人 PGLS 抗体对
01AB02090
6-phosphogluconolactonase (PGLS) is a cytosolic enzyme of the oxidative branch of the pentose phosphate pathway that catalyzes the hydrolysis of 6-phospho-D-glucono-1,5-lactone to 6-phospho-D-gluconate. This reaction is essential for the production of NADPH and ribose-5-phosphate, which support redox homeostasis and nucleotide biosynthesis, respectively. As a soluble monomeric protein, PGLS ensures efficient pentose phosphate flux; its deficiency leads to reduced glutathione levels and increased reactive oxygen species, impairing cell growth. Clinically, PGLS is linked to hemolytic anemia and is frequently upregulated in several malignancies, including glioblastoma, breast, and hepatocellular cancers. In these oncogenic contexts, PGLS promotes rapid cell proliferation and maintains redox balance, often correlating with poor prognosis and immune modulation within the tumor microenvironment.
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技术参数
- 靶点基因名
- PGLS
- 蛋白别名
- 6-phosphogluconolactonase; PGLS
- UniProt
- O95336
- 物种
- Human
产品详情
- 靶点名称
- PGLS
- 蛋白名称
- 6-phosphogluconolactonase
- 蛋白别名
- 6-phosphogluconolactonase; 6PGL
- 靶点基因名
- PGLS
- UniProt
- O95336
- 来源物种
- Homo sapiens (Human)
- 物种反应性
- Human
背景介绍
6-phosphogluconolactonase (PGLS) is a cytosolic enzyme of the oxidative branch of the pentose phosphate pathway that catalyzes the hydrolysis of 6-phospho-D-glucono-1,5-lactone to 6-phospho-D-gluconate. This reaction is essential for the production of NADPH and ribose-5-phosphate, which support redox homeostasis and nucleotide biosynthesis, respectively. As a soluble monomeric protein, PGLS ensures efficient pentose phosphate flux; its deficiency leads to reduced glutathione levels and increased reactive oxygen species, impairing cell growth. Clinically, PGLS is linked to hemolytic anemia and is frequently upregulated in several malignancies, including glioblastoma, breast, and hepatocellular cancers. In these oncogenic contexts, PGLS promotes rapid cell proliferation and maintains redox balance, often correlating with poor prognosis and immune modulation within the tumor microenvironment.