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Total 24 results found since Jan 2013.

Genetic Regulation of Liver Metabolites and Transcripts Linking to Biochemical-Clinical Parameters
Conclusion In summary, this study is the first to combine metabolomics, transcriptomics, and genome-wide association studies in a porcine model. Our results improve understanding of the genetic regulation of metabolites which link to transcripts and finally biochemical-clinical parameters. Further, high-performance profiling of metabolites as intermediate phenotypes is a potentially powerful approach to uncover how genetic variation affects metabolic and health status. Our results advance knowledge in areas of biomedical and agricultural interest and identify potential correlates of biomarkers, SNPs-metabolites, SNPs-tran...
Source: Frontiers in Genetics - April 16, 2019 Category: Genetics & Stem Cells Source Type: research

Roles for cytosolic NADPH redox in regulating pulmonary artery relaxation by thiol oxidation-elicited subunit dimerization of Protein Kinase G 1α
Abstract The activity of glucose-6-phosphate dehydrogenase (G6PD) appears to control a vascular smooth muscle relaxing mechanism regulated through cytosolic NADPH oxidation. Since our recent studies suggest thiol oxidation-elicited dimerization of the 1α form of protein kinase G (PKG1α) contributes to the relaxation of isolated endothelium-removed bovine pulmonary arteries (BPA) to peroxide and responses to hypoxia, we investigated if cytosolic NADPH oxidation promoted relaxation by PKG1α dimerization. Relaxation of BPA to G6PD inhibitors, 6-aminonicotinamide (6-AN) and epiandrosterone (studied under hypoxia to...
Source: American Journal of Physiology. Heart and Circulatory Physiology - May 24, 2013 Category: Physiology Authors: Neo BH, Patel D, Kandhi S, Wolin MS Tags: Am J Physiol Heart Circ Physiol Source Type: research

Roles for cytosolic NADPH redox in regulating pulmonary artery relaxation by thiol oxidation-elicited subunit dimerization of protein kinase G1{alpha}
The activity of glucose-6-phosphate dehydrogenase (G6PD) appears to control a vascular smooth muscle relaxing mechanism regulated through cytosolic NADPH oxidation. Since our recent studies suggest that thiol oxidation-elicited dimerization of the 1α form of protein kinase G (PKG1α) contributes to the relaxation of isolated endothelium-removed bovine pulmonary arteries (BPA) to peroxide and responses to hypoxia, we investigated whether cytosolic NADPH oxidation promoted relaxation by PKG1α dimerization. Relaxation of BPA to G6PD inhibitors 6-aminonicotinamide (6-AN) and epiandrosterone (studied under hypo...
Source: AJP: Heart and Circulatory Physiology - August 1, 2013 Category: Cardiology Authors: Neo, B. H., Patel, D., Kandhi, S., Wolin, M. S. Tags: VASCULAR BIOLOGY AND MICROCIRCULATION Source Type: research

Inhibition of Calcium/Calmodulin-Dependent Protein Kinase II α Suppresses Oxidative Stress in Cerebral Ischemic Rats Through Targeting Glucose 6-Phosphate Dehydrogenase.
Inhibition of Calcium/Calmodulin-Dependent Protein Kinase IIα Suppresses Oxidative Stress in Cerebral Ischemic Rats Through Targeting Glucose 6-Phosphate Dehydrogenase. Neurochem Res. 2019 Mar 27;: Authors: Wei Y, Wang R, Teng J Abstract Ischemic stroke is a leading cause of mortality and morbidity worldwide, and oxidative stress plays a significant role in the ischemia stage and reperfusion stage. Previous studies have indicated that both calcium/calmodulin-dependent protein kinase II (CaMKII) and glucose 6-phosphate dehydrogenase (G6PD) are involved in the oxidative stress. Thus, the aim of this st...
Source: Neurochemical Research - March 26, 2019 Category: Neuroscience Authors: Wei Y, Wang R, Teng J Tags: Neurochem Res Source Type: research

Thioredoxin-interacting protein regulates glucose metabolism and improves the intracellular redox state in bovine oocytes during in vitro maturation.
Abstract The extent of glucose metabolism during oocyte maturation is closely related to oocyte developmental potential. Thioredoxin-interacting protein (TXNIP) is an α-arrestin family protein that negatively regulates glucose uptake into cells. However, little information is available regarding the function of TXNIP in bovine oocytes. Accordingly, the present study was performed to investigate the influence of TXNIP on glucose metabolism in bovine oocytes during in vitro maturation. Pharmacological inhibition of TXNIP by azaserine enhanced glucose uptake and imparted a specific metabolic effect on glycolysis and...
Source: Am J Physiol Endocri... - January 13, 2020 Category: Endocrinology Authors: Jiang X, Pang Y, Zhao S, Hao H, Zhao X, Du W, Wang Y, Zhu H Tags: Am J Physiol Endocrinol Metab Source Type: research

Nutrient Regulation of mRNA Splicing Gene Regulation
Expression of G6PD is controlled by changes in the degree of splicing of the G6PD mRNA in response to nutrients in the diet. This regulation involves an exonic splicing enhancer (ESE) in exon 12 of the mRNA. Using the G6PD model, we demonstrate that nutrients and hormones control the activity of serine-arginine-rich (SR) proteins, a family of splicing co-activators, and thereby regulate the splicing of G6PD mRNA. In primary rat hepatocyte cultures, insulin increased the amount of phosphorylated SR proteins, and this effect was counteracted by arachidonic acid. The results of RNA affinity analysis with nuclear extracts from...
Source: Journal of Biological Chemistry - January 25, 2013 Category: Chemistry Authors: Walsh, C. M., Suchanek, A. L., Cyphert, T. J., Kohan, A. B., Szeszel-Fedorowicz, W., Salati, L. M. Tags: RNA Source Type: research

Caveolin-1 upregulation in diabetic fibroblasts and wounded tissues: implication for understanding the underlying mechanisms of non-healing diabetic ulcers.
Abstract A heightened state of oxidative stress and senescence of fibroblasts constitute potential therapeutic targets in non-healing diabetic wounds. Here, we studied the underlying mechanism mediating diabetes-induced cellular senescence using in vitro cultured dermal fibroblasts and in vivo circular wounds. Our results demonstrated that the total antioxidant capacity, mRNA levels of thioredoxinreductase and glucose-6-phosphate dehydrogenase as well as the ratio of NADPH/NADP were markedly decreased in fibroblasts from patients with type 2 diabetes (DFs). Consistent with this shifts in favor of excessive reactiv...
Source: American Journal of Physiology. Endocrinology and Metabolism - August 13, 2013 Category: Physiology Authors: Bitar MS, Abdel-Halim SM, Al-Mulla F Tags: Am J Physiol Endocrinol Metab Source Type: research

Caveolin-1/PTRF upregulation constitutes a mechanism for mediating p53-induced cellular senescence: implications for evidence-based therapy of delayed wound healing in diabetes
A heightened state of oxidative stress and senescence of fibroblasts constitute potential therapeutic targets in nonhealing diabetic wounds. Here, we studied the underlying mechanism mediating diabetes-induced cellular senescence using in vitro cultured dermal fibroblasts and in vivo circular wounds. Our results demonstrated that the total antioxidant capacity and mRNA levels of thioredoxinreductase and glucose-6-phosphate dehydrogenase as well as the ratio of NADPH/NADP were decreased markedly in fibroblasts from patients with type 2 diabetes (DFs). Consistent with this shift in favor of excessive reactive oxygen species,...
Source: AJP: Endocrinology and Metabolism - October 15, 2013 Category: Endocrinology Authors: Bitar, M. S., Abdel-Halim, S. M., Al-Mulla, F. Tags: Articles Source Type: research

TIGAR regulates glycolysis in ischemic kidney proximal tubules.
Abstract Tp53-induced glycolysis and apoptosis regulator (TIGAR) activation blocks glycolytic ATP synthesis by inhibiting phosphofructokinase-1 (PFK-1) activity. Our data indicate that TIGAR is selectively induced and activated in renal outermedullary proximal straight tubules (PST) following ischemia/reperfusion injury (IRI) in a p53-dependent manner. Under severe ischemic conditions, TIGAR expression persisted through 48 hours post-injury and induced loss of renal function and histological damage. Further, TIGAR upregulation inhibited PFK-1 activity, glucose 6-phosphate dehydrogenase (G6PD) activity and induced ...
Source: American Journal of Physiology. Renal Physiology - December 10, 2014 Category: Physiology Authors: Kim J, Devalaraja-Narashimha K, Padanilam BJ Tags: Am J Physiol Renal Physiol Source Type: research

Glucose 6-phosphate dehydrogenase knockdown enhances IL-8 expression in HepG2 cells via oxidative stress and NF-κB signaling pathway
Conclusions: G6PD deficiency predisposes cells to enhanced production of pro-inflammatory cytokine IL-8. Mechanistically, G6PD deficiency up-regulates IL-8 through oxidative stress and NF-κB pathway. The palmitate-induced inflammation in G6PD-deficient HepG2 cells could serve as an in vitro model to study the role of altered redox homeostasis in chronic hepatic inflammation.
Source: Journal of Inflammation - April 24, 2015 Category: Allergy & Immunology Authors: Hung-Chi YangMei-Ling ChengYi-Syuan HuaYi-Hsuan WuHsin-Ru LinHui-Ya LiuHung-Yao HoDaniel Chiu Source Type: research

ΔNp63α-responsive microRNAs modulate the expression of metabolic enzymes in squamous cell carcinoma cells.
Abstract MicroRNAs, whose transcription is regulated by members of the tumor protein p53 family, modulate the expression of numerous metabolic enzymes, significantly altering tumor cell response to chemotherapeutic treatments. The role for ΔNp63α-regulated microRNAs in regulation of cell cycle arrest, apoptosis and autophagy in squamous cell carcinoma (SCC) cells upon cisplatin exposure has been reported. The current study indicated that the selected microRNA targets differentially regulated by ΔNp63α in cisplatin-sensitive and cisplatin-resistant SCC cells could alter the expression of a few metabolic enzymes...
Source: Current Pharmaceutical Biotechnology - June 19, 2015 Category: Biotechnology Authors: Ratovitski EA Tags: Curr Pharm Biotechnol Source Type: research

Abstract A49: Carcinoma-associated fibroblasts in the tumor microenvironment affect growth, invasiveness, and drug response of human pancreatic cancer cells
Pancreatic cancer is one of the most aggressive malignancies, with a 5-year overall survival of less than 5%. Tumor drug resistance to conventional chemotherapy, such as gemcitabine, is often a significant contributor to poor overall survival. One of the common mechanisms of gemcitabine resistance is activation of cell signaling via increased phosphorylation of Mitogen-Activated kinase (MAP) kinases, leading to increased tumor survival and reduced sensitivity to chemotherapeutic agents. A growing body of evidence suggests that the CXCL12/CXCR4 signal transduction axis in the tumor microenvironment is an important mediator ...
Source: Cancer Research - June 30, 2015 Category: Cancer & Oncology Authors: Sanani, A. A., Patel, B., Duarte, A., Bansal, N., Bhagat, T., Rattigan, Y., Maitra, A., Verma, A., Banerjee, D. Tags: Inflammation/Stroma Source Type: research

G6PD downregulation triggered growth inhibition and induced apoptosis by regulating STAT3 signaling pathway in esophageal squamous cell carcinoma
Abstract There is growing evidence that glucose-6-phosphate dehydrogenase (G6PD) is tightly associated with development and progression of many human tumors. However, its precise molecular mechanisms in esophageal squamous cell carcinoma (ESCC) remain unknown. In the current study, we found that G6PD messenger RNA (mRNA) and protein levels in ESCC cell lines (Eca109, EC1, and EC9706 cells) were significantly higher than that in normal esophageal epithelial cell line Het-1A (P < 0.05) and specific small interfering RNA (siRNA) against G6PD significantly reduced the levels of G6PD mRNA and protein in EC1 cell...
Source: Tumor Biology - August 6, 2015 Category: Cancer & Oncology Source Type: research

Twist promotes reprogramming of glucose metabolism in breast cancer cells through PI3K/AKT and p53 signaling pathways.
In this study, we found that glucose consumption and lactate production were increased and mitochondrial mass was decreased in Twist-overexpressing MCF10A mammary epithelial cells compared with vector-expressing MCF10A cells. Moreover, these Twist-induced phenotypic changes were augmented by hypoxia. The expression of some glucose metabolism-related genes such as PKM2, LDHA, and G6PD was also found to be upregulated. Mechanistically, activated β1-integrin/FAK/PI3K/AKT/mTOR and suppressed P53 signaling were responsible for the observed EMR. Knockdown of Twist reversed the effects of Twist on EMR in Twist-overexpressing MCF...
Source: Oncotarget - September 8, 2015 Category: Cancer & Oncology Tags: Oncotarget Source Type: research

Viruses, Vol. 7, Pages 6689-6706: Glucose-6-Phosphate Dehydrogenase Enhances Antiviral Response through Downregulation of NADPH Sensor HSCARG and Upregulation of NF-κB Signaling
This study examined the mechanism underlying this phenomenon by measuring the expression of antiviral genes—tumor necrosis factor alpha (TNF-α) and GTPase myxovirus resistance 1 (MX1)—in G6PD-knockdown cells upon human coronavirus 229E (HCoV-229E) and enterovirus 71 (EV71) infection. Molecular analysis revealed that the promoter activities of TNF-α and MX1 were downregulated in G6PD-knockdown cells, and that the IκB degradation and DNA binding activity of NF-κB were decreased. The HSCARG protein, a nicotinamide adenine dinucleotide phosphate (NADPH) sensor and negative regulator of NF-κB, was upregulated in G6PD-k...
Source: Viruses - December 17, 2015 Category: Virology Authors: Yi-Hsuan WuDaniel ChiuHsin-Ru LinHsiang-Yu TangMei-Ling ChengHung-Yao Ho Tags: Article Source Type: research