoglutaric Acids); 27O7W4T232 (Spironolactone); 2968PHW8QP (Citric Acid); 8ID597Z82X (alpha-ketoglutaric acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170907
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.117.09819


  6 / 4127 MEDLINE  
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[PMID]:28827812
[Au] Autor:Irnov I; Wang Z; Jannetty ND; Bustamante JA; Rhee KY; Jacobs-Wagner C
[Ad] Endereço:Microbial Sciences Institute, Yale University, West Haven, CT, United States of America.
[Ti] Título:Crosstalk between the tricarboxylic acid cycle and peptidoglycan synthesis in Caulobacter crescentus through the homeostatic control of α-ketoglutarate.
[So] Source:PLoS Genet;13(8):e1006978, 2017 Aug.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To achieve robust replication, bacteria must integrate cellular metabolism and cell wall growth. While these two processes have been well characterized, the nature and extent of cross-regulation between them is not well understood. Here, using classical genetics, CRISPRi, metabolomics, transcriptomics and chemical complementation approaches, we show that a loss of the master regulator Hfq in Caulobacter crescentus alters central metabolism and results in cell shape defects in a nutrient-dependent manner. We demonstrate that the cell morphology phenotype in the hfq deletion mutant is attributable to a disruption of α-ketoglutarate (KG) homeostasis. In addition to serving as a key intermediate of the tricarboxylic acid (TCA) cycle, KG is a by-product of an enzymatic reaction required for the synthesis of peptidoglycan, a major component of the bacterial cell wall. Accumulation of KG in the hfq deletion mutant interferes with peptidoglycan synthesis, resulting in cell morphology defects and increased susceptibility to peptidoglycan-targeting antibiotics. This work thus reveals a direct crosstalk between the TCA cycle and cell wall morphogenesis. This crosstalk highlights the importance of metabolic homeostasis in not only ensuring adequate availability of biosynthetic precursors, but also in preventing interference with cellular processes in which these intermediates arise as by-products.
[Mh] Termos MeSH primário: Caulobacter crescentus/genética
Parede Celular/genética
Ciclo do Ácido Cítrico/genética
Fator Proteico 1 do Hospedeiro/genética
[Mh] Termos MeSH secundário: Caulobacter crescentus/crescimento & desenvolvimento
Ciclo Celular/genética
Parede Celular/metabolismo
Replicação do DNA/genética
Homeostase
Ácidos Cetoglutáricos/metabolismo
Metabolômica
Peptidoglicano/biossíntese
Peptidoglicano/genética
Deleção de Sequência/genética
Transcriptoma/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Host Factor 1 Protein); 0 (Ketoglutaric Acids); 0 (Peptidoglycan); 8ID597Z82X (alpha-ketoglutaric acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170823
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006978


  7 / 4127 MEDLINE  
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[PMID]:28813658
[Au] Autor:Chisolm DA; Savic D; Moore AJ; Ballesteros-Tato A; León B; Crossman DK; Murre C; Myers RM; Weinmann AS
[Ad] Endereço:Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
[Ti] Título:CCCTC-Binding Factor Translates Interleukin 2- and α-Ketoglutarate-Sensitive Metabolic Changes in T Cells into Context-Dependent Gene Programs.
[So] Source:Immunity;47(2):251-267.e7, 2017 Aug 15.
[Is] ISSN:1097-4180
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Despite considerable research connecting cellular metabolism with differentiation decisions, the underlying mechanisms that translate metabolite-sensitive activities into unique gene programs are still unclear. We found that aspects of the interleukin-2 (IL-2)-sensitive effector gene program in CD4 and CD8 T cells in type 1 conditions (Th1) were regulated by glutamine and alpha-ketoglutarate (αKG)-induced events, in part through changes in DNA and histone methylation states. We further identified a mechanism by which IL-2- and αKG-sensitive metabolic changes regulated the association of CCCTC-binding factor (CTCF) with select genomic sites. αKG-sensitive CTCF sites were often associated with loci containing IL-2- and αKG-sensitive genome organization patterns and gene expression in T cells. IL-2- and αKG-sensitive CTCF sites in T cells were also associated with genes from developmental pathways that had αKG-sensitive expression in embryonic stem cells. The data collectively support a mechanism wherein CTCF serves to translate αKG-sensitive metabolic changes into context-dependent differentiation gene programs.
[Mh] Termos MeSH primário: Diferenciação Celular
Interleucina-2/metabolismo
Ácidos Cetoglutáricos/metabolismo
Proteínas Repressoras/metabolismo
Células Th1/imunologia
[Mh] Termos MeSH secundário: Animais
Fator de Ligação a CCCTC
Diferenciação Celular/genética
Células Cultivadas
Microambiente Celular
Metilação de DNA
Feminino
Regulação da Expressão Gênica
Glutamina/metabolismo
Histonas/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Proteínas Repressoras/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CCCTC-Binding Factor); 0 (Ctcf protein, mouse); 0 (Histones); 0 (Interleukin-2); 0 (Ketoglutaric Acids); 0 (Repressor Proteins); 0RH81L854J (Glutamine); 8ID597Z82X (alpha-ketoglutaric acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170817
[St] Status:MEDLINE


  8 / 4127 MEDLINE  
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[PMID]:28764105
[Au] Autor:Zeng W; Zhang H; Xu S; Fang F; Zhou J
[Ad] Endereço:Key Laboratory of Industrial Biotechnology of Ministry of Education, School of Biotechnology, Jiangnan University, Wuxi 214122, Jiangsu, China; National Engineering Laboratory for Cereal Fermentation Technology, Jiangnan University, Wuxi 214122, Jiangsu, China.
[Ti] Título:Biosynthesis of keto acids by fed-batch culture of Yarrowia lipolytica WSH-Z06.
[So] Source:Bioresour Technol;243:1037-1043, 2017 Nov.
[Is] ISSN:1873-2976
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Both α-ketoglutarate (α-KG) and pyruvate (PYR) are important organic acids with promising applications in the food, pharmaceutical and chemical industries. During the production of α-KG by different microorganisms, PYR is always present as a by-product. Strategies have been applied to eliminate PYR accumulation since it can bring difficulties to the downstream separation process. However, modern separation technologies have already conquered this problem. Therefore, this study was aimed at simultaneously enhancing α-KG and PYR production by Yarrowia lipolytica WSH-Z06. Using a fed-batch strategy, in which the initial glycerol concentration was 50g·L , the residual glycerol concentration was maintained 20-30g·L by constant feeding at a rate of 1.25g·L ·h . The titers of α-KG and PYR were increased by 9.6% and 176.8%, and reached 67.4g·L and 39.1g·L , respectively. The final yield of keto acids was 0.71g·g glycerol, which is 42.0% higher than that of the optimal batch fermentation.
[Mh] Termos MeSH primário: Ácidos Cetoglutáricos
Yarrowia
[Mh] Termos MeSH secundário: Técnicas de Cultura Celular por Lotes
Glicerol
Cetoácidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Keto Acids); 0 (Ketoglutaric Acids); 8ID597Z82X (alpha-ketoglutaric acid); PDC6A3C0OX (Glycerol)
[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


  9 / 4127 MEDLINE  
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[PMID]:28714978
[Au] Autor:Liu PS; Wang H; Li X; Chao T; Teav T; Christen S; Di Conza G; Cheng WC; Chou CH; Vavakova M; Muret C; Debackere K; Mazzone M; Huang HD; Fendt SM; Ivanisevic J; Ho PC
[Ad] Endereço:Department of Fundamental Oncology, Faculty of Biology and Medicine, University of Lausanne, Epalinges, Switzerland.
[Ti] Título:α-ketoglutarate orchestrates macrophage activation through metabolic and epigenetic reprogramming.
[So] Source:Nat Immunol;18(9):985-994, 2017 Sep.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glutamine metabolism provides synergistic support for macrophage activation and elicitation of desirable immune responses; however, the underlying mechanisms regulated by glutamine metabolism to orchestrate macrophage activation remain unclear. Here we show that the production of α-ketoglutarate (αKG) via glutaminolysis is important for alternative (M2) activation of macrophages, including engagement of fatty acid oxidation (FAO) and Jmjd3-dependent epigenetic reprogramming of M2 genes. This M2-promoting mechanism is further modulated by a high αKG/succinate ratio, whereas a low ratio strengthens the proinflammatory phenotype in classically activated (M1) macrophages. As such, αKG contributes to endotoxin tolerance after M1 activation. This study reveals new mechanistic regulations by which glutamine metabolism tailors the immune responses of macrophages through metabolic and epigenetic reprogramming.
[Mh] Termos MeSH primário: Reprogramação Celular/imunologia
Epigênese Genética
Ácidos Cetoglutáricos/imunologia
Ativação de Macrófagos/imunologia
Macrófagos/imunologia
[Mh] Termos MeSH secundário: Animais
Imunoprecipitação da Cromatina
Ciclo do Ácido Cítrico/imunologia
Ácidos Graxos/metabolismo
Perfilação da Expressão Gênica
Glutamina/metabolismo
Glicólise/imunologia
Ácidos Cetoglutáricos/metabolismo
Lipopolissacarídeos
Macrófagos/metabolismo
Metabolômica
Camundongos
NF-kappa B/imunologia
Oxirredução
Fosforilação Oxidativa
Fenótipo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Análise de Sequência de RNA
Ácido Succínico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids); 0 (Ketoglutaric Acids); 0 (Lipopolysaccharides); 0 (NF-kappa B); 0RH81L854J (Glutamine); 8ID597Z82X (alpha-ketoglutaric acid); AB6MNQ6J6L (Succinic Acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3796


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[PMID]:28642005
[Au] Autor:Wang X; Inaoka DK; Shiba T; Balogun EO; Allmann S; Watanabe YI; Boshart M; Kita K; Harada S
[Ad] Endereço:Department of Biomedical Chemistry, School of International Health, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan; School of Tropical Medicine and Global Health, Nagasaki University, Nagasaki 852-8523, Japan.
[Ti] Título:Expression, purification, and crystallization of type 1 isocitrate dehydrogenase from Trypanosoma brucei brucei.
[So] Source:Protein Expr Purif;138:56-62, 2017 Oct.
[Is] ISSN:1096-0279
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Isocitrate dehydrogenases (IDHs) are metabolic enzymes that catalyze the oxidative decarboxylation of isocitrate to α-ketoglutarate. Depending on the electron acceptor and subcellular localization, these enzymes are classified as NADP -dependent IDH1 in the cytosol or peroxisomes, NADP -dependent IDH2 and NAD -dependent IDH3 in mitochondria. Trypanosoma brucei is a protozoan parasite that causes African sleeping sickness in humans and Nagana disease in animals. Here, for the first time, a putative glycosomal T. brucei type 1 IDH (TbIDH1) was expressed in Escherichia coli and purified for crystallographic study. Surprisingly, the putative NADP -dependent TbIDH1 has higher activity with NAD compared with NADP as electron acceptor, a unique characteristic among known eukaryotic IDHs which encouraged us to crystallize TbIDH1 for future biochemical and structural studies. Methods of expression and purification of large amounts of recombinant TbIDH1 with improved solubility to facilitate protein crystallization are presented.
[Mh] Termos MeSH primário: Isocitrato Desidrogenase/genética
NADP/metabolismo
NAD/metabolismo
Proteínas de Protozoários/genética
Proteínas Recombinantes de Fusão/genética
Trypanosoma brucei brucei/química
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Clonagem Molecular
Cristalização
Escherichia coli/genética
Escherichia coli/metabolismo
Expressão Gênica
Vetores Genéticos/química
Vetores Genéticos/metabolismo
Isocitrato Desidrogenase/isolamento & purificação
Isocitrato Desidrogenase/metabolismo
Isocitratos/metabolismo
Ácidos Cetoglutáricos/metabolismo
Peso Molecular
Proteínas de Protozoários/isolamento & purificação
Proteínas de Protozoários/metabolismo
Proteínas Recombinantes de Fusão/isolamento & purificação
Proteínas Recombinantes de Fusão/metabolismo
Trypanosoma brucei brucei/enzimologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Isocitrates); 0 (Ketoglutaric Acids); 0 (Protozoan Proteins); 0 (Recombinant Fusion Proteins); 0U46U6E8UK (NAD); 320-77-4 (isocitric acid); 53-59-8 (NADP); 8ID597Z82X (alpha-ketoglutaric acid); EC 1.1.1.41 (Isocitrate Dehydrogenase)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170624
[St] Status:MEDLINE



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