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glucose-6-phosphate dehydrogenase A-

a G202A/A376G mutant
Also Known As:
G6PD A-
Networked: 86 relevant articles (7 outcomes, 11 trials/studies)

Relationship Network

Bio-Agent Context: Research Results

Experts

1. Clark, Taane G: 4 articles (01/2021 - 08/2009)
2. Campino, Susana: 3 articles (01/2021 - 08/2009)
3. Drakeley, Chris: 3 articles (01/2021 - 05/2010)
4. Prchal, Josef T: 3 articles (01/2021 - 01/2016)
5. Reading, N Scott: 3 articles (01/2021 - 01/2016)
6. Ware, Russell E: 3 articles (07/2013 - 12/2008)
7. Bousema, Teun: 2 articles (01/2021 - 05/2010)
8. Dicko, Alassane: 2 articles (01/2021 - 11/2010)
9. Tiono, Alfred B: 2 articles (01/2021 - 11/2012)
10. Gladwin, Mark T: 2 articles (11/2020 - 01/2020)

Related Diseases

1. Malaria
2. Glucosephosphate Dehydrogenase Deficiency
3. Neoplasms (Cancer)
4. Thalassemia
01/01/2017 - ": Overall, 11% of children had a sickle cell variant, 19% of boys were G6PD A- hemizygotes, 12% and 10% of girls were G6PD A- hetero- or homozygotes, respectively, and 12% of children had α-thalassemia. "
07/01/2014 - "Here, we performed genotyping of five published single nucleotide polymorphisms, the α-thalassemia genotype, the G6PD A (-) variant deficiency, and the β(S) haplotype in a large series of SCA patients with well-defined stroke phenotypes. "
01/01/2014 - "The most prominent red blood cell polymorphism was heterozygous α(+)-thalassemia (37.8%), followed by the G6PD(A) deficiency (16.4%), heterozygous sickle cell trait (15.9%), G6PD(A-) deficiency (13.5%) and homozygous α(+)-thalassemia (5.2%). "
11/01/2017 - "The prevalences (heterozygotes plus homozygotes) of sickle hemoglobin (28% Tororo, 25% Jinja, 7% Kanungu), α-thalassemia (53% Tororo, 45% Jinja, 18% Kanungu) and G6PD A- (29% Tororo, 18% Jinja, 8% Kanungu) were significantly greater in Tororo and Jinja compared to Kanungu (p<0.0001 for all three alleles); prevalences were also significantly greater in Tororo compared to Jinja for α-thalassemia (p=0.03) and G6PD A- (p<0.0001). "
06/16/2011 - "To verify the accuracy of proposed genetic modifiers influencing stroke risk in SCA, we performed genotyping for 38 published single nucleotide polymorphisms (SNPs), as well as α-thalassemia, G6PD A(-) variant deficiency, and β-globin haplotype in 2 cohorts of children with well-defined stroke phenotypes (130 stroke, 103 nonstroke). "
5. Favism

Related Drugs and Biologics

1. Enzymes
2. Glucosephosphate Dehydrogenase (Glucose 6 Phosphate Dehydrogenase)
3. Biomarkers (Surrogate Marker)
4. Sickle Hemoglobin
5. B7-H1 Antigen
6. Immune Checkpoint Inhibitors
7. Nucleotides
8. Membrane Proteins (Integral Membrane Proteins)
9. Primaquine
10. DNA (Deoxyribonucleic Acid)

Related Therapies and Procedures

1. Therapeutics