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 活性可被高浓度 D-Glucose (HY-B0389) (5.6 和 25mM，72 小时) 抑制，导致 MIN6 细胞中 ROS 及细胞凋亡增加，细胞增殖及胰岛素分泌减少^[2]。
Glucose-6-phosphate dehydrogenase 活性可被 Aldosterone (HY-113313) (1-100 nM，24 小时) 抑制，导致血管反应性受损和内皮功能障碍^[3]。
在转染了 G6PD cDNA 的 NIH 3T3 细胞中，由 G6PD 过表达产生的 Glucose-6-phosphate dehydrogenase 会诱导肿瘤发生，且其致瘤特性与 Glucose-6-phosphate dehydrogenase 活性正相关^[5]。
Glucose-6-phosphate dehydrogenase 活性在较低的金属离子 (Cu²⁺, Al³⁺, Zn²⁺, and Cd²⁺) 浓度下增强 (0.025-0.1 μM，2 小时)，而在较高的金属浓度下 (0.2 和 0.4 μM，2 小时) 减弱^[6]。
NADPH (0.01-0.05 mM) 以非竞争性方式抑制 Glucose-6-phosphate dehydrogenase，K_i 值为 0.144 mM^[6]。

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

与野生型小鼠相比，G6PD 基因缺陷小鼠模型中葡萄糖水平显著升高，胰岛素分泌量显著降低^[2]。
与 Glucose-6-phosphate dehydrogenase 正常表达的心肌病小鼠模型相比，Glucose-6-phosphate dehydrogenase 缺乏可预防心肌病小鼠模型中的心脏肥大和心肌细胞中的蛋白质聚集 (通过将 hR120GCryAB 转基因心肌病模型与 G6PD 基因缺陷模型杂交，获得Glucose-6-phosphate dehydrogenase 活性降低的 hR120GCryAB 转基因心肌病小鼠模型)^[4]。

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

9001-40-5

固体

White to off-white

6-磷酸葡萄糖脱氢酶, 微生物

Room temperature in continental US; may vary elsewhere.

Please store the product under the recommended conditions in the Certificate of Analysis.

• [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]