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Condition: G6PD

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Total 24 results found since Jan 2013.

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

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

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

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

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

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

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

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

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