Glucose-6-phosphate dehydrogenase, Microorganism  (Synonyms: G6PD)

Glucose-6-phosphate dehydrogenase, Microorganism (G6PD) is the rate-limiting enzyme of the pentose phosphate pathway. Glucose-6-phosphate dehydrogenase, Microorganism is a primary source of NADPH in antioxidant pathways, nitric oxide synthase, NADPH oxidase, cytochrome p450 systems, and others. Glucose-6-phosphate dehydrogenase, Microorganism is applicable in research related to diabetes, endothelial dysfunction, cancer, and cardiomyopathy^{[1][2][3][4][5]}.

Glucose-6-phosphate dehydrogenase activity can be inhibited by high concentrations of D-Glucose (HY-B0389) (5.6 and 25 mM, 72 hours), leading to increased ROS and apoptosis in MIN6 cells, and decreased cell proliferation and insulin secretion^[2].
Glucose-6-phosphate dehydrogenase activity can be inhibited by Aldosterone (HY-113313) (1-100 nM, 24 hours), resulting in impaired vascular reactivity and endothelial dysfunction^[3].
In NIH 3T3 cells transfected with G6PD cDNA, Glucose-6-phosphate dehydrogenase produced by G6PD overexpression induces tumorigenesis, with its oncogenic properties positively correlated with Glucose-6-phosphate dehydrogenase activity^[5].
Glucose-6-phosphate dehydrogenase activity is enhanced at lower metal ion concentrations (Cu²⁺, Al³⁺, Zn²⁺, and Cd²⁺) (0.025-0.1 μM, 2 hours), but weakened at higher metal concentrations (0.2 and 0.4 μM, 2 hours)^[6].
NADPH (0.01-0.05 mM) inhibits Glucose-6-phosphate dehydrogenase in a non-competitive manner, with a K_i value of 0.144 mM^[6]。

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Compared to wild-type mice, glucose levels are significantly increased and insulin secretion is significantly reduced in the G6PD gene-deficient mouse model^[2].
Compared to the cardiomyopathy mouse model with normal expression of Glucose-6-phosphate dehydrogenase, the absence of Glucose-6-phosphate dehydrogenase can prevent cardiac hypertrophy and protein aggregation in cardiomyocytes in the cardiomyopathy mouse model (by crossing the hR120GCryAB transgenic cardiomyopathy model with the G6PD gene-deficient model, resulting in a hR120GCryAB transgenic cardiomyopathy mouse model with reduced Glucose-6-phosphate dehydrogenase activity)^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

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[Glucose-6-phosphate dehydrogenase, Microorganism]

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• [1]. Stanton RC. Glucose-6-phosphate dehydrogenase, NADPH, and cell survival. IUBMB Life. 2012 May;64(5):362-9.  [Content Brief]

  [2]. Zhang Z, et al. High glucose inhibits glucose-6-phosphate dehydrogenase, leading to increased oxidative stress and beta-cell apoptosis. FASEB J. 2010 May;24(5):1497-505.  [Content Brief]

  [3]. Leopold JA, et al. Aldosterone impairs vascular reactivity by decreasing glucose-6-phosphate dehydrogenase activity. Nat Med. 2007 Feb;13(2):189-97.  [Content Brief]

  [4]. Rajasekaran NS, et al. Human alpha B-crystallin mutation causes oxido-reductive stress and protein aggregation cardiomyopathy in mice. Cell. 2007 Aug 10;130(3):427-39.  [Content Brief]

  [5]. Kuo W, et al. Human glucose-6-phosphate dehydrogenase (G6PD) gene transforms NIH 3T3 cells and induces tumors in nude mice. Int J Cancer. 2000 Mar 15;85(6):857-64.  [Content Brief]

  [6]. Sun L, et al. Kinetic properties of glucose 6-phosphate dehydrogenase and inhibition effects of several metal ions on enzymatic activity in vitro and cells. Sci Rep. 2024 Mar 9;14(1):5806.  [Content Brief]