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1
Li, Quan, Xiangyang Li, and Hui Lin. "Proteomic Analysis Reveals Growth Inhibition of Coriolus versicolor by Methanol Extracts of Cinnamomum camphora Xylem." International Journal of Polymer Science 2021 (August 21, 2021): 1–9. http://dx.doi.org/10.1155/2021/6337906.
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The extracts of decay-resistant tree species are important research objects for the future development of wood preservatives. To understand the antifungal mechanisms of Coriolus versicolor inhibition with methanol extracts of C. camphora xylem, the protein profiles of C. versicolor were analyzed using 2-DE followed by MALDI-TOF/MS and bioinformatic analyses. The results showed that 41 protein spots were obviously changed among the 366-385 protein spots of C. versicolor treated with methanol extracts of C. camphora xylem. Twenty-one protein spots were upregulated, and 20 protein spots were downregulated. Cellular localization was performed to identify these differential proteins, and biological process and functional analysis found that 9 of these proteins were in the cytoplasm, 6 were intracellular, and 5 were in the mitochondrion. A total of 18.8% were mapped to small-molecule metabolic processes, 12.5% to cellular amino acid metabolic processes, and 10.9% to cellular nitrogen compound metabolic processes. Twenty-five percent of the differential proteins were associated with ion bonding, 15% with oxidoreductase activity, and 15% with ATPase activity and transmembrane transport activity. Downregulated expression of aspartate aminotransferase, ATP synthase alpha chain, DEAD/DEAH-box helicase, and phosphoglycerate kinase showed that the methanol extracts of C. camphora xylem disrupted functional aspects such as nitrogen and carbon metabolism, energy metabolism, hormone signal response, and glucose metabolism, eventually leading to C. versicolor inhibition.
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Slayton, Mark, Abhishek Gupta, Bijinu Balakrishnan, and Vishwajeet Puri. "CIDE Proteins in Human Health and Disease." Cells 8, no. 3 (March 13, 2019): 238. http://dx.doi.org/10.3390/cells8030238.
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Cell death-Inducing DNA Fragmentation Factor Alpha (DFFA)-like Effector (CIDE) proteins have emerged as lipid droplet-associated proteins that regulate fat metabolism. There are three members in the CIDE protein family—CIDEA, CIDEB, and CIDEC (also known as fat-specific protein 27 (FSP27)). CIDEA and FSP27 are primarily expressed in adipose tissue, while CIDEB is expressed in the liver. Originally, based upon their homology with DNA fragmentation factors, these proteins were identified as apoptotic proteins. However, recent studies have changed the perception of these proteins, redefining them as regulators of lipid droplet dynamics and fat metabolism, which contribute to a healthy metabolic phenotype in humans. Despite various studies in humans and gene-targeting studies in mice, the physiological roles of CIDE proteins remains elusive. This review will summarize the known physiological role and metabolic pathways regulated by the CIDE proteins in human health and disease.
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Aleshin, Vasily A., Artem V. Artiukhov, Thilo Kaehne, Anastasia V. Graf, and Victoria I. Bunik. "Daytime Dependence of the Activity of the Rat Brain Pyruvate Dehydrogenase Corresponds to the Mitochondrial Sirtuin 3 Level and Acetylation of Brain Proteins, All Regulated by Thiamine Administration Decreasing Phosphorylation of PDHA Ser293." International Journal of Molecular Sciences 22, no. 15 (July 27, 2021): 8006. http://dx.doi.org/10.3390/ijms22158006.
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Coupling glycolysis and mitochondrial tricarboxylic acid cycle, pyruvate dehydrogenase (PDH) complex (PDHC) is highly responsive to cellular demands through multiple mechanisms, including PDH phosphorylation. PDHC also produces acetyl-CoA for protein acetylation involved in circadian regulation of metabolism. Thiamine (vitamin B1) diphosphate (ThDP) is known to activate PDH as both coenzyme and inhibitor of the PDH inactivating kinases. Molecular mechanisms integrating the function of thiamine-dependent PDHC into general redox metabolism, underlie physiological fitness of a cell or an organism. Here, we characterize the daytime- and thiamine-dependent changes in the rat brain PDHC function, expression and phosphorylation, assessing their impact on protein acetylation and metabolic regulation. Morning administration of thiamine significantly downregulates both the PDH phosphorylation at Ser293 and SIRT3 protein level, the effects not observed upon the evening administration. This action of thiamine nullifies the daytime-dependent changes in the brain PDHC activity and mitochondrial acetylation, inducing diurnal difference in the cytosolic acetylation and acetylation of total brain proteins. Screening the daytime dependence of central metabolic enzymes and proteins of thiol/disulfide metabolism reveals that thiamine also cancels daily changes in the malate dehydrogenase activity, opposite to those of the PDHC activity. Correlation analysis indicates that thiamine abrogates the strong positive correlation between the total acetylation of the brain proteins and PDHC function. Simultaneously, thiamine heightens interplay between the expression of PDHC components and total acetylation or SIRT2 protein level. These thiamine effects on the brain acetylation system change metabolic impact of acetylation. The changes are exemplified by the thiamine enhancement of the SIRT2 correlations with metabolic enzymes and proteins of thiol-disulfide metabolism. Thus, we show the daytime- and thiamine-dependent changes in the function and phosphorylation of brain PDHC, contributing to regulation of the brain acetylation system and redox metabolism. The daytime-dependent action of thiamine on PDHC and SIRT3 may be of therapeutic significance in correcting perturbed diurnal regulation.
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Olalde-Portugal, Víctor, José Luis Cabrera-Ponce, Argel Gastelum-Arellanez, Armando Guerrero-Rangel, Robert Winkler, and Silvia Valdés-Rodríguez. "Proteomic analysis and interactions network in leaves of mycorrhizal and nonmycorrhizal sorghum plants under water deficit." PeerJ 8 (April 23, 2020): e8991. http://dx.doi.org/10.7717/peerj.8991.
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For understanding the water deficit stress mechanism in sorghum, we conducted a physiological and proteomic analysis in the leaves of Sorghum bicolor L. Moench (a drought tolerant crop model) of non-colonized and colonized plants with a consortium of arbuscular mycorrhizal fungi. Physiological results indicate that mycorrhizal fungi association enhances growth and photosynthesis in plants, under normal and water deficit conditions. 2D-electrophoresis profiles revealed 51 differentially accumulated proteins in response to water deficit, of which HPLC/MS successfully identified 49. Bioinformatics analysis of protein–protein interactions revealed the participation of different metabolic pathways in nonmycorrhizal compared to mycorrhizal sorghum plants under water deficit. In noninoculated plants, the altered proteins are related to protein synthesis and folding (50S ribosomal protein L1, 30S ribosomal protein S10, Nascent polypeptide-associated complex subunit alpha), coupled with multiple signal transduction pathways, guanine nucleotide-binding beta subunit (Rack1) and peptidyl-prolyl-cis-trans isomerase (ROC4). In contrast, in mycorrhizal plants, proteins related to energy metabolism (ATP synthase-24kDa, ATP synthase β), carbon metabolism (malate dehydrogenase, triosephosphate isomerase, sucrose-phosphatase), oxidative phosphorylation (mitochondrial-processing peptidase) and sulfur metabolism (thiosulfate/3-mercaptopyruvate sulfurtransferase) were found. Our results provide a set of proteins of different metabolic pathways involved in water deficit produced by sorghum plants alone or associated with a consortium of arbuscular mycorrhizal fungi isolated from the tropical rain forest Los Tuxtlas Veracruz, México.
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Chiang, John Y. L., Preeti Pathak, Hailiang Liu, Ajay Donepudi, Jessica Ferrell, and Shannon Boehme. "Intestinal Farnesoid X Receptor and Takeda G Protein Couple Receptor 5 Signaling in Metabolic Regulation." Digestive Diseases 35, no. 3 (2017): 241–45. http://dx.doi.org/10.1159/000450981.
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Bile acids play a critical role in the regulation of glucose, lipid and energy metabolisms by activating the nuclear bile acid receptor farnesoid X receptor (FXR) and membrane G protein-coupled bile acid receptor-1 (aka takeda G protein couple receptor 5, TGR5) signaling. Paradoxical roles of FXR in the regulation of glucose and lipid metabolism and metabolic disorder have been reported recently. The activation or inhibition of intestinal FXR signaling has been shown to improve insulin and glucose sensitivity and energy metabolism to prevent diabetes, obesity and non-alcoholic fatty liver disease (NAFLD). TGR5 has an anti-inflammatory function in the intestine and stimulates glucagon-like peptide-1 (GLP-1) secretion in the intestine to stimulate insulin secretion from the pancreas. The role of TGR5 in metabolism and metabolic regulation is not clear and warrants further study. FXR and TGR5 are co-expressed in the ileum and colon. These 2 bile acid-activated receptors may cooperate to stimulate GLP-1 secretion and improve hepatic metabolism. FXR and TGR5 dual agonists may have therapeutic potential for treating diabetes and NAFLD.
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Phillips, Darci, Angel M. Aponte, Raul Covian, Edward Neufeld, Zu-Xi Yu, and Robert S. Balaban. "Homogenous protein programming in the mammalian left and right ventricle free walls." Physiological Genomics 43, no. 21 (November 2011): 1198–206. http://dx.doi.org/10.1152/physiolgenomics.00121.2011.
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Despite identical cardiac outputs, the right (RV) and left ventricle (LV) have very different embryological origins and resting workload. These differences suggest that the ventricles have different protein programming with regard to energy metabolism and contractile elements. The objective of this study was to determine the relative RV and LV protein expression levels, with an emphasis on energy metabolism. The RV and LV protein contents of the rabbit and porcine heart were determined with quantitative gel electrophoresis (2D-DIGE), mass spectrometry, and optical spectroscopy techniques. Surprisingly, the expression levels for more than 600 RV and LV proteins detected were similar. This included proteins many different compartments and metabolic pathways. In addition, no isoelectric shifts were detected in 2D-DIGE consistent with no differential posttranslational modifications in these proteins. Analysis of the RV and LV metabolic response to work revealed that the metabolic rate increases much faster with workload in the RV compared with LV. This implies that the generally lower metabolic stress of the RV actually approaches LV metabolic stress at maximum workloads. Thus, identical levels of energy conversion and mechanical elements in the RV and LV may be driven by the performance requirements at maximum workloads. In summary, the ventricles of the heart manage the differences in overall workload by modifying the amounts of cytosol, not its composition. The constant myocyte composition in the LV and RV implies that the ratio of energy metabolism and contractile elements may be optimal for the sustained cardiac contractile activity in the mammalian heart.
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Zhou, Suping, Marsha Palmer, Jing Zhou, Sarabjit Bhatti, Kevin J. Howe, Tara Fish, and Theodore W. Thannhauser. "Differential Root Proteome Expression in Tomato Genotypes with Contrasting Drought Tolerance Exposed to Dehydration." Journal of the American Society for Horticultural Science 138, no. 2 (March 2013): 131–41. http://dx.doi.org/10.21273/jashs.138.2.131.
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A comparative proteomics study using isobaric tags for relative and absolute quantitation (iTRAQ) was performed on a mesophytic tomato (Solanum lycopersicum) cultivar and a dehydration-resistant wild species (Solanum chilense) to identify proteins that play key roles in tolerance to water deficit stress. In tomato ‘Walter’ LA3465, 130 proteins were identified, of which 104 (80%) were repressed and 26 (20%) were induced. In S. chilense LA1958, a total of 170 proteins were identified with 106 (62%) repressed and 64 (38%) induced. According to their putative molecular functions, the differentially expressed proteins belong to the following subgroups: stress proteins, gene expression, nascent protein processing, protein folding, protein degradation, carbohydrate metabolism, amino acid and nucleotide metabolism, lipid metabolism, signal transduction, and cell cycle regulation. Based on changes in protein abundance induced by the dehydration treatment, cellular metabolic activities and protein biosynthesis were suppressed by the stress. In S. chilense, dehydration treatment led to elevated accumulation of proteins involved in post-transcriptional gene regulation and fidelity in protein translation including prefoldin, which promotes protein folding without the use of adenosine-5′-triphosphate (ATP), several hydrophilic proteins, and calmodulin in the calcium signal transduction pathway. Those protein changes were not found in the susceptible tomato, ‘Walter’. Within each functional protein group, proteins showing opposite changes (dehydration induced vs. repressed) in the two species were identified and roles of those proteins in conferring tolerance to water deficit stress are discussed. Information provided in this report will be useful for selection of proteins or genes in analyzing or improving dehydration tolerance in tomato cultivars.
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Herrmann, Abigail G., Ruth F. Deighton, Thierry Le Bihan, Mailis C. McCulloch, James L. Searcy, Lorraine E. Kerr, and James McCulloch. "Adaptive Changes in the Neuronal Proteome: Mitochondrial Energy Production, Endoplasmic Reticulum Stress, and Ribosomal Dysfunction in the Cellular Response to Metabolic Stress." Journal of Cerebral Blood Flow & Metabolism 33, no. 5 (January 16, 2013): 673–83. http://dx.doi.org/10.1038/jcbfm.2012.204.
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Impaired energy metabolism in neurons is integral to a range of neurodegenerative diseases, from Alzheimer's disease to stroke. To investigate the complex molecular changes underpinning cellular adaptation to metabolic stress, we have defined the proteomic response of the SH-SY5Y human neuroblastoma cell line after exposure to a metabolic challenge of oxygen glucose deprivation (OGD) in vitro. A total of 958 proteins across multiple subcellular compartments were detected and quantified by label-free liquid chromatography mass spectrometry. The levels of 130 proteins were significantly increased ( P < 0.01) after OGD and the levels of 63 proteins were significantly decreased ( P < 0.01) while expression of the majority of proteins (765) was not altered. Network analysis identified novel protein–protein interactomes involved with mitochondrial energy production, protein folding, and protein degradation, indicative of coherent and integrated proteomic responses to the metabolic challenge. Approximately one third (61) of the differentially expressed proteins was associated with the endoplasmic reticulum and mitochondria. Electron microscopic analysis of these subcellular structures showed morphologic changes consistent with the identified proteomic alterations. Our investigation of the global cellular response to a metabolic challenge clearly shows the considerable adaptive capacity of the proteome to a slowly evolving metabolic challenge.
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Zhao, Zifeng, Lei Yin, Feihua Wu, and Xin Tong. "Hepatic metabolic regulation by nuclear factor E4BP4." Journal of Molecular Endocrinology 66, no. 1 (January 2021): R15—R21. http://dx.doi.org/10.1530/jme-20-0239.
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Discovered as a b-ZIP transcription repressor 30 years ago, E4 promoter-binding protein 4 (E4BP4) has been shown to play critical roles in immunity, circadian rhythms, and cancer progression. Recent research has highlighted E4BP4 as a novel regulator of metabolisms in various tissues. In this review, we focus on the function and mechanisms of hepatic E4BP4 in regulating lipid and glucose homeostasis, bile metabolism, as well as xenobiotic metabolism. Finally, E4BP4-specific targets will be discussed for the prevention and treatment of metabolic disorders.
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Xu, Man, Run-Qing Xue, Yi Lu, Su-Yun Yong, Qing Wu, Yan-Ling Cui, Xiao-Ting Zuo, Xiao-Jiang Yu, Ming Zhao, and Wei-Jin Zang. "Choline ameliorates cardiac hypertrophy by regulating metabolic remodelling and UPRmt through SIRT3-AMPK pathway." Cardiovascular Research 115, no. 3 (August 27, 2018): 530–45. http://dx.doi.org/10.1093/cvr/cvy217.
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Abstract Aims Cardiac hypertrophy is characterized by a shift in metabolic substrate utilization, but the molecular events underlying the metabolic remodelling remain poorly understood. We explored metabolic remodelling and mitochondrial dysfunction in cardiac hypertrophy and investigated the cardioprotective effects of choline. Methods and results The experiments were conducted using a model of ventricular hypertrophy by partially banding the abdominal aorta of Sprague Dawley rats. Cardiomyocyte size and cardiac fibrosis were significantly increased in hypertrophic hearts. In vitro cardiomyocyte hypertrophy was induced by exposing neonatal rat cardiomyocytes to angiotensin II (Ang II) (10−6 M, 24 h). Choline attenuated the mito-nuclear protein imbalance and activated the mitochondrial-unfolded protein response (UPRmt) in the heart, thereby preserving the ultrastructure and function of mitochondria in the context of cardiac hypertrophy. Moreover, choline inhibited myocardial metabolic dysfunction by promoting the expression of proteins involved in ketone body and fatty acid metabolism in response to pressure overload, accompanied by the activation of sirtuin 3/AMP-activated protein kinase (SIRT3-AMPK) signalling. In vitro analyses demonstrated that SIRT3 siRNA diminished choline-mediated activation of ketone body metabolism and UPRmt, as well as inhibition of hypertrophic signals. Intriguingly, serum from choline-treated abdominal aorta banding models (where β-hydroxybutyrate was increased) attenuated Ang II-induced myocyte hypertrophy, which indicates that β-hydroxybutyrate is important for the cardioprotective effects of choline. Conclusion Choline attenuated cardiac dysfunction by modulating the expression of proteins involved in ketone body and fatty acid metabolism, and induction of UPRmt; this was likely mediated by activation of the SIRT3-AMPK pathway. Taken together, these results identify SIRT3-AMPK as a key cardiac transcriptional regulator that helps orchestrate an adaptive metabolic response to cardiac stress. Choline treatment may represent a new therapeutic strategy for optimizing myocardial metabolism in the context of hypertrophy and heart failure.
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Li, Jinda, Xia Du, Qian Feng, and Hong Yan. "EXTRACELLULAR DIFFERENTIAL PROTEOME ANALYSIS OF SUBSTRATES OF DIFFERENT LIGNIN MODEL COMPOUNDS DEGRADED BY ASPERGILLUS FUMIGATUS G-13." Journal of Environmental Engineering and Landscape Management 28, no. 3 (September 23, 2020): 137–47. http://dx.doi.org/10.3846/jeelm.2020.12695.
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Aspergillus fumigatus G-13 has the potential to degrade lignocellulose biomass. The purpose of this work is to analyze the extracellular soluble secretory protein of lignocellulose degradation by Aspergillus fumigatus G-13. The research used ferulic acid, sinapic acid and p-coumaric acid as carbon sources. By controlling the culture conditions, adding cellulose co-substrate and auxiliary carbon source, the enzymatic production law of Aspergillus fumigatus G-13 degradation of three lignin model compounds was investigated. The two groups with the greatest difference in enzyme activity expression were screened, and high throughput quantitative proteomics analysis using iTRAQ. iTRAQ analysis showed that a total of 3862 protein spots changed significantly, of which 2103 down-regulated proteins and 1759 up-regulated proteins. The differential proteins involved in the degradation process of lignin model compounds are concentrated in dioxygenase, oxidoreductase, ferulic acid esterase B-2, isoamyl alcohol oxidase, bifunctional catalase peroxidase CAT2, cellulase, cytochrome P450 monooxygenase, flavin-binding monooxygenase, etc. Lignin-related differential abundance proteins were mapped to 128 metabolic pathways. Significantly enriched pathways include metabolic pathways, glyceride metabolism, oxidative phosphorylation, riboflavin metabolism, peroxisomes, riboflavin metabolism. The information presented in this paper is helpful to better understand the lignocellulose degradation mechanisms of A. fumigatus G-13.
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Hao, Min, De Ji, Lin Li, Lianlin Su, Wei Gu, Liya Gu, Qiaohan Wang, Tulin Lu, and Chunqin Mao. "Mechanism of Curcuma wenyujin Rhizoma on Acute Blood Stasis in Rats Based on a UPLC-Q/TOF-MS Metabolomics and Network Approach." Molecules 24, no. 1 (December 27, 2018): 82. http://dx.doi.org/10.3390/molecules24010082.
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Rhizome of Curcuma wenyujin, which is called EZhu in China, is a traditional Chinese medicine used to treat blood stasis for many years. However, the underlying mechanism of EZhu is not clear at present. In this study, plasma metabolomics combined with network pharmacology were used to elucidate the therapeutic mechanism of EZhu in blood stasis from a metabolic perspective. The results showed that 26 potential metabolite markers of acute blood stasis were screened, and the levels were all reversed to different degrees by EZhu preadministration. Metabolic pathway analysis showed that the improvement of blood stasis by Curcuma wenyujin rhizome was mainly related to lipid metabolism (linoleic acid metabolism, ether lipid metabolism, sphingolipid metabolism, glycerophospholipid metabolism, and arachidonic acid metabolism) and amino acid metabolisms (tryptophan metabolism, lysine degradation). The component-target-pathway network showed that 68 target proteins were associated with 21 chemical components in EZhu. Five metabolic pathways of the network, including linoleic acid metabolism, sphingolipid metabolism, glycerolipid metabolism, arachidonic acid metabolism, and steroid hormone biosynthesis, were consistent with plasma metabolomics results. In conclusion, plasma metabolomics combined with network pharmacology can be helpful to clarify the mechanism of EZhu in improving blood stasis and to provide a literature basis for further research on the therapeutic mechanism of EZhu in clinical practice.
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Wang, Xueting, Shouxiang Sun, Xiaojuan Cao, and Jian Gao. "Quantitative Phosphoproteomic Analysis Reveals the Regulatory Networks of Elovl6 on Lipid and Glucose Metabolism in Zebrafish." International Journal of Molecular Sciences 21, no. 8 (April 19, 2020): 2860. http://dx.doi.org/10.3390/ijms21082860.
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Elongation of very long-chain fatty acids protein 6 (Elovl6) has been reported to be associated with clinical treatments of a variety of metabolic diseases. However, there is no systematic and comprehensive study to reveal the regulatory role of Elovl6 in mRNA, protein and phosphorylation levels. We established the first knock-out (KO), elovl6−/−, in zebrafish. Compared with wild type (WT) zebrafish, KO presented significant higher whole-body lipid content and lower content of fasting blood glucose. We utilized RNA-Seq, tandem mass tag (TMT) labeling-based quantitative technology and liquid chromatography-tandem mass spectrometry (LC-MS/MS) to perform the transcriptomic, proteomic and phosphoproteomic analyses of livers from WT and elovl6−/− zebrafish. There were 734 differentially expressed genes (DEG) and 559 differentially expressed proteins (DEP) between elovl6−/− and WT zebrafish, identified out of quantifiable 47251 transcripts and 5525 proteins. Meanwhile, 680 differentially expressed phosphoproteins (DEPP) with 1054 sites were found out of quantifiable 1230 proteins with 3604 sites. Gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) analysis of the transcriptomic and proteomic data further suggested that the abnormal lipid metabolism and glucose metabolism in KO were mainly related to fatty acid degradation and biosynthesis, glycolysis/gluconeogenesis and PPAR signaling pathway. Based on phosphoproteomic analyses, some kinases critical for lipid metabolism and glucose metabolism, including ribosomal protein S6 kinase (Rps6kb), mitogen-activated protein kinase14 (Mapk14) and V-akt murine thymoma viral oncogene homolog 2-like (Akt2l), were identified. These results allowed us to catch on the regulatory networks of elovl6 on lipid and glucose metabolism in zebrafish. To our knowledge, this is the first multi-omic study of zebrafish lacking elovl6, which provides strong datasets to better understand many lipid/glucose metabolic risks posed to human health.
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Fu, Minnie, and Xiaoyong Yang. "The sweet tooth of the circadian clock." Biochemical Society Transactions 45, no. 4 (July 3, 2017): 871–84. http://dx.doi.org/10.1042/bst20160183.
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The endogenous circadian clock is a key regulator of daily metabolic processes. On the other hand, circadian clocks in a broad range of tissues can be tuned by extrinsic and intrinsic metabolic cues. The bidirectional interaction between circadian clocks and metabolism involves both transcriptional and post-translational mechanisms. Nuclear receptors exemplify the transcriptional programs that couple molecular clocks to metabolism. The post-translational modifications of the core clock machinery are known to play a key role in metabolic entrainment of circadian clocks. O-linked N-acetylglucosamine modification (O-GlcNAcylation) of intracellular proteins is a key mediator of metabolic response to nutrient availability. This review highlights our current understanding of the role of protein O-GlcNAcylation in mediating metabolic input and output of the circadian clock.
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Milley, J. R. "Ovine fetal leucine kinetics and protein metabolism during acute metabolic acidosis." American Journal of Physiology-Endocrinology and Metabolism 272, no. 2 (February 1, 1997): E275—E281. http://dx.doi.org/10.1152/ajpendo.1997.272.2.e275.
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Fetal acidosis is associated with poor fetal growth. Because protein accretion is an important component of fetal growth, we used seven chronically prepared fetal lambs (10-16 days postoperation) to find whether fetal metabolic acidosis affected fetal protein accretion, and, if so, whether such effects were due to decreased synthesis or increased breakdown of proteins. Fetal leucine kinetics were measured during infusion of [1-(14)C]leucine by the reciprocal pool method. After control measurements, metabolic acidosis was induced by fetal infusion of 0.5 N HCl, and the measurements were repeated. Although fetal leucine concentration rose (164 +/- 11 vs. 216 +/- 15 microM; P < 0.001), fetal leucine uptake fell during acidosis (3.33 +/- 0.30 vs. 1.43 +/- 0.35 micromol x kg(-1) x min(-1); P < 0.05). However, the influx of leucine from protein breakdown increased (12.6 +/- 2.6 vs. 14.7 +/- 2.6 micromol x kg(-1) x min(-1); P < 0.02). The incorporation of leucine into fetal protein was unaffected by acidosis, so that fetal protein accretion fell (0.48 +/- 1.04 vs. -2.32 +/- 1.53 micromol x kg(-1) x min(-1); P < 0.001). Fetal leucine decarboxylation increased during acidosis (2.85 +/- 0.33 vs. 3.75 +/- 0.61 micromol x kg(-1) x min(-1); P < 0.05). We conclude that fetal metabolic acidosis stimulates pathways to degrade both protein and at least one of the subsequently derived amino acids, leucine. The consequence of such changes induced by acidosis is decreased protein accretion, a finding incompatible with normal fetal growth.
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Dang, Thao Thi Phuong, Linh My Dao, Anh Man Huynh, and Dan Thi Hanh Vo. "Transgenic Drosophila melanogaster model of metabolic disorders." Science and Technology Development Journal - Natural Sciences 4, no. 4 (November 9, 2020): 811–17. http://dx.doi.org/10.32508/stdjns.v4i4.929.
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Metabolic syndrome is a collection of disorders related to metabolisms such as obesity, lipid disorders, hyper/hypoglycemia, ... Metabolic syndrome can lead to cardiovascular diseases, strokes, and diabetes - the leading death causes in the world. In many cases, metabolic disorders are original by the redundant/ reduction of insulin- the most important hormone in metabolism regulation. Both of them are involved in beta-cells dysfunction. Many mechanisms related to this phenomenon has been approved, notably mitochondrial dysfunction and the Ubiquitin proteasome system impairment. UCH-L1 is a protein belonging to the Ubiquitin proteasome system and highly expressed in beta cells. Previous studies reported that decrease UCH-L1 function can alter metabolism and lead to b cell apoptosis under various nutritional conditions, however, the mechanism has not been clarified. In this study, we proposed a Drosophila melanogaster model that expresses many symptoms of metabolic syndrome, by knocking down dUCH (Drosophila homolog of UCH-L1) specifically in Insulin-producing cells. Our fruit fly model had abnormal metabolism, physiology, loss of insulinproducing cells, and mitochondria over-workload, similar to metabolic syndrome in humans. These results suggested that this model is suitable for further studies on the role of UCH-L1 in b cells, as well as a potential model in metabolism diseases' drug screening.
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NOY, Noa. "Retinoid-binding proteins: mediators of retinoid action." Biochemical Journal 348, no. 3 (June 7, 2000): 481–95. http://dx.doi.org/10.1042/bj3480481.
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Active vitamin A metabolites, known as retinoids, are essential for multiple physiological processes, ranging from vision to embryonic development. These small hydrophobic compounds associate in vivo with soluble proteins that are present in a variety of cells and in particular extracellular compartments, and which bind different types of retinoids with high selectivity and affinity. Traditionally, retinoid-binding proteins were viewed as transport proteins that act by solubilizing and protecting their labile ligands in aqueous spaces. It is becoming increasingly clear, however, that, in addition to this general role, retinoid-binding proteins have diverse and specific functions in regulating the disposition, metabolism and activities of retinoids. Some retinoid-binding proteins appear to act by sequestering their ligands, thereby generating concentration gradients that allow cells to take up retinoids from extracellular pools and metabolic steps to proceed in energetically unfavourable directions. Other retinoid-binding proteins regulate the metabolic fates of their ligands by protecting them from some enzymes while allowing metabolism by others. In these cases, delivery of a bound retinoid from the binding protein to the ‘correct’ enzyme is likely to be mediated by direct and specific interactions between the two proteins. One retinoid-binding protein was reported to enhance the ability of its ligand to regulate gene transcription by directly delivering this retinoid to the transcription factor that is activated by it. ‘Channelling’ of retinoids between their corresponding binding protein and a particular protein target thus seems to be a general theme through which some retinoid-binding proteins exert their effects.
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Braccia, Clarissa, Bhakti Prinsi, Mara Colzani, Alessandra A. Altomare, Luca Espen, Yoon-Mi Lee, Giancarlo Aldini, and Kyung-Jin Yeum. "Protocol Optimization of Proteomic Analysis of Korean Ginseng (Panax ginseng Meyer)." Separations 8, no. 4 (April 19, 2021): 53. http://dx.doi.org/10.3390/separations8040053.
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The benefits of ginseng have been mainly attributed to its triterpenoids, called ginsenosides. Recent genome sequencing of the Panax ginseng has paved the way for in-depth proteomic studies of this medicinal plant. The current study was conducted to deepen the proteomic information on the root proteome of Korean ginseng. Proteomic workflow was optimized by testing two different strategies, characterized by the phenol extraction procedure, the presence or the absence of SDS-PAGE fractionation step, and nano-scale liquid chromatographic tandem mass spectrometry (nLC-MS/MS) analysis. The results highlighted an evident improvement of proteome extraction by the combination of phenol extraction with SDS-PAGE before the nLC-MS/MS analysis. In addition, a dramatic impact of the steaming process (the treatment to produce red ginseng from ginseng) on protein properties was observed. Overall, the analyses of Korean ginseng permitted the characterization of a total of 2412 proteins. A large number of identified proteins belonged to the functional categories of protein and carbon/energy metabolism (22.4% and 14.6%, respectively). The primary and secondary metabolisms are major metabolic pathways, which emerged from the proteomic analysis. In addition, a large number of proteins known to play an important role in response to (a)biotic stresses were also identified. The current proteomic study not only confirmed the previous transcriptomic and proteomic reports but also extended proteomic information, including the main metabolic pathways involved in Korean ginseng.
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Sjögren, Klara, Kin-Chuen Leung, Warren Kaplan, Margaret Gardiner-Garden, James Gibney, and Ken K. Y. Ho. "Growth hormone regulation of metabolic gene expression in muscle: a microarray study in hypopituitary men." American Journal of Physiology-Endocrinology and Metabolism 293, no. 1 (July 2007): E364—E371. http://dx.doi.org/10.1152/ajpendo.00054.2007.
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Muscle is a target of growth hormone (GH) action and a major contributor to whole body metabolism. Little is known about how GH regulates metabolic processes in muscle or the extent to which muscle contributes to changes in whole body substrate metabolism during GH treatment. To identify GH-responsive genes that regulate substrate metabolism in muscle, we studied six hypopituitary men who underwent whole body metabolic measurement and skeletal muscle biopsies before and after 2 wk of GH treatment (0.5 mg/day). Transcript profiles of four subjects were analyzed using Affymetrix GeneChips. Serum insulin-like growth factor I (IGF-I) and procollagens I and III were measured by RIA. GH increased serum IGF-I and procollagens I and III, enhanced whole body lipid oxidation, reduced carbohydrate oxidation, and stimulated protein synthesis. It induced gene expression of IGF-I and collagens in muscle. GH reduced expression of several enzymes regulating lipid oxidation and energy production. It reduced calpain 3, increased ribosomal protein L38 expression, and displayed mixed effects on genes encoding myofibrillar proteins. It increased expression of circadian gene CLOCK, and reduced that of PERIOD. In summary, GH exerted concordant effects on muscle expression and blood levels of IGF-I and collagens. It induced changes in genes regulating protein metabolism in parallel with a whole body anabolic effect. The discordance between muscle gene expression profiles and metabolic responses suggests that muscle is unlikely to contribute to GH-induced stimulation of whole body energy and lipid metabolism. GH may regulate circadian function in skeletal muscle by modulating circadian gene expression with possible metabolic consequences.
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Rajas, Fabienne, Amandine Gautier-Stein, and Gilles Mithieux. "Glucose-6 Phosphate, a Central Hub for Liver Carbohydrate Metabolism." Metabolites 9, no. 12 (November 20, 2019): 282. http://dx.doi.org/10.3390/metabo9120282.
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Cells efficiently adjust their metabolism according to the abundance of nutrients and energy. The ability to switch cellular metabolism between anabolic and catabolic processes is critical for cell growth. Glucose-6 phosphate is the first intermediate of glucose metabolism and plays a central role in the energy metabolism of the liver. It acts as a hub to metabolically connect glycolysis, the pentose phosphate pathway, glycogen synthesis, de novo lipogenesis, and the hexosamine pathway. In this review, we describe the metabolic fate of glucose-6 phosphate in a healthy liver and the metabolic reprogramming occurring in two pathologies characterized by a deregulation of glucose homeostasis, namely type 2 diabetes, which is characterized by fasting hyperglycemia; and glycogen storage disease type I, where patients develop severe hypoglycemia during short fasting periods. In these two conditions, dysfunction of glucose metabolism results in non-alcoholic fatty liver disease, which may possibly lead to the development of hepatic tumors. Moreover, we also emphasize the role of the transcription factor carbohydrate response element-binding protein (ChREBP), known to link glucose and lipid metabolisms. In this regard, comparing these two metabolic diseases is a fruitful approach to better understand the key role of glucose-6 phosphate in liver metabolism in health and disease.
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Leff, T. "AMP-activated protein kinase regulates gene expression by direct phosphorylation of nuclear proteins." Biochemical Society Transactions 31, no. 1 (February 1, 2003): 224–27. http://dx.doi.org/10.1042/bst0310224.
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One of the primary functions of AMP-activated protein kinase (AMPK) is to regulate the metabolic pathways in response to reduced cellular energy charge. Most of the known targets of the kinase are cytoplasmic enzymes involved in both catabolic and anabolic metabolism. In addition, activation of AMPK in many cells results in changes in the pattern of gene expression. Although some of these effects are undoubtedly secondary responses to modified cellular metabolism, it is possible that in addition to its well-characterized function in the cytoplasm, AMPK also directly phosphorylates and regulates proteins involved in gene transcription. There are now several examples of transcription factors, cofactors and components of the transcriptional core machinery that are directly phosphorylated and regulated by AMPK. Here I review these examples and discuss the significance of AMPK activity in the nucleus.
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Soumoy, Laura, Corentin Schepkens, Mohammad Krayem, Ahmad Najem, Vanessa Tagliatti, Ghanem E. Ghanem, Sven Saussez, Jean-Marie Colet, and Fabrice Journe. "Metabolic Reprogramming in Metastatic Melanoma with Acquired Resistance to Targeted Therapies: Integrative Metabolomic and Proteomic Analysis." Cancers 12, no. 5 (May 22, 2020): 1323. http://dx.doi.org/10.3390/cancers12051323.
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Treatments of metastatic melanoma underwent an impressive development over the past few years, with the emergence of small molecule inhibitors targeting mutated proteins, such as BRAF, NRAS, or cKIT. However, since a significant proportion of patients acquire resistance to these therapies, new strategies are currently being considered to overcome this issue. For this purpose, melanoma cell lines with mutant BRAF, NRAS, or cKIT and with acquired resistances to BRAF, MEK, or cKIT inhibitors, respectively, were investigated using both 1H-NMR-based metabonomic and protein microarrays. The 1H-NMR profiles highlighted a similar go and return pattern in the metabolism of the BRAF, NRAS, and cKIT mutated cell lines. Indeed, melanoma cells exposed to mutation-specific inhibitors underwent metabolic disruptions following acute exposure but partially recovered their basal metabolism in long-term exposure, most likely acquiring resistance skills. The protein microarrays inquired about the potential cellular mechanisms used by the resistant cells to escape drug treatment, by showing decreased levels of proteins linked to the drug efficacy, especially in the downstream part of the MAPK signaling pathway. Integrating metabonomic and proteomic findings revealed some metabolic pathways (i.e., glutaminolysis, choline metabolism, glutathione production, glycolysis, oxidative phosphorylation) and key proteins (i.e., EPHA2, DUSP4, and HIF-1A) as potential targets to discard drug resistance.
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Prusinkiewicz, Martin A., and Joe S. Mymryk. "Metabolic Control by DNA Tumor Virus-Encoded Proteins." Pathogens 10, no. 5 (May 6, 2021): 560. http://dx.doi.org/10.3390/pathogens10050560.
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Viruses co-opt a multitude of host cell metabolic processes in order to meet the energy and substrate requirements for successful viral replication. However, due to their limited coding capacity, viruses must enact most, if not all, of these metabolic changes by influencing the function of available host cell regulatory proteins. Typically, certain viral proteins, some of which can function as viral oncoproteins, interact with these cellular regulatory proteins directly in order to effect changes in downstream metabolic pathways. This review highlights recent research into how four different DNA tumor viruses, namely human adenovirus, human papillomavirus, Epstein–Barr virus and Kaposi’s associated-sarcoma herpesvirus, can influence host cell metabolism through their interactions with either MYC, p53 or the pRb/E2F complex. Interestingly, some of these host cell regulators can be activated or inhibited by the same virus, depending on which viral oncoprotein is interacting with the regulatory protein. This review highlights how MYC, p53 and pRb/E2F regulate host cell metabolism, followed by an outline of how each of these DNA tumor viruses control their activities. Understanding how DNA tumor viruses regulate metabolism through viral oncoproteins could assist in the discovery or repurposing of metabolic inhibitors for antiviral therapy or treatment of virus-dependent cancers.
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James, Joel, Mathews Valuparampil Varghese, Mikhail Vasilyev, Paul R. Langlais, Stevan P. Tofovic, Olga Rafikova, and Ruslan Rafikov. "Complex III Inhibition-Induced Pulmonary Hypertension Affects the Mitochondrial Proteomic Landscape." International Journal of Molecular Sciences 21, no. 16 (August 8, 2020): 5683. http://dx.doi.org/10.3390/ijms21165683.
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The mitochondria play a vital role in controlling cell metabolism and regulating crucial cellular outcomes. We previously demonstrated that chronic inhibition of the mitochondrial complex III in rats by Antimycin A (AA) induced sustained pulmonary vasoconstriction. On the metabolic level, AA-induced mitochondrial dysfunction resulted in a glycolytic shift that was reported as the primary contributor to pulmonary hypertension pathogenesis. However, the regulatory proteins driving this metabolic shift with complex III inhibition are yet to be explored. Therefore, to delineate the mechanisms, we followed changes in the rat lung mitochondrial proteome throughout AA treatment. Rats treated with AA for up to 24 days showed a disturbed mitochondrial proteome with significant changes in 28 proteins (p < 0.05). We observed a time-dependent decrease in the expression of key proteins that regulate fatty acid oxidation, the tricarboxylic acid cycle, the electron transport chain, and amino acid metabolism, indicating a correlation with diminished mitochondrial function. We also found a significant dysregulation in proteins that controls the protein import machinery and the clearance and detoxification of oxidatively damaged peptides via proteolysis and mitophagy. This could potentially lead to the onset of mitochondrial toxicity due to misfolded protein stress. We propose that chronic inhibition of mitochondrial complex III attenuates mitochondrial function by disruption of the global mitochondrial metabolism. This potentially aggravates cellular proliferation by initiating a glycolytic switch and thereby leads to pulmonary hypertension.
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Zhang, Youjun, and Alisdair R. Fernie. "On the Detection and Functional Significance of the Protein–Protein Interactions of Mitochondrial Transport Proteins." Biomolecules 10, no. 8 (July 25, 2020): 1107. http://dx.doi.org/10.3390/biom10081107.
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Protein–protein assemblies are highly prevalent in all living cells. Considerable evidence has recently accumulated suggesting that particularly transient association/dissociation of proteins represent an important means of regulation of metabolism. This is true not only in the cytosol and organelle matrices, but also at membrane surfaces where, for example, receptor complexes, as well as those of key metabolic pathways, are common. Transporters also frequently come up in lists of interacting proteins, for example, binding proteins that catalyze the production of their substrates or that act as relays within signal transduction cascades. In this review, we provide an update of technologies that are used in the study of such interactions with mitochondrial transport proteins, highlighting the difficulties that arise in their use for membrane proteins and discussing our current understanding of the biological function of such interactions.
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Bukke, Vidyasagar Naik, Rosanna Villani, Moola Archana, Agata Wawrzyniak, Krzysztof Balawender, Stanislaw Orkisz, Luca Ferraro, Gaetano Serviddio, and Tommaso Cassano. "The Glucose Metabolic Pathway as A Potential Target for Therapeutics: Crucial Role of Glycosylation in Alzheimer’s Disease." International Journal of Molecular Sciences 21, no. 20 (October 19, 2020): 7739. http://dx.doi.org/10.3390/ijms21207739.
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Glucose uptake in the brain decreases because of normal aging but this decline is accelerated in Alzheimer’s disease (AD) patients. In fact, positron emission tomography (PET) studies have shown that metabolic reductions in AD patients occur decades before the onset of symptoms, suggesting that metabolic deficits may be an upstream event in at least some late-onset cases. A decrease in availability of glucose content induces a considerable impairment/downregulation of glycosylation, which is an important post-translational modification. Glycosylation is an important and highly regulated mechanism of secondary protein processing within cells and it plays a crucial role in modulating stability of proteins, as carbohydrates are important in achieving the proper three-dimensional conformation of glycoproteins. Moreover, glycosylation acts as a metabolic sensor that links glucose metabolism to normal neuronal functioning. All the proteins involved in β-amyloid (Aβ) precursor protein metabolism have been identified as candidates of glycosylation highlighting the possibility that Aβ metabolism could be regulated by their glycosylation. Within this framework, the present review aims to summarize the current understanding on the role of glycosylation in the etiopathology of AD, emphasizing the idea that glucose metabolic pathway may represent an alternative therapeutic option for targeting AD. From this perspective, the pharmacological modulation of glycosylation levels may represent a ‘sweet approach’ to treat AD targeting new mechanisms independent of the amyloid cascade and with comparable impacts in familial and sporadic AD.
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Kuang, Heqian, Cheng-hsin Wei, Tiannan Wang, Jennifer Eastep, Yang Li, and Guoxun Chen. "Vitamin A status affects weight gain and hepatic glucose metabolism in rats fed a high-fat diet." Biochemistry and Cell Biology 97, no. 5 (October 2019): 545–53. http://dx.doi.org/10.1139/bcb-2018-0284.
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Whether vitamin A (VA) has a role in the development of metabolic abnormalities associated with intake of a high-fat diet (HFD) is unclear. Sprague–Dawley rats after weaning were fed an isocaloric VA sufficient HFD (VAS-HFD) or a VA deficient HFD (VAD-HFD) for 8 weeks. Body mass, food intake, liver and adipose tissue mass, and the hepatic expression levels of key proteins for metabolism were determined. VAD-HFD rats had lower body, liver, and epididymal fat mass than VAS-HFD rats. VAD-HFD rats had lower hepatic protein expression levels of cytochrome P450 26A1, glucokinase, and phosphoenolpyruvate carboxykinase than VAS-HFD rats. VAD-HFD rats had higher protein levels of glycogen synthase kinase (GSK)-3α and lower levels of GSK-3β, but not glycogen synthase, than VAS-HFD rats. VAD-HFD rats had higher hepatic levels of insulin receptor substrate-1 (IRS-1), insulin receptor β-subunit, mitogen-activated protein kinase proteins, and peroxisome proliferator-activated receptor-gamma coactivator 1α mRNA, and lower level of IRS-2 protein than VAS-HFD rats. These results indicate that in a HFD setting, VA deficiency attenuated HFD-induced obesity, and VA status altered the expression levels of proteins required for glucose metabolism and insulin signaling. We conclude that VA status contributes to the regulation of hepatic glucose and lipid metabolism in a HFD setting, and may regulate hepatic carbohydrate metabolism.
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Li, Yun, Wu, Qu, Duan, and Jiang. "Combination of Transcriptomic, Proteomic, and Metabolomic Analysis Reveals the Ripening Mechanism of Banana Pulp." Biomolecules 9, no. 10 (September 23, 2019): 523. http://dx.doi.org/10.3390/biom9100523.
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The banana is one of the most important fruits in the world. Bananas undergo a rapid ripening process after harvest, resulting in a short shelf. In this study, the mechanism underlying pulp ripening of harvested bananas was investigated using integrated transcriptomic, proteomic, and metabolomic analysis. Ribonucleic acid sequencing (RNA-Seq) revealed that a great number of genes related to transcriptional regulation, signal transduction, cell wall modification, and secondary metabolism were up-regulated during pulp ripening. At the protein level, 84 proteins were differentially expressed during pulp ripening, most of which were associated with energy metabolism, oxidation-reduction, cell wall metabolism, and starch degradation. According to partial least squares discriminant analysis, 33 proteins were identified as potential markers for separating different ripening stages of the fruit. In addition to ethylene’s central role, auxin signal transduction might be involved in regulating pulp ripening. Moreover, secondary metabolism, energy metabolism, and the protein metabolic process also played an important role in pulp ripening. In all, this study provided a better understanding of pulp ripening of harvested bananas.
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Wang, Yinan, Mengke Wang, Min Li, Te Zhao, and Lin Zhou. "Cinnamaldehyde inhibits the growth of Phytophthora capsici through disturbing metabolic homoeostasis." PeerJ 9 (April 30, 2021): e11339. http://dx.doi.org/10.7717/peerj.11339.
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Background Phytophthora capsici Leonian (P. capsici) can cause wilting and roots rotting on pepper and other cash crops. The new fungicide cinnamaldehyde (CA) has high activity against this pathogen. However, its potential mechanism is still unknown. Methods In order to gain insights into the mechanism, isobaric tags for relative and absolute quantification (iTRAQ)-based quantitative proteomics was used to analyze P. capsici treated with CA. The iTRAQ results were evaluated by parallel reaction monitoring (PRM) analysis and quantitative real-time PCR (qRT-PCR) analysis. Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis was used to speculate the biochemical pathways that the agent may act on. Results The results showed that 1502 differentially expressed proteins were identified, annotated and classified into 209 different terms (like metabolic process, cellular process, single-organism process) based on Gene Ontology (GO) functional enrichment analysis and nine different pathways (glyoxylate and dicarboxylate metabolism, fatty acid metabolism and so on) based on the Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. This study suggested that CA disordered fatty acid metabolism, polysaccharide metabolism and leucine metabolism. Based on PRM analysis, five proteins including CAMK/CAMK1 protein kinase, glucan 1,3-beta-glucosidase, 1,3-beta-glucanosyltransferase, methylcrotonoyl-CoA carboxylase subunit alpha and isovaleryl-CoA dehydrogenase were down-regulated in P. capsici treated with CA. Furthermore, the qRT-PCR analysis showed that the gene expression level of the interested proteins was consistent with the protein expression level, except for CAMK/CAMK1 protein kinase, acetyl-CoA carboxylase and fatty acid synthase subunit alpha. Conclusions CA destroyed the metabolic homoeostasisof P. capsici, which led to cell death. This is the first proteomic analysis of P. capsici treated with CA, which may provide an important information for exploring the mechanism of the fungicide CA against P. capsici.
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Ashour, Amal, Mingzhan Xue, Maryam Al-Motawa, Paul J. Thornalley, and Naila Rabbani. "Glycolytic overload-driven dysfunction of periodontal ligament fibroblasts in high glucose concentration, corrected by glyoxalase 1 inducer." BMJ Open Diabetes Research & Care 8, no. 2 (October 2020): e001458. http://dx.doi.org/10.1136/bmjdrc-2020-001458.
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IntroductionPatients with diabetes have increased risk of periodontal disease, with increased risk of weakening of periodontal ligament and tooth loss. Periodontal ligament is produced and maintained by periodontal ligament fibroblasts (PDLFs). We hypothesized that metabolic dysfunction of PDLFs in hyperglycemia produces an accumulation of the reactive glycating agent, methylglyoxal (MG), leading to increased formation of the major advanced glycation endproduct, MG-H1 and PDLF dysfunction. The aim of this study was to assess if there is dicarbonyl stress and functional impairment of human PDLFs in primary culture in high glucose concentration—a model of hyperglycemia, to characterize the metabolic drivers of it and explore remedial intervention by the glyoxalase 1 inducer dietary supplement, trans-resveratrol and hesperetin combination (tRES-HESP).Research design and methodsHuman PDLFs were incubated in low and high glucose concentration in vitro. Metabolic and enzymatic markers of MG and glucose control were quantified and related changes in the cytoplasmic proteome and cell function—binding to collagen-I, assessed. Reversal of PDLF dysfunction by tRES-HESP was explored.ResultsIn high glucose concentration cultures, there was a ca. twofold increase in cellular MG, cellular protein MG-H1 content and decreased attachment of PDLFs to collagen-I. This was driven by increased hexokinase-2 linked glucose metabolism and related increased MG formation. Proteomics analysis revealed increased abundance of chaperonins, heat shock proteins (HSPs), Golgi-to-endoplasmic reticulum transport and ubiquitin E3 ligases involved in misfolded protein degradation in high glucose concentration, consistent with activation of the unfolded protein response by increased misfolded MG-modified proteins. PDLF dysfunction was corrected by tRES-HESP.ConclusionsIncreased hexokinase-2 linked glucose metabolism produces dicarbonyl stress, increased MG-modified protein, activation of the unfolded protein response and functional impairment of PDLFs in high glucose concentration. tRES-HESP resolves this at source by correcting increased glucose metabolism and may be of benefit in prevention of diabetic periodontal disease.
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Bruggeman, Frank J., Robert Planqué, Douwe Molenaar, and Bas Teusink. "Searching for principles of microbial physiology." FEMS Microbiology Reviews 44, no. 6 (September 21, 2020): 821–44. http://dx.doi.org/10.1093/femsre/fuaa034.
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ABSTRACT Why do evolutionarily distinct microorganisms display similar physiological behaviours? Why are transitions from high-ATP yield to low(er)-ATP yield metabolisms so widespread across species? Why is fast growth generally accompanied with low stress tolerance? Do these regularities occur because most microbial species are subject to the same selective pressures and physicochemical constraints? If so, a broadly-applicable theory might be developed that predicts common microbiological behaviours. Microbial systems biologists have been working out the contours of this theory for the last two decades, guided by experimental data. At its foundations lie basic principles from evolutionary biology, enzyme biochemistry, metabolism, cell composition and steady-state growth. The theory makes predictions about fitness costs and benefits of protein expression, physicochemical constraints on cell growth and characteristics of optimal metabolisms that maximise growth rate. Comparisons of the theory with experimental data indicates that microorganisms often aim for maximisation of growth rate, also in the presence of stresses; they often express optimal metabolisms and metabolic proteins at optimal concentrations. This review explains the current status of the theory for microbiologists; its roots, predictions, experimental evidence and future directions.
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Balatskyi, Volodymyr V., Oksana L. Palchevska, Lina Bortnichuk, Ana-Maria Gan, Anna Myronova, Larysa L. Macewicz, Viktor O. Navrulin, et al. "β-Catenin Regulates Cardiac Energy Metabolism in Sedentary and Trained Mice." Life 10, no. 12 (December 17, 2020): 357. http://dx.doi.org/10.3390/life10120357.
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The role of canonical Wnt signaling in metabolic regulation and development of physiological cardiac hypertrophy remains largely unknown. To explore the function of β-catenin in the regulation of cardiac metabolism and physiological cardiac hypertrophy development, we used mice heterozygous for cardiac-specific β-catenin knockout that were subjected to a swimming training model. β-Catenin haploinsufficient mice subjected to endurance training displayed a decreased β-catenin transcriptional activity, attenuated cardiomyocytes hypertrophic growth, and enhanced activation of AMP-activated protein kinase (AMPK), phosphoinositide-3-kinase–Akt (Pi3K–Akt), and mitogen-activated protein kinase/extracellular signal-regulated kinases 1/2 (MAPK/Erk1/2) signaling pathways compared to trained wild type mice. We further observed an increased level of proteins involved in glucose aerobic metabolism and β-oxidation along with perturbed activity of mitochondrial oxidative phosphorylation complexes (OXPHOS) in trained β-catenin haploinsufficient mice. Taken together, Wnt/β-catenin signaling appears to govern metabolic regulatory programs, sustaining metabolic plasticity in adult hearts during the adaptation to endurance training.
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Eckert, J., P. A. Pugh, J. G. Thompson, H. Niemann, and H. R. Tervit. "Exogenous protein affects developmental competence and metabolic activity of bovine pre-implantation embryos in vitro." Reproduction, Fertility and Development 10, no. 4 (1998): 327. http://dx.doi.org/10.1071/r98077.
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The role of exogenous protein during bovine pre-implantation embryo development in two in vitro production systems was investigated. Morphological development, survival after vitrification and metabolic activity before and after vitrification were recorded in blastocysts generated in vitro in synthetic oviduct fluid (SOF) medium in the presence of either bovine serum albumin (BSA) or polyvinyl-alcohol (PVA). Metabolic activity was determined by measuring oxygen consumption, glucose and pyruvate uptake as well as lactate production. Development to blastocysts and survival after vitrification were reduced significantly in medium lacking protein. Of the metabolic parameters measured, only pyruvate uptake was increased significantly in embryos cultured in medium supplemented with PVA. Whereas in BSA-supplemented medium pyruvate uptake was correlated with lactate production, in PVA-supplemented medium glucose uptake was correlated with lactate production. Lactate production increased significantly after vitrification as compared with fresh embryos. Thus, exogenously added protein significantly alters oxidative metabolism. In medium lacking protein, the additional pyruvate may be used for the maintenance of intracellular amino acid pools. Vitrification appears to alter glycolytic metabolic profiles indicating a stress-response. In conclusion, the perturbed metabolism corresponding to reduced developmental capacity of embryos produced under protein-free conditions emphasizes the ambiguity between maximum develop-ment, technical and hygienic requirements and physiological demands of the early bovine embryo in vitro. The use of well-defined recombinant proteins might assist in closing this gap.
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Mudry, Jonathan M., Julie Massart, Ferenc L. M. Szekeres, and Anna Krook. "TWIST1 and TWIST2 regulate glycogen storage and inflammatory genes in skeletal muscle." Journal of Endocrinology 224, no. 3 (March 2015): 303–13. http://dx.doi.org/10.1530/joe-14-0474.
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TWIST proteins are important for development of embryonic skeletal muscle and play a role in the metabolism of tumor and white adipose tissue. The impact of TWIST on metabolism in skeletal muscle is incompletely studied. Our aim was to assess the impact of TWIST1 and TWIST2 overexpression on glucose and lipid metabolism. In intact mouse muscle, overexpression of Twist reduced total glycogen content without altering glucose uptake. Expression of TWIST1 or TWIST2 reducedPdk4mRNA, while increasing mRNA levels ofIl6,Tnfα, andIl1β. Phosphorylation of AKT was increased and protein abundance of acetyl CoA carboxylase (ACC) was decreased in skeletal muscle overexpressing TWIST1 or TWIST2. Glycogen synthesis and fatty acid oxidation remained stable in C2C12 cells overexpressing TWIST1 or TWIST2. Finally, skeletal muscle mRNA levels remain unaltered inob/obmice, type 2 diabetic patients, or in healthy subjects before and after 3 months of exercise training. Collectively, our results indicate that TWIST1 and TWIST2 are expressed in skeletal muscle. Overexpression of these proteins impacts proteins in metabolic pathways and mRNA level of cytokines. However, skeletal muscle levels of TWIST transcripts are unaltered in metabolic diseases.
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Valle-Mendiola, Arturo, and Isabel Soto-Cruz. "Energy Metabolism in Cancer: The Roles of STAT3 and STAT5 in the Regulation of Metabolism-Related Genes." Cancers 12, no. 1 (January 3, 2020): 124. http://dx.doi.org/10.3390/cancers12010124.
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A central characteristic of many types of cancer is altered energy metabolism processes such as enhanced glucose uptake and glycolysis and decreased oxidative metabolism. The regulation of energy metabolism is an elaborate process involving regulatory proteins such as HIF (pro-metastatic protein), which reduces oxidative metabolism, and some other proteins such as tumour suppressors that promote oxidative phosphorylation. In recent years, it has been demonstrated that signal transducer and activator of transcription (STAT) proteins play a pivotal role in metabolism regulation. STAT3 and STAT5 are essential regulators of cytokine- or growth factor-induced cell survival and proliferation, as well as the crosstalk between STAT signalling and oxidative metabolism. Several reports suggest that the constitutive activation of STAT proteins promotes glycolysis through the transcriptional activation of hypoxia-inducible factors and therefore, the alteration of mitochondrial activity. It seems that STAT proteins function as an integrative centre for different growth and survival signals for energy and respiratory metabolism. This review summarises the functions of STAT3 and STAT5 in the regulation of some metabolism-related genes and the importance of oxygen in the tumour microenvironment to regulate cell metabolism, particularly in the metabolic pathways that are involved in energy production in cancer cells.
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Yan, Xue, Aurélie Budin-Verneuil, Yanick Auffray, and Vianney Pichereau. "Proteome phenotyping of ΔrelA mutants in Enterococcus faecalis V583." Canadian Journal of Microbiology 60, no. 8 (August 2014): 525–31. http://dx.doi.org/10.1139/cjm-2014-0254.
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The (p)ppGpp synthetase RelA contributes to stress adaptation and virulence in Enterococcus faecalis V583. A 2-dimensional electrophoresis proteomic analysis of 2 relA mutants, i.e., ΔrelA carrying a complete deletion of the relA gene, and ΔrelAsp that is deleted from only its 3′ extremity, showed that 31 proteins were deregulated in 1 or both of these mutants. Mass spectrometry identification of these proteins showed that 10 are related to translation, including 5 ribosomal proteins, 3 proteins involved in translation elongation, and 2 proteins in tRNA synthesis; 14 proteins are involved in diverse metabolisms and biosynthesis (8 in sugar and energy metabolisms, 2 in fatty acid biosynthesis, 2 in amino acid biosynthesis, and 2 in nucleotide metabolism). Five proteins were relevant to the adaptation to different environmental stresses, i.e., SodA and a Dps family protein, 2 cold-shock domain proteins, and Ef1744, which is a general stress protein that plays an important role in the response to ethanol stress. The potential role of these proteins in the development of stress phenotypes associated with these mutations is discussed.
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Nawaz, Gul, Babar Usman, Haowen Peng, Neng Zhao, Ruizhi Yuan, Yaoguang Liu, and Rongbai Li. "Knockout of Pi21 by CRISPR/Cas9 and iTRAQ-Based Proteomic Analysis of Mutants Revealed New Insights into M. oryzae Resistance in Elite Rice Line." Genes 11, no. 7 (July 2, 2020): 735. http://dx.doi.org/10.3390/genes11070735.
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Rice blast (Magnaporthe oryzae) is a devastating disease affecting rice production globally. The development of cultivars with host resistance has been proved to be the best strategy for disease management. Several rice-resistance genes (R) have been recognized which induce resistance to blast in rice but R gene-mediated mechanisms resulting in defense response still need to be elucidated. Here, mutant lines generated through CRISPR/Cas9 based targeted mutagenesis to investigate the role of Pi21 against blast resistance and 17 mutant plants were obtained in T0 generation with the mutation rate of 66% including 26% bi-allelic, 22% homozygous, 12% heterozygous, and 3% chimeric and 17 T-DNA-free lines in T1 generation. The homozygous mutant lines revealed enhanced resistance to blast without affecting the major agronomic traits. Furthermore, comparative proteome profiling was adopted to study the succeeding proteomic regulations, using iTRAQ-based proteomic analysis. We identified 372 DEPs, among them 149 up and 223 were down-regulated, respectively. GO analysis revealed that the proteins related to response to stimulus, photosynthesis, carbohydrate metabolic process, and small molecule metabolic process were up-regulated. The most of DEPs were involved in metabolic, ribosomal, secondary metabolites biosynthesis, and carbon metabolism pathways. 40S ribosomal protein S15 (P31674), 50S ribosomal protein L4, L5, L6 (Q10NM5, Q9ZST0, Q10L93), 30S ribosomal protein S5, S9 (Q6YU81, Q850W6, Q9XJ28), and succinate dehydrogenase (Q9S827) were hub-proteins. The expression level of genes related to defense mechanism, involved in signaling pathways of jasmonic acid (JA), salicylic acid (SA), and ethylene metabolisms were up-regulated in mutant line after the inoculation of the physiological races of M. oryzae as compared to WT. Our results revealed the fundamental value of genome editing and expand knowledge about fungal infection avoidance in rice.
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Pinto, Samuel K., Séverine Lamon, Erin J. Stephenson, Ming Kalanon, Jasmine Mikovic, Lauren G. Koch, Steven L. Britton, John A. Hawley, and Donny M. Camera. "Expression of microRNAs and target proteins in skeletal muscle of rats selectively bred for high and low running capacity." American Journal of Physiology-Endocrinology and Metabolism 313, no. 3 (September 1, 2017): E335—E343. http://dx.doi.org/10.1152/ajpendo.00043.2017.
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Impairments in mitochondrial function and substrate metabolism are implicated in the etiology of obesity and Type 2 diabetes. MicroRNAs (miRNAs) can degrade mRNA or repress protein translation and have been implicated in the development of such disorders. We used a contrasting rat model system of selectively bred high- (HCR) or low- (LCR) intrinsic running capacity with established differences in metabolic health to investigate the molecular mechanisms through which miRNAs regulate target proteins mediating mitochondrial function and substrate oxidation processes. Quantification of select miRNAs using the rat miFinder miRNA PCR array revealed differential expression of 15 skeletal muscles (musculus tibialis anterior) miRNAs between HCR and LCR rats (14 with higher expression in LCR; P < 0.05). Ingenuity Pathway Analysis predicted these altered miRNAs to collectively target multiple proteins implicated in mitochondrial dysfunction and energy substrate metabolism. Total protein abundance of citrate synthase (CS; miR-19 target) and voltage-dependent anion channel 1 (miR-7a target) were higher in HCR compared with LCR cohorts (~57 and ~26%, respectively; P < 0.05). A negative correlation was observed for miR-19a-3p and CS ( r = 0.32, P = 0.015) protein expression. To determine whether miR-19a-3p can regulate CS in vitro, we performed luciferase reporter and transfection assays in C2C12 myotubes. MiR-19a-3p binding to the CS untranslated region did not change luciferase reporter activity; however, miR-19a-3p transfection decreased CS protein expression (∼70%; P < 0.05). The differential miRNA expression targeting proteins implicated in mitochondrial dysfunction and energy substrate metabolism may contribute to the molecular basis, mediating the divergent metabolic health profiles of LCR and HCR rats.
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Dusejovska, M., B. Stankova, M. Vecka, A. Pisarikova, E. Tvrzicka, and A. Zak. "SELECTED ASPECTS OF PROTEIN METABOLISM IN METABOLIC SYNDROME." Atherosclerosis Supplements 9, no. 1 (May 2008): 249. http://dx.doi.org/10.1016/s1567-5688(08)70999-1.
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Kurpińska, Anna, Agnieszka Jarosz, and Wiesław Skrzypczak. "Parameters of protein and iron metabolism in dairy cows during periparturient period." Acta Scientiarum Polonorum Zootechnica 18, no. 3 (January 15, 2020): 3–10. http://dx.doi.org/10.21005/asp.2019.18.3.01.
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Koshel, Ivanna. "Level of Arachidonic Acid and State of Peroxidation Processes in Patients with Aspirin-Intolerant Polypous Rhinosinusitis." Galician Medical Journal 23, no. 4 (November 5, 2016): 2016410. http://dx.doi.org/10.21802/gmj.2016.4.10.
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The main peculiarity of aspirin-intolerant polypous rhinosinusitis pathogenesis is the presence of “genetic block” of constitutive cyclooxygenase being the key enzyme of the arachidonic acid metabolism. It justifies the necessity of studying its metabolic peculiarities.The objective of the research was to determine the level of arachidonic acid as well as the state of lipid and protein peroxidation processes in patients with aspirin-intolerant polypous rhinosinusitis.Materials and methods. The levels of arachidonic acid, malondialdehyde and oxidative modification of serum proteins were studied in 20 patients with aspirin-intolerant polypous rhinosinusitis and 7 healthy individuals.Results. Significantly elevated levels of arachidonic levels were observed. The search for alternative metabolic pathways stimulated lipid and protein peroxidation processes and led to the increase in the levels of malondialdehyde and oxidative modification of serum proteins. The peculiarities of biochemical changes indicated pro-inflammatory orientation of lipid metabolism.Conclusions. The obtained data confirmed the hypothesis of “genetic block” of the arachidonic acid metabolism as the main pathogenetic component of aspirin-intolerant polypous rhinosinusitis and allowed us to clearly interpret biochemical picture of the disease.
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Shi, Lei, and Benjamin P. Tu. "Protein acetylation as a means to regulate protein function in tune with metabolic state." Biochemical Society Transactions 42, no. 4 (August 1, 2014): 1037–42. http://dx.doi.org/10.1042/bst20140135.
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Protein acetylation has emerged as a prominent post-translational modification that can occur on a wide variety of proteins. The metabolite acetyl-CoA is a key intermediate in energy metabolism that also serves as the acetyl group donor in protein acetylation modifications. Therefore such acetylation modifications might be coupled to the intracellular availability of acetyl-CoA. In the present article, we summarize recent evidence suggesting that the particular protein acetylation modifications enable the regulation of protein function in tune with acetyl-CoA availability and thus the metabolic state of the cell.
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Koksharova, Olga A., Ivan O. Butenko, Olga V. Pobeguts, Nina A. Safronova, and Vadim M. Govorun. "The First Proteomic Study of Nostoc sp. PCC 7120 Exposed to Cyanotoxin BMAA under Nitrogen Starvation." Toxins 12, no. 5 (May 9, 2020): 310. http://dx.doi.org/10.3390/toxins12050310.
Full textAbstract:
The oldest prokaryotic photoautotrophic organisms, cyanobacteria, produce many different metabolites. Among them is the water-soluble neurotoxic non-protein amino acid beta-N-methylamino-L-alanine (BMAA), whose biological functions in cyanobacterial metabolism are of fundamental scientific and practical interest. An early BMAA inhibitory effect on nitrogen fixation and heterocyst differentiation was shown in strains of diazotrophic cyanobacteria Nostoc sp. PCC 7120, Nostoc punctiforme PCC 73102 (ATCC 29133), and Nostoc sp. strain 8963 under conditions of nitrogen starvation. Herein, we present a comprehensive proteomic study of Nostoc (also called Anabaena) sp. PCC 7120 in the heterocyst formation stage affecting by BMAA treatment under nitrogen starvation conditions. BMAA disturbs proteins involved in nitrogen and carbon metabolic pathways, which are tightly co-regulated in cyanobacteria cells. The presented evidence shows that exogenous BMAA affects a key nitrogen regulatory protein, PII (GlnB), and some of its protein partners, as well as glutamyl-tRNA synthetase gltX and other proteins that are involved in protein synthesis, heterocyst differentiation, and nitrogen metabolism. By taking into account the important regulatory role of PII, it becomes clear that BMAA has a severe negative impact on the carbon and nitrogen metabolism of starving Nostoc sp. PCC 7120 cells. BMAA disturbs carbon fixation and the carbon dioxide concentrating mechanism, photosynthesis, and amino acid metabolism. Stress response proteins and DNA repair enzymes are upregulated in the presence of BMAA, clearly indicating severe intracellular stress. This is the first proteomic study of the effects of BMAA on diazotrophic starving cyanobacteria cells, allowing a deeper insight into the regulation of the intracellular metabolism of cyanobacteria by this non-protein amino acid.
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Toyoshima, Masakazu, Yuma Tokumaru, Fumio Matsuda, and Hiroshi Shimizu. "Assessment of Protein Content and Phosphorylation Level in Synechocystis sp. PCC 6803 under Various Growth Conditions Using Quantitative Phosphoproteomic Analysis." Molecules 25, no. 16 (August 6, 2020): 3582. http://dx.doi.org/10.3390/molecules25163582.
Full textAbstract:
The photosynthetic apparatus and metabolic enzymes of cyanobacteria are subject to various controls, such as transcriptional regulation and post-translational modifications, to ensure that the entire cellular system functions optimally. In particular, phosphorylation plays key roles in many cellular controls such as enzyme activity, signal transduction, and photosynthetic apparatus restructuring. Therefore, elucidating the governing functions of phosphorylation is crucial to understanding the regulatory mechanisms underlying metabolism and photosynthesis. In this study, we determined protein content and phosphorylation levels to reveal the regulation of intracellular metabolism and photosynthesis in Synechocystis sp. PCC 6803; for this, we obtained quantitative data of proteins and their phosphorylated forms involved in photosynthesis and metabolism under various growth conditions (photoautotrophic, mixotrophic, heterotrophic, dark, and nitrogen-deprived conditions) using targeted proteomic and phosphoproteomic analyses with nano-liquid chromatography-triple quadrupole mass spectrometry. The results indicated that in addition to the regulation of protein expression, the regulation of phosphorylation levels of cyanobacterial photosynthetic apparatus and metabolic enzymes was pivotal for adapting to changing environmental conditions. Furthermore, reduced protein levels of CpcC and altered phosphorylation levels of CpcB, ApcA, OCP, and PsbV contributed to the cellular response of the photosynthesis apparatus to nitrogen deficiency.
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Youssef, Nermeen, Scott Campbell, Amy Barr, Manoj Gandhi, Beth Hunter, Vernon Dolinsky, Jason R. B. Dyck, Alexander S. Clanachan, and Peter E. Light. "Hearts lacking plasma membrane KATP channels display changes in basal aerobic metabolic substrate preference and AMPK activity." American Journal of Physiology-Heart and Circulatory Physiology 313, no. 3 (September 1, 2017): H469—H478. http://dx.doi.org/10.1152/ajpheart.00612.2016.
Full textAbstract:
Cardiac ATP-sensitive K+ (KATP) channels couple changes in cellular metabolism to membrane excitability and are activated during metabolic stress, although under basal aerobic conditions, KATP channels are thought to be predominately closed. Despite intense research into the roles of KATP channels during metabolic stress, their contribution to aerobic basal cardiac metabolism has not been previously investigated. Hearts from Kir6.2+/+ and Kir6.2−/− mice were perfused in working mode, and rates of glycolysis, fatty acid oxidation, and glucose oxidation were measured. Changes in activation/expression of proteins regulating metabolism were probed by Western blot analysis. Despite cardiac mechanical function and metabolic efficiency being similar in both groups, hearts from Kir6.2−/− mice displayed an approximately twofold increase in fatty acid oxidation and a 0.45-fold reduction in glycolytic rates but similar glucose oxidation rates compared with hearts from Kir6.2+/+ mice. Kir6.2−/− hearts also possessed elevated levels of activated AMP-activated protein kinase (AMPK), higher glycogen content, and reduced mitochondrial density. Moreover, activation of AMPK by isoproterenol or diazoxide was significantly blunted in Kir6.2−/− hearts. These data indicate that KATP channel ablation alters aerobic basal cardiac metabolism. The observed increase in fatty acid oxidation and decreased glycolysis before any metabolic insult may contribute to the poor recovery observed in Kir6.2−/− hearts in response to exercise or ischemia-reperfusion injury. Therefore, KATP channels may play an important role in the regulation of cardiac metabolism through AMPK signaling. NEW & NOTEWORTHY In this study, we show that genetic ablation of plasma membrane ATP-sensitive K+ channels results in pronounced changes in cardiac metabolic substrate preference and AMP-activated protein kinase activity. These results suggest that ATP-sensitive K+ channels may play a novel role in regulating metabolism in addition to their well-documented effects on ionic homeostasis during periods of stress.
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Nie, Cunxi, Fei Xie, Ning Ma, Yueyu Bai, Wenju Zhang, and Xi Ma. "Nutrients Mediate Bioavailability and Turnover of Proteins in Mammals." Current Protein & Peptide Science 20, no. 7 (June 27, 2019): 661–65. http://dx.doi.org/10.2174/1389203720666190125111235.
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As a major component of biologically active compounds in the body, proteins contribute to the synthesis of body tissues for the renewal and growth of the body. The high level of dietary protein and the imbalance of amino acid (AA) composition in mammals result in metabolic disorders, inefficient utilization of protein resources and increased nitrogen excretion. Fortunately, nutritional interventions can be an effective way of attenuating the nitrogen excretion and increasing protein utilization, which include, but are not limited to, formulating the AA balance and protein-restricted diet supplementing with essential AAs, and adding probiotics in the diet. This review highlights recent advances in the turnover of dietary proteins and mammal’s metabolism for health, in order to improve protein bioavailability through nutritional approach.
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Jaeger, Cassie, Ali Q. Khazaal, Canxin Xu, Mingwei Sun, Stacey L. Krager, and Shelley A. Tischkau. "Aryl Hydrocarbon Receptor Deficiency Alters Circadian and Metabolic Rhythmicity." Journal of Biological Rhythms 32, no. 2 (March 27, 2017): 109–20. http://dx.doi.org/10.1177/0748730417696786.
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PAS domain–containing proteins can act as environmental sensors that capture external stimuli to allow coordination of organismal physiology with the outside world. These proteins permit diverse ligand binding and heterodimeric partnership, allowing for varied combinations of PAS-dependent protein-protein interactions and promoting crosstalk among signaling pathways. Previous studies report crosstalk between circadian clock proteins and the aryl hydrocarbon receptor (AhR). Activated AhR forms a heterodimer with the circadian clock protein Bmal1 and thereby functionally inhibits CLOCK/Bmal1 activity. If physiological activation of AhR through naturally occurring, endogenous ligands inhibits clock function, it seems plausible to hypothesize that decreased AhR expression releases AhR-induced inhibition of circadian rhythms. Because both AhR and the clock are important regulators of glucose metabolism, it follows that decreased AhR will also alter metabolic function. To test this hypothesis, rhythms of behavior, metabolic outputs, and circadian and metabolic gene expression were measured in AhR-deficient mice. Genetic depletion of AhR enhanced behavioral responses to changes in the light-dark cycle, increased rhythmic amplitude of circadian clock genes in the liver, and altered rhythms of glucose and insulin. This study provides evidence of AhR-induced inhibition that influences circadian rhythm amplitude.
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Mendonca, Caroll M., Sho Yoshitake, Hua Wei, Anne Werner, Samantha S. Sasnow, Theodore W. Thannhauser, and Ludmilla Aristilde. "Hierarchical routing in carbon metabolism favors iron-scavenging strategy in iron-deficient soilPseudomonasspecies." Proceedings of the National Academy of Sciences 117, no. 51 (December 3, 2020): 32358–69. http://dx.doi.org/10.1073/pnas.2016380117.
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High-affinity iron (Fe) scavenging compounds, or siderophores, are widely employed by soil bacteria to survive scarcity in bioavailable Fe. Siderophore biosynthesis relies on cellular carbon metabolism, despite reported decrease in both carbon uptake and Fe-containing metabolic proteins in Fe-deficient cells. Given this paradox, the metabolic network required to sustain the Fe-scavenging strategy is poorly understood. Here, through multiple13C-metabolomics experiments with Fe-replete and Fe-limited cells, we uncover how soilPseudomonasspecies reprogram their metabolic pathways to prioritize siderophore biosynthesis. Across the three species investigated (Pseudomonas putidaKT2440,Pseudomonas protegensPf-5, andPseudomonas putidaS12), siderophore secretion is higher during growth on gluconeogenic substrates than during growth on glycolytic substrates. In response to Fe limitation, we capture decreased flux toward the tricarboxylic acid (TCA) cycle during the metabolism of glycolytic substrates but, due to carbon recycling to the TCA cycle via enhanced anaplerosis, the metabolism of gluconeogenic substrates results in an increase in both siderophore secretion (up to threefold) and Fe extraction (up to sixfold) from soil minerals. During simultaneous feeding on the different substrate types, Fe deficiency triggers a hierarchy in substrate utilization, which is facilitated by changes in protein abundances for substrate uptake and initial catabolism. Rerouted metabolism further promotes favorable fluxes in the TCA cycle and the gluconeogenesis–anaplerosis nodes, despite decrease in several proteins in these pathways, to meet carbon and energy demands for siderophore precursors in accordance with increased proteins for siderophore biosynthesis. Hierarchical carbon metabolism thus serves as a critical survival strategy during the metal nutrient deficiency.
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Xavier, Joana C., Wim Hordijk, Stuart Kauffman, Mike Steel, and William F. Martin. "Autocatalytic chemical networks at the origin of metabolism." Proceedings of the Royal Society B: Biological Sciences 287, no. 1922 (March 11, 2020): 20192377. http://dx.doi.org/10.1098/rspb.2019.2377.
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Modern cells embody metabolic networks containing thousands of elements and form autocatalytic sets of molecules that produce copies of themselves. How the first self-sustaining metabolic networks arose at life's origin is a major open question. Autocatalytic sets smaller than metabolic networks were proposed as transitory intermediates at the origin of life, but evidence for their role in prebiotic evolution is lacking. Here, we identify reflexively autocatalytic food-generated networks (RAFs)—self-sustaining networks that collectively catalyse all their reactions—embedded within microbial metabolism. RAFs in the metabolism of ancient anaerobic autotrophs that live from H 2 and CO 2 provided with small-molecule catalysts generate acetyl-CoA as well as amino acids and bases, the monomeric components of protein and RNA, but amino acids and bases without organic catalysts do not generate metabolic RAFs. This suggests that RAFs identify attributes of biochemical origins conserved in metabolic networks. RAFs are consistent with an autotrophic origin of metabolism and furthermore indicate that autocatalytic chemical networks preceded proteins and RNA in evolution. RAFs uncover intermediate stages in the emergence of metabolic networks, narrowing the gaps between early Earth chemistry and life.
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Xu, Chenping, Zhongchun Jiang, and Bingru Huang. "Nitrogen Deficiency-induced Protein Changes in Immature and Mature Leaves of Creeping Bentgrass." Journal of the American Society for Horticultural Science 136, no. 6 (November 2011): 399–407. http://dx.doi.org/10.21273/jashs.136.6.399.
Full textAbstract:
Nitrogen (N) deficiency inhibits plant growth and induces leaf senescence through regulating various metabolic processes. The objectives of this study were to examine protein changes in response to N deficiency in immature and mature leaves of a perennial grass species and determine major metabolic processes affected by N deficiency through proteomic profiling. Creeping bentgrass (Agrostis stolonifera cv. Penncross) plants were originally fertilized with a diluted 36N–2.6P–5K fertilizer. After 14 days acclimation in a growth chamber, plants were grown in a nutrient solution containing 6 mm nitrate (control) or without N (N deficiency). Immature leaves (upper first and second not yet fully expanded leaves) and mature leaves (lower fully expanded leaves) were separated at 28 days of treatment for protein analysis. Two-dimensional electrophoresis and mass spectrometry analysis were used to identify protein changes in immature and mature leaves in response to N deficiency. The abundance of many proteins in both immature and mature leaves decreased with N deficiency, including those involved in photosynthesis, photorespiration, and amino acid metabolism (hydroxypyruvate reductase, serine hydroxymethyltransferase, alanine aminotransferase, glycine decarboxylase complex, glycolate oxidase), protein protection [heat shock protein (HSP)/HSP 70, chaperonin 60 and FtsH-like protein], and RNA stability (RNA binding protein). The reduction in protein abundance under N deficiency was greater in mature leaves than in immature leaves. The abundance of small HSP and metalloendopeptidase increased under N deficiency only in immature leaves. These results suggest that N deficiency accelerated protein degradation in immature and mature leaves of creeping bentgrass, particularly those proteins associated with energy and metabolism, but to a lesser extent in immature leaves. Immature leaves were also able to accumulate proteins with chaperone functions and for N reutilization, which could protect leaves from senescence under N deficiency.