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Most individuals with G6PD deficiency are asymptomatic.When it induces hemolysis, the effect is usually short-lived. [5]Most people who develop symptoms are male, due to the X-linked pattern of inheritance, but female carriers can be affected due to unfavorable lyonization or skewed X-inactivation, where random inactivation of an X-chromosome in certain cells creates a population of G6PD ...
The selection and use of essential medicines: report of the WHO Expert Committee, 2017 (including the 20th WHO Model List of Essential Medicines and the 6th Model List of Essential Medicines for Children). Geneva: World Health Organization. hdl: 10665/259481. ISBN 978-92-4-121015-7. ISSN 0512-3054. WHO technical report series; no. 1006.
G6PD inhibitors are under investigation to treat cancers and other conditions. [18] In vitro cell proliferation assay indicates that G6PD inhibitors, DHEA (dehydroepiandrosterone) and ANAD (6-aminonicotinamide), effectively decrease the growth of AML cell lines.
It forms ribulose 5-phosphate from 6-phosphogluconate: 6-phospho-D-gluconate + NAD(P) + D-Ribulose 5-phosphate + CO2 + NAD(P)H + H + It is an oxidative carboxylase that catalyses the oxidative decarboxylation of 6-phosphogluconate into ribulose 5-phosphate in the presence of NADP.
The reaction is the second NADPH releasing reaction in the pentose phosphate pathway, the first being catalyzed by glucose-6-phosphate dehydrogenase. 3-keto-6-phosphogluconate then rapidly (in an irreversible reaction) decarboxylates to CO 2 and ribulose-5-phosphate, which is the precursor to many vital metabolic processes.
XDH and AOX dual deficiency Xanthine dehydrogenase and aldehyde oxidase combined deficiency XDH deficiency Xanthine dehydrogenase deficiency XDP X-linked dystonia-parkinsonism XDR TB Extensively drug-resistant tuberculosis: XHED X-linked hypohidrotic ectodermal dysplasia: XLMTM X-linked myotubular myopathy: XLOS X-linked Opitz G/BBB syndrome
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