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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
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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
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Human Monoclonal Glucose-6-Phosphate Dehydrogenase Primary Antibody for FACS, IHC - ABIN969161
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
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Human Monoclonal Glucose-6-Phosphate Dehydrogenase Primary Antibody for FACS, IHC - ABIN969162
Brajovich, Rucci, Acosta, Cotorruelo, García Borrás, Racca, Biondi, Racca: Effects of aging on antioxidant response and phagocytosis in senescent erythrocytes. in Immunological investigations 2009
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Human Polyclonal Glucose-6-Phosphate Dehydrogenase Primary Antibody for ELISA, WB - ABIN253103
Guindo, Fairhurst, Doumbo, Wellems, Diallo: X-linked G6PD deficiency protects hemizygous males but not heterozygous females against severe malaria. in PLoS medicine 2007
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
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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
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.
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.
Data indicate the tetramer as the most active form of glucose-6-phosphate dehydrogenase (G6PDH).
Data suggest that G6PD PT materials can be stored at 4 degrees C and used for up to one month and can be stored at -20 degrees C for one year and yield >90% enzyme activity. Exposure to warm temperatures, especially with elevated humidity, should be avoided. Desiccant should always be used to mitigate humidity effects
We found that 2 G6PD variant genotypes were associated with elevated sTfR (show TFRC Antibodies) concentrations, which limits the accuracy of sTfR (show TFRC Antibodies) as a biomarker of iron status in this population.
immature reticulocytes (CD71 (show TFRC Antibodies)+) targeted by P. vivax invasion are enzymatically normal, even in hemizygous G6PD-Mahidol G487A mutants; thus, allowing the normal growth, development, and high parasite density in severely deficient samples
review of the state of the art in G6PD deficiency, describing 217 mutations in the g6pd gene; also compiled information about 31 new mutations, 16 that were not recognized and 15 more that have recently been reported; found that class I mutations have the most deleterious effects on the structure and stability of the protein
We now provide an additional evidence form Palestinian G6PD-deficient subjects for a possible role of 3' UTR (show UTS2R Antibodies) c.*+357 A>G, c.1365-13T>C, and/or c.1311C>T polymorphism for G6PD deficiency, suggesting that not only a single variation in the exonic or exonic intronic boundaries, but also a haplotype of G6PD should considered as a cause for G6PD deficiency.
This work reviews and discusses rationales and challenges of G6PD screening program in Gaza Strip. We advocate adopting a national neonatal G6PD screening program in Gaza Strip to identify children at risk and promote wellness and health for Palestine.
From the study it appears that Ala44Gly and Gly163Ser are the most common G6PD mutations in Dhaka, Bangladesh. This is the first study of G6PD mutations in Bangladesh.
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.
We envisage these data and models finding utility when investigating the muscle-specific functions of the 11beta-HSD1/G6PT/H6PDH triad.
Data suggest that Gh (growth hormone (show GH1 Antibodies)) represses H6pd through locally produced Igf1 (insulin-like growth factor 1 (show IGF1 Antibodies)); Gh directly represses Hsd11b1 (11-beta-hydroxysteroid dehydrogenase 1 (show HSD11B1 Antibodies)) mRNA rather than acting via Igf1 (show IGF1 Antibodies) receptor.
These results suggest that increased H6PDH expression specifically in adipose tissue is sufficient to cause intra-adipose glucocorticoid production and adverse metabolic phenotypes.
Findings suggest that increased hepatic H6PDH and G6PT (show G6PC Antibodies) production contribute to 11beta-HSD1 (show HSD11B1 Antibodies) upregulation of local glucocorticoid action that may be related to the development of type 2 diabetes.
These data are consistent with an 11beta-HSD1-independent function for H6PDH in which sarcoplasmic reticulum G6P metabolism and NAD/NADH redox status are important for maintaining muscle homeostasis.
High-glucose-mediated decrease in G6PD activity may provide a mechanistic explanation for the gradual loss of beta cells in patients with diabetes.
Data suggest that glucose-6-phosphate dehydrogenase (G6PD) is the only NADPH (show FDXR Antibodies)-producing enzyme activated in response to oxidative stress.
Data suggest that aberrant increase of glucose-6-phosphate dehydrogenase in obese and/or diabetic subjects would alter lipid metabolism and adipocytokine expression, thereby resulting in failure of lipid homeostasis and insulin (show INS Antibodies) resistance in adipocytes
Required for 11 beta-hydroxysteroid dehydrogenase type 1 activity
Data postulate that increased glycogen (show GYS1 Antibodies) synthesis may reflect increased flux of glucose-6-phosphate (H6PDH substrate) through to glycogen (show GYS1 Antibodies) in the absence of hexose-6-phosphate dehydrogenase mediated metabolism.
There are 2 forms of glucose-6-phosphate dehydrogenase. G form is X-linked and H form, encoded by this gene, is autosomally linked. This H form shows activity with other hexose-6-phosphates, especially galactose-6-phosphate, whereas the G form is specific for glucose-6-phosphate. Both forms are present in most tissues, but H form is not found in red cells.
, 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
, G6PD, H form
, GDH/6PGL endoplasmic bifunctional protein
, glucose 1- dehydrogenase
, glucose dehydrogenase
, glucose dehyrogenase
, glucose-6-phosphate dehydrogenase, salivary
, glucose oxidase
, glucose 1-dehydrogenase
, glucose-6-phosphate dehydrogenase 1
, glucose-6-phosphate 1-dehydrogenase 2
, glucose-6-phosphate dehydrogenase X-linked, pseudogene 1