Glucose-6-phosphate dehydrogenase, Microorganism

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].

Product Specifications

CAS Number

[9001-40-5]

Product Name Alternative

G6PD

UNSPSC

12352204

Hazard Statement

H302, H315, H319, H335

Target

Endogenous Metabolite

Type

Enzyme

Related Pathways

Metabolic Enzyme/Protease

Applications

Metabolism-sugar/lipid metabolism

Field of Research

Cancer; Metabolic Disease

Assay Protocol

https://www.medchemexpress.com/glucose-6-phosphate-dehydrogenase-microorganism.html

Solubility

H2O : ≥ 100 mg/mL

Smiles

[Glucose-6-phosphatedehydrogenase,Microorganism]

Precautions

H302, H315, H319, H335

References & Citations

[1]Stanton RC. Glucose-6-phosphate dehydrogenase, NADPH, and cell survival. IUBMB Life. 2012 May;64 (5) :362-9.|[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. |[3]Leopold JA, et al. Aldosterone impairs vascular reactivity by decreasing glucose-6-phosphate dehydrogenase activity. Nat Med. 2007 Feb;13 (2) :189-97.|[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.|[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.|[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.