FDX1 as a key regulator in cuproptosis pathway could promote cuproptosis in endometriosis cells. Interestingly, FDX1 interacts with G6PD, and reduces its protein stability, which predominantly affects the cellular redox-regulating systems. Then, the reduced G6PD activity enhances cuproptosis via down-regulating NADPH and GSH levels.

2023年4月29日 · FDX1 as a key regulator in cuproptosis pathway could promote cuproptosis in endometriosis cells. Interestingly, FDX1 interacts with G6PD, and reduces its protein stability, which predominantly affects the cellular redox-regulating systems. Then, the reduced G6PD activity enhances cuproptosis via down-regulating NADPH and GSH levels.

fdx1作为铜凋亡途径的关键调节因子可以促进子宫内膜异位细胞的铜凋亡。 有趣的是，FDX1 与 G6PD 相互作用，并降低其蛋白质稳定性，这主要影响细胞氧化还原调节系统。

2025年2月8日 · Enables glucose-6-phosphate dehydrogenase activity and identical protein binding activity. Involved in pentose-phosphate shunt, oxidative branch. Acts upstream of or within several processes, including NADP biosynthetic process; erythrocyte development; and maintenance of blood vessel diameter homeostasis by renin-angiotensin. Is active in cytosol.

2024年4月30日 · FDX1 interaction with G6PD reduces its stability, disrupting the cellular redox regulation. This diminishes G6PD activity, lowering NADPH and GSH levels, ultimately promoting cuproptosis and inhibiting endometriotic cell proliferation and metastasis [14].

Data were represented as mean ± SEM. from publication: FDX1 enhances endometriosis cell cuproptosis via G6PD-mediated redox homeostasis | Cuproptosis is a new form of programmed cell death,...

2023年4月29日 · FDX1 as a key regulator in cuproptosis pathway could promote cuproptosis in endometriosis cells. Interestingly, FDX1 interacts with G6PD, and reduces its protein stability, which...

但铜异位症在子宫内膜异位症进展中的作用尚不清楚。在这里，我们发现在小鼠模型中，铜异位症抑制子宫内膜异位症细胞的生长和异位子宫内膜组织的生长。fdx1作为铜倾通路的关键调控因子，可促进子宫内膜异位症细胞铜倾。有趣的是，fdx1与g6pd

2025年1月15日 · Using CRISPR-Cas9 for a genome-wide loss-of-function screen, researchers identified several genes involved in copper ion carrier-induced cell death, including ferredoxin 1 (FDX1), lipolytransferase 1 (LIPT1), lipoyl synthase (LIAS), dihydrolipoamide dehydrogenase (DLD), dihydrolipoamide S-acetyltransferase (DLAT), pyruvate dehydrogenase E1 ...

FDX1 as a key regulator in cuproptosis pathway could promote cuproptosis in endometriosis cells. Interestingly, FDX1 interacts with G6PD, and reduces its protein stability, which predominantly afects the cellular redox-regulating systems. Then, the reduced G6PD activity enhances cuproptosis via down-regulating NADPH and GSH levels.