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Glucose-6-phosphate dehydrogenase

glucose-6-phosphate dehydrogenase, G6PD
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. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, ACID, HAD, catalase, AGE
Papers using glucose-6-phosphate dehydrogenase antibodies
Global and gene-specific promoter methylation changes are related to anti-B[a]PDE-DNA adduct levels and influence micronuclei levels in polycyclic aromatic hydrocarbon-exposed individuals.
Chiariotti Lorenzo, In PLoS ONE, 2008
An exogenous NADPH-regenerating system (1.3 mM NADP+, 3.3 mM glucose-6-phosphate, 0.4 U/ml glucose-6-phosphate dehydrogenase, and 3.3 mM magnesium chloride; BD Biosciences, Erembodegem, Belgium) required by ...
Preclinical evaluation of a potent novel DNA-dependent protein kinase inhibitor NU7441
Costanzo Vincenzo et al., In The EMBO Journal, 2005
... The antibodies used were anti-human G6PD goat polyclonal (Abcam), anti-Hsp27 mouse monoclonal (Santa ...
Regulation of telomerase by telomeric proteins
Wang Tzu-Chien V et al., In Journal of Biomedical Science, 2003
... The anti-G6PD antibody was from Genesis Biotech (Taiwan) ...
Cytochrome P450 phenotypic ratios for predicting herb-drug interactions in humans.
Keiser Jennifer, In PLoS ONE, 2001
... ) and Solution B (100×, 0.4 U/ml glucose-6-phosphate dehydrogenase) of the NADPH regenerating system were supplied by BD Biosciences (San Jose, CA, USA) ...
Cellular Prion Protein Promotes Brucella Infection into Macrophages
Katamine Shigeru et al., In The Journal of Experimental Medicine, 2001
... Anti–glucose-6-phosphate dehydrogenase (G6PDH) goat polyclonal antibody was obtained from Cortex Biochem.
Papers on glucose-6-phosphate dehydrogenase
1,25-Dihydroxyvitamin D induces the glutamate transporter SLC1A1 and alters glutamate handling in non-transformed mammary cells.
Welsh et al., Albany, United States. In Mol Cell Endocrinol, Feb 2016
In support of this concept, the expression of GCLC (which codes for the rate-limiting enzyme in GSH synthesis) and genes which generate reducing equivalents in the form of NADPH (ie, G6PD, PGD, IDH2) are elevated in 1,25D treated cells.
Safety of Live Liver Donation by Individuals With G6PD Deficiency: Initial Results and Comparative Study.
Rela et al., Chennai, India. In Transplantation, Feb 2016
BACKGROUND: G6PD deficiency (G6PDd) is the commonest genetic enzyme defect in the world.
NADP(+) binding effects tryptophan accessibility, folding and stability of recombinant B. malayi G6PD.
Saxena et al., Lucknow, India. In Int J Biol Macromol, Feb 2016
A homology model of BmG6PD constructed using human G6PD (PDB id: 2BH9) as a template indicated 34% α-helix, 19% β-sheet and 47% random coil conformations in the predicted model of the enzyme.
Preexisting conditions in pediatric ALL patients: Spectrum, frequency and clinical impact.
Kratz et al., Hannover, Germany. In Eur J Med Genet, Jan 2016
The following conditions were reported in more than one patient: Gilbert's disease (n=13), neurofibromatosis type I (n=8), ataxia telangiectasia (n=8), thalassemia (n=7), Nijmegen Breakage syndrome (n=6), cystic fibrosis (n=4), glucose-6-phosphate dehydrogenase deficiency (n=4), Noonan syndrome (n=2), Klinefelter syndrome (n=2), alpha-1-antitrypsin deficiency (n=2), primary ciliary dyskinesia (n=2).
Infants at risk of significant hyperbilirubinemia in poorly-resourced countries: evidence from a scoping review.
Slusher et al., Lagos, Nigeria. In World J Pediatr, Nov 2015
The factors most frequently associated with neonatal hyperbilirubinemia (in approximately 10% of all studies) were ABO and Rhesus incompatibilities, diabetes mellitus, glucose-6-phosphate dehydrogenase deficiency, prematurity/low birth weight, infection, birth trauma, and drug-induced labor.
Global burden of genetic disease and the role of genetic screening.
Puri et al., New Delhi, India. In Semin Fetal Neonatal Med, Oct 2015
In developing, as compared to western countries, hemoglobinopathies and glucose-6-phosphate dehydrogenase deficiency have a higher incidence due to severe falciparum malaria in the distant past, and autosomal recessive disorders have a higher frequency due to greater proportion of consanguineous marriages.
Parental education and the WHO neonatal G-6-PD screening program: a quarter century later.
Bhutani et al., Jerusalem, Israel. In J Perinatol, Oct 2015
Neonatal screening for glucose-6-phosphate dehydrogenase (G-6-PD) deficiency in any population with a male frequency >3-5%, combined with parental education regarding the dietary, environmental and sepsis-related triggers for hemolysis was recommended by the WHO (World Health Organization) Working Group in 1989.
[Alleviation of salt stress during maize seed germination by presoaking with exogenous sugar].
Ma et al., In Ying Yong Sheng Tai Xue Bao, Sep 2015
Exogenous Glc and Suc presoaking could increase the activities of superoxide dismutase (SOD), ascorbate peroxidase (APX), glutathione peroxidase (GPX), glutathione reductase (GR) and induce glucose-6-phosphate dehydrogenase (G6PDH) activity of maize shoot under salt stress.
Therapeutic potential of manipulating suicidal erythrocyte death.
Lang et al., Tübingen, Germany. In Expert Opin Ther Targets, 2014
AREAS COVERED: Stimulation of eryptosis contributes to anemia of several clinical conditions such as metabolic syndrome, diabetes, malignancy, hepatic failure, heart failure, uremia, hemolytic uremic syndrome, sepsis, fever, dehydration, mycoplasma infection, malaria, iron deficiency, sickle cell anemia, thalassemia, glucose-6-phosphate dehydrogenase deficiency and Wilson's disease.
Increase in Blood Glutathione and Erythrocyte Proteins Related to Glutathione Generation, Reduction and Utilization in African-American Old Women with Diabetes.
Guo et al., Wuhan, China. In J Sci Technol Environ, 2014
The erythrocyte levels of glutamate cysteine ligase catalytic subunit (GCLC), glucose-6-phosphate dehydrogenase (G6PD), glutathione reductase (GR), glutathione peroxidase-1 (GPx1), glutathione S-transferase-ρ1 (GST-ρ1) and glyoxalase I (Glo1) are comparable in nondiabetic young and old women, but significantly higher in diabetic patients than in age-matched nondiabetic controls.
Reappraisal of known malaria resistance loci in a large multicenter study.
Malaria Genomic Epidemiology Network et al., In Nat Genet, 2014
There was evidence of association at P < 1 × 10(-4) with the HBB, ABO, ATP2B4, G6PD and CD40LG loci, but previously reported associations at 22 other loci did not replicate in the multicenter analysis.
Tafenoquine plus chloroquine for the treatment and relapse prevention of Plasmodium vivax malaria (DETECTIVE): a multicentre, double-blind, randomised, phase 2b dose-selection study.
Kellam et al., Lima, Peru. In Lancet, 2014
Patients with glucose-6-phosphate dehydrogenase enzyme activity of less than 70% were excluded.
TAp73 enhances the pentose phosphate pathway and supports cell proliferation.
Yang et al., Hefei, China. In Nat Cell Biol, 2013
TAp73 activates the expression of glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting enzyme of the pentose phosphate pathway (PPP).
Glc-6-PD and PKG contribute to hypoxia-induced decrease in smooth muscle cell contractile phenotype proteins in pulmonary artery.
Gupte et al., Mobile, United States. In Am J Physiol Lung Cell Mol Physiol, 2012
Glc-6-PD activity was also elevated in hypoxic pulmonary arteries.
Glucose-6-phosphate dehydrogenase, NADPH, and cell survival.
Stanton, Boston, United States. In Iubmb Life, 2012
G6PD is under complex regulatory control and of central importance to many cellular processes. [Review]
Hemolysis and Mediterranean G6PD mutation (c.563 C>T) and c.1311 C>T polymorphism among Palestinians at Gaza Strip.
Prchal et al., Salt Lake City, United States. In Blood Cells Mol Dis, 2012
The Mediterranean mutation c.563T, while common among G6PD deficient Gaza Strip Palestinians and closely linked with the G6PD c.1311T polymorphism, does not account for most of the G6PD mutations in Gaza Strip population.
[Genetic factors in the occurrence of neonatal unconjugated hyperbilirubinemia].
Liu et al., Shenzhen, China. In Zhongguo Dang Dai Er Ke Za Zhi, 2012
UGT1A1 Gly71Arg and G6PD gene mutations may be involved in the development of neonatal unconjugated hyperbilirubinemia.
[Erythrocytic enzymopathy in Uzbekistan].
Ashrabhodzhaeva et al., In Lik Sprava, 2011
Deficiencies of erythrocytic G6PD in Uzbekistan are marked with diverse pathological phenotypes.
p53 regulates biosynthesis through direct inactivation of glucose-6-phosphate dehydrogenase.
Yang et al., Hefei, China. In Nat Cell Biol, 2011
The p53 protein binds to glucose-6-phosphate dehydrogenase (G6PD), the first and rate-limiting enzyme of the PPP, and prevents the formation of the active dimer.
Positively selected G6PD-Mahidol mutation reduces Plasmodium vivax density in Southeast Asians.
Sakuntabhai et al., Paris, France. In Science, 2010
effect of G6Pd-Mahidol(487A) variant in Southeast Asia on survival in vivax & falciparum malaria; results show positive selection has targeted Mahidol variant over past 1500 years; the variant reduces vivax but not falciparum parasite density
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