The Experts below are selected from a list of 228 Experts worldwide ranked by ideXlab platform
Valeria C Culotta - One of the best experts on this subject based on the ideXlab platform.
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the yeast copper zinc superoxide dismutase and the Pentose Phosphate Pathway play overlapping roles in oxidative stress protection
Journal of Biological Chemistry, 1996Co-Authors: Kimberly Hudak Slekar, Daniel J Kosman, Valeria C CulottaAbstract:Next Section Abstract In Saccharomyces cerevisiae, loss of cytosolic superoxide dismutase (Sod1) results in several air-dependent mutant phenotypes, including methionine auxotrophy and oxygen sensitivity. Here we report that these two sod1Δ phenotypes were specifically suppressed by elevated expression of the TKL1 gene, encoding transketolase of the Pentose Phosphate Pathway. The apparent connection between Sod1 and the Pentose Phosphate Pathway prompted an investigation of mutants defective in glucose-6-Phosphate dehydrogenase (Zwf1), which catalyzes the rate-limiting NADPH-producing step of this Pathway. We confirmed that zwf1Δ mutants are methionine auxotrophs and report that they also are oxygen-sensitive. We determined that a functional ZWF1 gene product was required for TKL1 to suppress sod1Δ, leading us to propose that increased flux through the oxidative reactions of the Pentose Phosphate Pathway can rescue sod1 methionine auxotrophy. To better understand this methionine growth requirement, we examined the sulfur compound requirements of sod1Δ and zwf1Δ mutants, and noted that these mutants exhibit the same apparent defect in sulfur assimilation. Our studies suggest that this defect results from the impaired redox status of aerobically grown sod1 and zwf1 mutants, implicating Sod1 and the Pentose Phosphate Pathway as being critical for maintenance of the cellular redox state.
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The yeast copper/zinc superoxide dismutase and the Pentose Phosphate Pathway play overlapping roles in oxidative stress protection.
Journal of Biological Chemistry, 1996Co-Authors: Kimberly Hudak Slekar, Daniel J Kosman, Valeria C CulottaAbstract:Next Section Abstract In Saccharomyces cerevisiae, loss of cytosolic superoxide dismutase (Sod1) results in several air-dependent mutant phenotypes, including methionine auxotrophy and oxygen sensitivity. Here we report that these two sod1Δ phenotypes were specifically suppressed by elevated expression of the TKL1 gene, encoding transketolase of the Pentose Phosphate Pathway. The apparent connection between Sod1 and the Pentose Phosphate Pathway prompted an investigation of mutants defective in glucose-6-Phosphate dehydrogenase (Zwf1), which catalyzes the rate-limiting NADPH-producing step of this Pathway. We confirmed that zwf1Δ mutants are methionine auxotrophs and report that they also are oxygen-sensitive. We determined that a functional ZWF1 gene product was required for TKL1 to suppress sod1Δ, leading us to propose that increased flux through the oxidative reactions of the Pentose Phosphate Pathway can rescue sod1 methionine auxotrophy. To better understand this methionine growth requirement, we examined the sulfur compound requirements of sod1Δ and zwf1Δ mutants, and noted that these mutants exhibit the same apparent defect in sulfur assimilation. Our studies suggest that this defect results from the impaired redox status of aerobically grown sod1 and zwf1 mutants, implicating Sod1 and the Pentose Phosphate Pathway as being critical for maintenance of the cellular redox state.
Kimberly Hudak Slekar - One of the best experts on this subject based on the ideXlab platform.
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the yeast copper zinc superoxide dismutase and the Pentose Phosphate Pathway play overlapping roles in oxidative stress protection
Journal of Biological Chemistry, 1996Co-Authors: Kimberly Hudak Slekar, Daniel J Kosman, Valeria C CulottaAbstract:Next Section Abstract In Saccharomyces cerevisiae, loss of cytosolic superoxide dismutase (Sod1) results in several air-dependent mutant phenotypes, including methionine auxotrophy and oxygen sensitivity. Here we report that these two sod1Δ phenotypes were specifically suppressed by elevated expression of the TKL1 gene, encoding transketolase of the Pentose Phosphate Pathway. The apparent connection between Sod1 and the Pentose Phosphate Pathway prompted an investigation of mutants defective in glucose-6-Phosphate dehydrogenase (Zwf1), which catalyzes the rate-limiting NADPH-producing step of this Pathway. We confirmed that zwf1Δ mutants are methionine auxotrophs and report that they also are oxygen-sensitive. We determined that a functional ZWF1 gene product was required for TKL1 to suppress sod1Δ, leading us to propose that increased flux through the oxidative reactions of the Pentose Phosphate Pathway can rescue sod1 methionine auxotrophy. To better understand this methionine growth requirement, we examined the sulfur compound requirements of sod1Δ and zwf1Δ mutants, and noted that these mutants exhibit the same apparent defect in sulfur assimilation. Our studies suggest that this defect results from the impaired redox status of aerobically grown sod1 and zwf1 mutants, implicating Sod1 and the Pentose Phosphate Pathway as being critical for maintenance of the cellular redox state.
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The yeast copper/zinc superoxide dismutase and the Pentose Phosphate Pathway play overlapping roles in oxidative stress protection.
Journal of Biological Chemistry, 1996Co-Authors: Kimberly Hudak Slekar, Daniel J Kosman, Valeria C CulottaAbstract:Next Section Abstract In Saccharomyces cerevisiae, loss of cytosolic superoxide dismutase (Sod1) results in several air-dependent mutant phenotypes, including methionine auxotrophy and oxygen sensitivity. Here we report that these two sod1Δ phenotypes were specifically suppressed by elevated expression of the TKL1 gene, encoding transketolase of the Pentose Phosphate Pathway. The apparent connection between Sod1 and the Pentose Phosphate Pathway prompted an investigation of mutants defective in glucose-6-Phosphate dehydrogenase (Zwf1), which catalyzes the rate-limiting NADPH-producing step of this Pathway. We confirmed that zwf1Δ mutants are methionine auxotrophs and report that they also are oxygen-sensitive. We determined that a functional ZWF1 gene product was required for TKL1 to suppress sod1Δ, leading us to propose that increased flux through the oxidative reactions of the Pentose Phosphate Pathway can rescue sod1 methionine auxotrophy. To better understand this methionine growth requirement, we examined the sulfur compound requirements of sod1Δ and zwf1Δ mutants, and noted that these mutants exhibit the same apparent defect in sulfur assimilation. Our studies suggest that this defect results from the impaired redox status of aerobically grown sod1 and zwf1 mutants, implicating Sod1 and the Pentose Phosphate Pathway as being critical for maintenance of the cellular redox state.
Marta Cascante - One of the best experts on this subject based on the ideXlab platform.
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Role of the Pentose Phosphate Pathway in Tumour Metabolism
Tumor Cell Metabolism, 2020Co-Authors: Adrián Benito, Josep J. Centelles, Santiago Diaz-moralli, Marta CascanteAbstract:The Pentose Phosphate Pathway plays a pivotal role in cellular physiology. It synthesizes the nucleotide precursor ribose-5-Phosphate and NADPH, required for redox homeostasis maintenance and lipogenesis. Cancer cells undergo metabolic reprogramming required to sustain proliferation and fully achieve malignant capabilities. Such metabolic reprogramming involves multiple metabolic Pathways, and the Pentose Phosphate Pathway becomes essential in tumour metabolism and biology. According to that, many changes occur in this metabolic Pathway over the tumorigenic process, and the enzymes in this Pathway become directly involved in the metabolism of cancer cells as well as in other important features of tumours. Also, a greater reliance on this Pathway has been detected in some types of tumours. In this chapter, a detailed view of the role of the Pentose Phosphate Pathway and its enzymes in tumour metabolism is provided. In addition, the potentiality of this Pathway as therapeutic target in cancer treatment is discussed.
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A model of the Pentose Phosphate Pathway in rat liver cells.
Molecular and Cellular Biochemistry, 1995Co-Authors: Llorenç Sabate, Rafael Franco, Enric I. Canela, Josep J. Centelles, Marta CascanteAbstract:A mathematical model based on kinetic data taken from the literature is presented for the Pentose Phosphate Pathway in fasted rat liver steady-state. Since the oxidative and non oxidative Pentose Phosphate Pathway can act independently, the complete (oxidative + non oxidative) and the non oxidative Pentose Pathway were simulated.
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A model of the Pentose Phosphate Pathway in rat liver cells
Molecular and Cellular Biochemistry, 1995Co-Authors: Llorenç Sabate, Rafael Franco, Enric I. Canela, Josep J. Centelles, Marta CascanteAbstract:A mathematical model based on kinetic data taken from the literature is presented for the Pentose Phosphate Pathway in fasted rat liver steady-state. Since the oxidative and non oxidative Pentose Phosphate Pathway can act independently, the complete (oxidative + non oxidative) and the non oxidative Pentose Pathway were simulated. Sensitivity analyses are reported which show that the fluxes are mainly regulated by D-glucose-6-Phosphate dehydrogenase (for the oxidative Pathway) and by transketolase (for the non oxidative Pathway). The most influent metabolites were the group ATP, ADP, P_1 and the group NADPH, NADP^+ (for the non oxidative Pathway).
Dario Ghigo - One of the best experts on this subject based on the ideXlab platform.
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the Pentose Phosphate Pathway an antioxidant defense and a crossroad in tumor cell fate
Free Radical Biology and Medicine, 2012Co-Authors: Chiara Riganti, Elena Gazzano, Manuela Polimeni, Elisabetta Aldieri, Dario GhigoAbstract:Abstract The Pentose Phosphate Pathway, one of the main antioxidant cellular defense systems, has been related for a long time almost exclusively to its role as a provider of reducing power and ribose Phosphate to the cell. In addition to this “traditional” correlation, in the past years multiple roles have emerged for this metabolic cascade, involving the cell cycle, apoptosis, differentiation, motility, angiogenesis, and the response to anti-tumor therapy. These findings make the Pentose Phosphate Pathway a very interesting target in tumor cells. This review summarizes the latest discoveries relating the activity of the Pentose Phosphate Pathway to various aspects of tumor metabolism, such as cell proliferation and death, tissue invasion, angiogenesis, and resistance to therapy, and discusses the possibility that drugs modulating the Pathway could be used as potential tools in tumor therapy.
Daniel J Kosman - One of the best experts on this subject based on the ideXlab platform.
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the yeast copper zinc superoxide dismutase and the Pentose Phosphate Pathway play overlapping roles in oxidative stress protection
Journal of Biological Chemistry, 1996Co-Authors: Kimberly Hudak Slekar, Daniel J Kosman, Valeria C CulottaAbstract:Next Section Abstract In Saccharomyces cerevisiae, loss of cytosolic superoxide dismutase (Sod1) results in several air-dependent mutant phenotypes, including methionine auxotrophy and oxygen sensitivity. Here we report that these two sod1Δ phenotypes were specifically suppressed by elevated expression of the TKL1 gene, encoding transketolase of the Pentose Phosphate Pathway. The apparent connection between Sod1 and the Pentose Phosphate Pathway prompted an investigation of mutants defective in glucose-6-Phosphate dehydrogenase (Zwf1), which catalyzes the rate-limiting NADPH-producing step of this Pathway. We confirmed that zwf1Δ mutants are methionine auxotrophs and report that they also are oxygen-sensitive. We determined that a functional ZWF1 gene product was required for TKL1 to suppress sod1Δ, leading us to propose that increased flux through the oxidative reactions of the Pentose Phosphate Pathway can rescue sod1 methionine auxotrophy. To better understand this methionine growth requirement, we examined the sulfur compound requirements of sod1Δ and zwf1Δ mutants, and noted that these mutants exhibit the same apparent defect in sulfur assimilation. Our studies suggest that this defect results from the impaired redox status of aerobically grown sod1 and zwf1 mutants, implicating Sod1 and the Pentose Phosphate Pathway as being critical for maintenance of the cellular redox state.
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The yeast copper/zinc superoxide dismutase and the Pentose Phosphate Pathway play overlapping roles in oxidative stress protection.
Journal of Biological Chemistry, 1996Co-Authors: Kimberly Hudak Slekar, Daniel J Kosman, Valeria C CulottaAbstract:Next Section Abstract In Saccharomyces cerevisiae, loss of cytosolic superoxide dismutase (Sod1) results in several air-dependent mutant phenotypes, including methionine auxotrophy and oxygen sensitivity. Here we report that these two sod1Δ phenotypes were specifically suppressed by elevated expression of the TKL1 gene, encoding transketolase of the Pentose Phosphate Pathway. The apparent connection between Sod1 and the Pentose Phosphate Pathway prompted an investigation of mutants defective in glucose-6-Phosphate dehydrogenase (Zwf1), which catalyzes the rate-limiting NADPH-producing step of this Pathway. We confirmed that zwf1Δ mutants are methionine auxotrophs and report that they also are oxygen-sensitive. We determined that a functional ZWF1 gene product was required for TKL1 to suppress sod1Δ, leading us to propose that increased flux through the oxidative reactions of the Pentose Phosphate Pathway can rescue sod1 methionine auxotrophy. To better understand this methionine growth requirement, we examined the sulfur compound requirements of sod1Δ and zwf1Δ mutants, and noted that these mutants exhibit the same apparent defect in sulfur assimilation. Our studies suggest that this defect results from the impaired redox status of aerobically grown sod1 and zwf1 mutants, implicating Sod1 and the Pentose Phosphate Pathway as being critical for maintenance of the cellular redox state.