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Human Glucose-6-Phosphate Dehydrogenase Protein expressed in HEK-293 Cells - ABIN2721523
Ai, Dachineni, Kumar, Alfonso, Marimuthu, Bhat: Aspirin inhibits glucose‑6‑phosphate dehydrogenase activity in HCT 116 cells through acetylation: Identification of aspirin-acetylated sites. in Molecular medicine reports 2016
The prevalence of G6PD deficiency in the present study was similar to that observed in other study populations in Brazil. Molecular analysis identified in all patients the presence of the genetic polymorphism G202A/A376G, more common in the Brazilian population with G6PD deficiency, which is directly estimated by enzyme activity level.
We screened 611 unrelated Chinese Hakka subjects for G6PD polymorphism. Seven mutation sites were detected from subjects in our study. G6PD Canton (c.1376 G-->T)(33.06%), G6PD Kaiping (c.1388 G-->A)(30.67%), and polymorphism (c.1311 C-->T)(25.89%) account for 89.62% of mutations, followed by G6PD Gaohe (c.95 A-->G)(5.97%), G6PD Chinese-5 (c.1024 C-->T)(3.58%), G6PD Maewo (c.1360 C-->T)(0.39%), and G6PD Viangchan (c.871...
Study identified G6PD as a downstream target of miR1 in pituitary tumor cells and suggested that G6PD plays important roles for mediating the inhibitory effect of miR1 on the growth of pituitary tumor cells.
Study demonstrated that high G6PD expression is a poor prognostic factor in bladder cancer, and the levels of G6PD expression increase with increasing tumor stage. Patients with bladder cancer with high G6PD expression had worse survival rates compared with those with lower G6PD expression in resected tumors.
G6PD-dificient patients were found to have an increased risk for cancers, especially for brain tumor; higher tumor G6PD expression was associated with poor patient survival in low grade glioma (LGG), but not in Glioblastoma multiforme. A prognostication model using expression levels of G6PD and 9 related genes (PSMA2, PSMB8, SHFM1, GSS, GSTK1, MGST2, POLD3, MSH2, MSH6) could independently predict LGG patient survival.
G6PD contributes to HCC migration and invasion of hepatocellular carcinoma cells by inducing epithelial-mesenchymal transition through activation of signal transducer and activator of transcription 3
Study provided detailed genotypes of G6PD deficiency in Guangdong province with minorities populations and identified various point mutations in G6PD gene.
Results showed that not only G6PD expression but also G6PD activity was significantly lowered along with 3D MCF-7 cells culture time.
An aggregate analysis of mosaic G6PD expression in two distinct ethnic cohorts has been reported.
Proportion of mutational types in G6PD and the degree of enzyme activity change in various mutational types were found in the neonates of Fujian Province. Three most common mutation types were c.1376G > T, c.1388G > A, and c.95A >G.
Chemical inhibitors against SIRT2 suppress G6PD activity, leading to reduced cell proliferation of leukaemia cells, but not normal hematopoietic stem and progenitor cells. Importantly, SIRT2 is overexpressed in clinical acute myeloid leukaemia samples, while K403 acetylation is downregulated and G6PD catalytic activity is increased comparing to that of normal control.
Treatment of erythrocytes with Bay 11-7082, parthenolide or DMF led to concentration-dependent eryptosis resulting from complete depletion of GSH. GSH depletion was due to strong inhibition of G6PDH activity.
Studies indicate that the activities of glucose-6-phosphate dehydrogenase (the rate-limiting enzyme in the pentose shunt) and glucose flux through the shunt pathway is increased in various lung cells including, the stem cells, in pulmonary hypertension.
These findings revealed a novel glucose metabolism-related mechanism of PAK4 in promoting colon cancer cell growth, suggesting that PAK4 and/or G6PD blockage might be a potential therapeutic strategy for colon cancer.
Aggregated across all genotypes, we find that increasing levels of G6PD deficiency are associated with decreasing risk of cerebral malaria, but with increased risk of severe malarial anaemia.
ATM/G6PD-driven redox metabolism promotes FLT3 inhibitor resistance in acute myeloid leukemia that can be successfully reversed.
We concluded that the MeltPro G6PD assay is useful as a diagnostic or screening tool for G6PD deficiency in clinical settings
The glucose-6-phosphate dehydrogenase enzymatic deficiency was significantly higher in males compared to females in Burkina Faso. (Review)
This work expands the current understanding of the biochemical underpinnings of G6PD variant pathogenicity.
This study assessed quantitatively the hemolytic risk with tafenoquine in female healthy volunteers heterozygous for the Mahidol(487A) glucose-6-phosphate dehydrogenase (G6PD)-deficient variant versus G6PD-normal females.
higher (p<0.05) levels of G6PD were observed in SCNT deme and in vitro-derived groups in comparison to somatic cell nuclear transfer conv
Glc-6-PD activity was also elevated in hypoxic pulmonary arteries.
Hyperthermia-induced Hsp90.eNOS preserves mitochondrial respiration in hyperglycemic endothelial cells by down-regulating Glut-1 and up-regulating G6PD activity.
Glc-6-PD and NADPH redox are crucially involved in the mechanism of hypoxic pulmonary artery contraction and, in turn, may play a key role in increasing pulmonary arterial pressure
Levels of G6PD and HPRT RNA were higher in female morulae and blastocysts than in males, but only G6PD levels were significantly different between the sexes
Overexpression of G6PD in vascular endothelial cells decreases reactive oxygen species accumulation in response to exogenous and endogenous oxidant stress and improves levels of bioavailable NO.
In bovine retinal endothelial cells & pericytes, aldosterone reduced G6PD mRNA. A reduction in G6PD may be an early response to aldosterone.
Glucose 6-phosphate dehydrogenase is regulated through c-Src-mediated tyrosine phosphorylation in endothelial cells.
G6PD protects ischemic brain injury through increasing pentose phosphate pathway.
Hepatic transcriptional profiling response to fava bean-induced oxidative stress in glucose-6-phosphate dehydrogenase-deficient mice has been reported.
20-HETE elicited mitochondrial superoxide production and promoted secretory phenotype of vascular smooth muscle cells by activating MAPK1-Elk-1, all of which are blocked by inhibition of G6PD.
yeast hydrolysate supplementation suppressed body fat accumulation by attenuating fatty acid synthesis through the downregulation of hepatic G6PD and malic enzyme activities.
Serine arginine splicing factor 3 is involved in enhanced splicing of glucose-6-phosphate dehydrogenase RNA in response to nutrients and hormones in liver
F2 homozygous Gpdx mutant with C57L/J background exhibited the G6PD activity of 0.9+/-0.1 U/g Hb, level similar to those of G6PD deficiency in human.
Control of hepatic nuclear superoxide production by glucose 6-phosphate dehydrogenase and NADPH oxidase-4
as compared with control mice, G6PD-deficient mice had increased oxidative stress, as manifested by decreased NADPH levels and decreased GSH levels, and increased markers of lipid peroxidation.
not indispensable for early embryo development; severe deficiency in the extraembryonic tissues impairs development of the placenta and causes death of the embryo; is indispensable for survival when the embryo is exposed to oxygen through its blood supply
G6PD is required for limiting oxidative mutagenesis in the mouse spleen; Gpdx(a-m2Neu) is the first hypomorphic allele of a mouse housekeeping gene associated with elevated somatic mutagenesis in vivo
G6PD is an essential myocardial antioxidant enzyme, required for maintaining cellular glutathione levels and protecting against oxidative stress-induced cardiac dysfunction during ischemia-reperfusion.
G6pd deleted ES cells are very sensitive to oxidants, activating an apoptotic pathway at oxidant concentrations otherwise sublethal for wt ES cells.
G6PD proves indispensable for definitive erythropoiesis.
The study findings demonstrate a novel association between G6PD-status and inducibility of CYP2A5 and indicate that oxidative stress is not likely the key regulator of CYP2A5 expression.
This gene encodes glucose-6-phosphate dehydrogenase. This protein is a cytosolic enzyme encoded by a housekeeping X-linked gene whose main function is to produce NADPH, a key electron donor in the defense against oxidizing agents and in reductive biosynthetic reactions. G6PD is remarkable for its genetic diversity. Many variants of G6PD, mostly produced from missense mutations, have been described with wide ranging levels of enzyme activity and associated clinical symptoms. G6PD deficiency may cause neonatal jaundice, acute hemolysis, or severe chronic non-spherocytic hemolytic anemia. Two transcript variants encoding different isoforms have been found for this gene.
, glucose-6-phosphate dehydrogenase, G6PD
, Glucose-6-phosphate 1-dehydrogenase
, glucose-6-phosphate 1-dehydrogenase (G6PD)
, glucose-6-phosphate dehydrogenase
, glucose-6-P dehydrogenase
, glucose-6-phosphate dehydrogenase X-linked
, glucose-6-phosphate dehydrogenase 2
, glucose-6-phosphate 1-dehydrogenase X