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Your search keyword '"Chaplen, Frank W. R."' showing total 34 results
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34 results on '"Chaplen, Frank W. R."'

2. Tumor necrosis factor-induced modulation of glyoxalase I activities through phosphorylation by PKA results in cell death and is accompanied by the formation of a specific methylglyoxal-derived AGE

Author

Van Herreweghe, Franky, Mao, Jianqiang, Chaplen, Frank W. R., Grooten, Johan, Gevaert, Kris, Vandekerckhove, Joel, and Vancompernolle, Katia

Subjects
Tumor necrosis factor -- Physiological aspects, Phosphorylation -- Physiological aspects, Enzymes -- Physiological aspects, Cytochemistry -- Research, Fibrosarcoma -- Physiological aspects, Mitochondria -- Physiological aspects, Oxygen -- Physiological aspects, Cell death -- Research, Science and technology
Abstract

Tumor necrosis factor (TNF)-induced cell death in the fibrosarcoma cell line L929 is a caspase-independent process that is characterized by increased production of reactive oxygen species (ROS) in the mitochondria. To elucidate this ROS-dependent cell death pathway, a comparative study of the phosphoproteins present in TNF-treated and control cells was performed. Here we report that TNF induces an increased phosphorylation of glyoxalase I that is mediated by protein kinase A and required for cell death. We also show that TNF induces a substantial increase in intracellular levels of methylglyoxal (MG) that leads to the formation of a specific MG-derived advanced glycation end product and that this formation occurs as a consequence of increased ROS production. These data indicate that MG modification of proteins is a targeted process and that MG may thus function as a signal molecule during the regulation of cell death. Furthermore, we provide evidence that the TNF-induced phosphorylation of glyoxalase I is not involved in detoxification of MG by means of the glyoxalase system, but that phosphorylated glyoxalase I is on the pathway leading to the formation of a specific MG-derived advanced glycation end product.

Published
2002

11. New adenovirus vectors for protein production and gene transfer

Author

Massie, Bernard, Mosser, Dick D., Koutroumanis, Maria, Vitté-Mony, Isabelle, Lamoureux, Linda, Couture, France, Paquet, Luc, Guilbault, Claire, Dionne, Julie, Chahla, Dounia, Jolicoeur, Pierre, Langelier, Yves, Betenbaugh, Michael J., editor, Chalmers, Jeffrey J., editor, Arathoon, Rob, editor, Chaplen, Frank W. R., editor, and Mastrangelo, Alison J., editor

Published
1998
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19. Cell therapy in kidney failure

Author

Humes, H. David, Funke, Angela J., Buffington, Deborah A., Betenbaugh, Michael J., editor, Chalmers, Jeffrey J., editor, Arathoon, Rob, editor, Chaplen, Frank W. R., editor, and Mastrangelo, Alison J., editor

Published
1998
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32. Genome scale metabolic reconstruction of Chlorella variabilis for exploring its metabolic potential for biofuels.

Author

Juneja A, Chaplen FWR, and Murthy GS

Subjects
Biomass, Chlorella cytology, Chlorella growth & development, Metabolic Flux Analysis, Metabolic Networks and Pathways, Models, Theoretical, Phenotype, Biofuels, Chlorella genetics, Chlorella metabolism, Genome, Metabolic Engineering methods
Abstract

A compartmentalized genome scale metabolic network was reconstructed for Chlorella variabilis to offer insight into various metabolic potentials from this alga. The model, iAJ526, was reconstructed with 1455 reactions, 1236 metabolites and 526 genes. 21% of the reactions were transport reactions and about 81% of the total reactions were associated with enzymes. Along with gap filling reactions, 2 major sub-pathways were added to the model, chitosan synthesis and rhamnose metabolism. The reconstructed model had reaction participation of 4.3 metabolites per reaction and average lethality fraction of 0.21. The model was effective in capturing the growth of C. variabilis under three light conditions (white, red and red+blue light) with fair agreement. This reconstructed metabolic network will serve an important role in systems biology for further exploration of metabolism for specific target metabolites and enable improved characteristics in the strain through metabolic engineering., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Published
2016
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33. Effects of selected electron transport chain inhibitors on 24-h hydrogen production by Synechocystis sp. PCC 6803.

Author

Burrows EH, Chaplen FW, and Ely RL

Subjects
Algorithms, Hydrogen isolation & purification, Electron Transport Chain Complex Proteins antagonists & inhibitors, Enzyme Inhibitors pharmacology, Hydrogen metabolism, Hydrogenase antagonists & inhibitors, Hydrogenase metabolism, Synechocystis drug effects, Synechocystis metabolism
Abstract

One factor limiting biosolar hydrogen (H(2)) production from cyanobacteria is electron availability to the hydrogenase enzyme. In order to optimize 24-h H(2) production this study used Response Surface Methodology and Q2, an optimization algorithm, to investigate the effects of five inhibitors of the photosynthetic and respiratory electron transport chains of Synechocystis sp. PCC 6803. Over 3 days of diurnal light/dark cycling, with the optimized combination of 9.4 mM KCN (3.1 μmol 10(10) cells(-1)) and 1.5 mM malonate (0.5 μmol 10(10) cells(-1)) the H(2) production was 30-fold higher, in EHB-1 media previously optimized for nitrogen (N), sulfur (S), and carbon (C) concentrations (Burrows et al., 2008). In addition, glycogen concentration was measured over 24 h with two light/dark cycling regimes in both standard BG-11 and EHB-1 media. The results suggest that electron flow as well as glycogen accumulation should be optimized in systems engineered for maximal H(2) output., (Copyright © 2010 Elsevier Ltd. All rights reserved.)

Published
2011
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34. Stimulation of insulin release by glyceraldehyde may not be similar to glucose.

Author

MacDonald MJ, Chaplen FW, Triplett CK, Gong Q, and Drought H

Subjects
Animals, Cells, Cultured, Female, Male, Rats, Rats, Sprague-Dawley, Glucose metabolism, Glyceraldehyde administration & dosage, Insulin metabolism, Islets of Langerhans drug effects, Islets of Langerhans metabolism
Abstract

Glyceraldehyde (GA) has been used to study insulin secretion for decades and it is widely assumed that beta-cell metabolism of GA after its phosphorylation by triokinase is similar to metabolism of glucose; that is metabolism through distal glycolysis and oxidation in mitochondria. New data supported by existing information indicate that this is true for only a small amount of GA's metabolism and also suggest why GA is toxic. GA is metabolized at 10-20% the rate of glucose in pancreatic islets, even though GA is a more potent insulin secretagogue. GA also inhibits glucose metabolism to CO2 out of proportion to its ability to replace glucose as a fuel. This study is the first to measure methylglyoxal (MG) in beta-cells and shows that GA causes large increases in MG in INS-1 cells and d-lactate in islets but MG does not mediate GA-induced insulin release. GA severely lowers NAD(P) and increases NAD(P)H in islets. High NADH combined with GA's metabolism to CO2 may initially hyperstimulate insulin release, but a low cytosolic NAD/NADH ratio will block glycolysis at glyceraldehyde phosphate (GAP) dehydrogenase and divert GAP toward MG and D-lactate formation. Accumulation of D-lactate and 1-phosphoglycerate may explain why GA makes the beta-cell acidic. Reduction of both GA and MG by abundant beta-cell aldehyde reductases will lower the cytosolic NADPH/NADP ratio, which is normally high.

Published
2006
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