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anti-Human Glucose-6-Phosphate Dehydrogenase Antibodies:
anti-Rat (Rattus) Glucose-6-Phosphate Dehydrogenase Antibodies:
anti-Mouse (Murine) Glucose-6-Phosphate Dehydrogenase Antibodies:
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Human Polyclonal Glucose-6-Phosphate Dehydrogenase Primary Antibody for IHC (fro), IHC (p) - ABIN151702
Orr, Li, Wang, Li, Wang, Rong, Xu, Mastroberardino, Greenamyre, Li: N-terminal mutant huntingtin associates with mitochondria and impairs mitochondrial trafficking. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2008
Show all 17 Pubmed References
Human Polyclonal Glucose-6-Phosphate Dehydrogenase Primary Antibody for ICC, IF - ABIN4314533
Kato, Nicholson, Neiman, Rantalainen, Holmes, Barrett, Uhlén, Nilsson, Spector, Schwenk: Variance decomposition of protein profiles from antibody arrays using a longitudinal twin model. in Proteome science 2011
Show all 3 Pubmed References
Human Monoclonal Glucose-6-Phosphate Dehydrogenase Primary Antibody for FACS, IHC - ABIN969162
Louicharoen, Patin, Paul, Nuchprayoon, Witoonpanich, Peerapittayamongkol, Casademont, Sura, Laird, Singhasivanon, Quintana-Murci, Sakuntabhai: Positively selected G6PD-Mahidol mutation reduces Plasmodium vivax density in Southeast Asians. in Science (New York, N.Y.) 2009
Show all 2 Pubmed References
Human Monoclonal Glucose-6-Phosphate Dehydrogenase Primary Antibody for FACS, IHC - ABIN969161
Brajovich, Rucci, Acosta, Cotorruelo, García Borrás, Racca, Biondi, Racca: Effects of aging on antioxidant response and phagocytosis in senescent erythrocytes. in Immunological investigations 2009
Show all 2 Pubmed References
Human Polyclonal Glucose-6-Phosphate Dehydrogenase Primary Antibody for ICC, IF - ABIN4314534
Dammeyer, Arnér: Human Protein Atlas of redox systems - what can be learnt? in Biochimica et biophysica acta 2010
Show all 2 Pubmed References
Human Polyclonal Glucose-6-Phosphate Dehydrogenase Primary Antibody for IHC (p), WB - ABIN651229
Guo, Li, Myatt, Nathanielsz, Sun: Sexually dimorphic effects of maternal nutrient reduction on expression of genes regulating cortisol metabolism in fetal baboon adipose and liver tissues. in Diabetes 2013
Human Polyclonal Glucose-6-Phosphate Dehydrogenase Primary Antibody for ELISA, IHC - ABIN4314528
Guindo, Fairhurst, Doumbo, Wellems, Diallo: X-linked G6PD deficiency protects hemizygous males but not heterozygous females against severe malaria. in PLoS medicine 2007
Human Polyclonal Glucose-6-Phosphate Dehydrogenase Primary Antibody for WB - ABIN3042413
Hu, Zhang, Tang, Su, Li, Chen, Zhang, Cai, Zhu: Variant G6PD levels promote tumor cell proliferation or apoptosis via the STAT3/5 pathway in the human melanoma xenograft mouse model. in BMC cancer 2014
G6PD contributes to HCC (show FAM126A Antibodies) migration and invasion of hepatocellular carcinoma cells by inducing epithelial-mesenchymal transition through activation of signal transducer and activator of transcription 3 (show STAT3 Antibodies)
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 (show SIRT2 Antibodies) suppress G6PD activity, leading to reduced cell proliferation of leukaemia cells, but not normal hematopoietic stem and progenitor cells. Importantly, SIRT2 (show SIRT2 Antibodies) 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 (show PAK4 Antibodies) in promoting colon cancer cell growth, suggesting that PAK4 (show PAK4 Antibodies) 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.
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
Hyperthermia-induced Hsp90 (show HSP90 Antibodies).eNOS (show NOS3 Antibodies) preserves mitochondrial respiration in hyperglycemic endothelial cells by down-regulating Glut-1 (show SLC2A1 Antibodies) 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 (show HPRT1 Antibodies) 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.
ATM (show ATM Antibodies)/G6PD-driven redox metabolism promotes FLT3 (show FLT3 Antibodies) inhibitor resistance in acute myeloid leukemia (show BCL11A Antibodies) that can be successfully reversed.
20-HETE elicited mitochondrial superoxide production and promoted secretory phenotype of vascular smooth muscle cells by activating MAPK1 (show MAPK1 Antibodies)-Elk-1 (show ELK1 Antibodies), 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 (show SLU7 Antibodies) 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 (show NOX4 Antibodies)
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.
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
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