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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...
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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.
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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.
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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.
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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
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Study provided detailed genotypes of G6PD deficiency in Guangdong province with minorities populations and identified various point mutations in G6PD gene.
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Results showed that not only G6PD expression but also G6PD activity was significantly lowered along with 3D MCF-7 cells culture time.
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An aggregate analysis of mosaic G6PD expression in two distinct ethnic cohorts has been reported.
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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.
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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.
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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.
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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.
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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.
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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.
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ATM/G6PD-driven redox metabolism promotes FLT3 inhibitor resistance in acute myeloid leukemia that can be successfully reversed.
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We concluded that the MeltPro G6PD assay is useful as a diagnostic or screening tool for G6PD deficiency in clinical settings
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The glucose-6-phosphate dehydrogenase enzymatic deficiency was significantly higher in males compared to females in Burkina Faso. (Review)
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This work expands the current understanding of the biochemical underpinnings of G6PD variant pathogenicity.
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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.
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only in the case of G6PD and TALDO, the ratio of BrdU incorporation to DNA was significantly changed. The presented results together with our previously published studies illustrate the complexity of the influence of genes coding for central carbon metabolism on the control of DNA replication in human fibroblasts, and indicate which of them are especially important in this process.
