In this study, we identify FDX1 as a mammalian CcO assembly factor. Our findings showing reduced oxygen consumption, decreased abundance of CcO, reduced levels of heme a/a 3, and COX15-based partial rescue of COX1 in FDX1 null cells support the role of FDX1 in CcO biogenesis via heme a/a 3 biosynthesis (Figs. 1, 2, and 5). Our results are in ...

首先得搞清楚 FDX1 在 铜死亡 过程中所起的作用，一方面，FDX1参与调节蛋白质 (包括 DLAT) 的 硫辛酰化。 另一方面，FDX1 将 Cu2+ 还原成更具毒性的 Cu+，导致 Fe-S 簇蛋白 合成的抑制，诱导细胞死亡。 铜死亡发生的条件是细胞内出现铜离子的过载，FDX1 会和过载的 Cu2+作用，导致铜死亡的发生，这个过程是消耗FDX1，所以发生铜死亡的细胞会导致FDX1量下降. 您好，麻烦问一下您，这个问题解决了吗，我也困扰好久了. 如题，FDX1是铜死亡的主要调控点，其存在促 …

在大鼠心肌细胞系中使用基于 CRISPR-Cas9 的功能丧失研究，我们证明了 FDX1 在线粒体呼吸和能量产生中的基本需求。我们将线粒体呼吸减少归因于细胞色素 c 氧化酶 （CcO） 丰度和组装的特异性降低，CcO 是一种线粒体血红素-铜氧化酶和线粒体呼吸链的末端酶。

2023年10月17日 · This finding links FDX1 function to heme a biosynthesis, and places it upstream of COX15 in CcO biogenesis like its ancestral yeast homolog. Taken together, our work has identified FDX1 as a critical CcO biogenesis factor in mammalian cells.

FDX1 Is Essential for ES-Mediated Rescue of Mitochondrial Respiration in Cu-Depleted Cells. Previous studies reported that ES treatment results in an increase in mitochondrial Cu content and that loss of FDX1 conferred resistance to ES-mediated killing (8, 11, 15). Taken together, these results suggest that FDX1 may

Up-regulation of FDX1 promoted elesclomol-induced cuproptosis against glioblastoma both in vitro and in vivo. FDX1 knockdown can reverse the inhibitory effect of elesclomol on tumor cells. Conclusions: Elesclomol inhibits glioblastoma development via inducing cuproptosis, regulated by NFκB1/FDX1 axis.

补充铜未能挽救 cco 生物发生，但血红素合酶 cox15 的过度表达部分挽救了 fdx1 敲除细胞中 cox1 的丰度。 这一发现将 FDX1 功能与血红素生物合成联系起来，并将其置于 CcO 生物合成中 COX15 的上游，就像其祖先酵母同源物一样。

Here, we demonstrate that copper is released from elesclomol within mitochondria via FDX1, and outside of mitochondria in an FDX1-independent manner to make copper available to mitochondrial and nonmitochondrial cuproenzymes, respectively.

AB017. NFκB1 regulates FDX1 to facilitate elesclomol-induced cuproptosis against glioblastoma - Wu- Chinese Clinical Oncology. Article Options. Download. The PDF file you selected should load here if your Web browser has a PDF reader plug-in installed (for example, a recent version of Adobe Acrobat Reader).

Ferredoxin 1 (FDX1): direct target of cuproptosis, encoding a small iron– sulfur protein that transfers electrons from NADPH through ferredoxin reductase to mitochondrial cytochrome P450, involved in steroid, vitamin D, and bile acid metabolism. Lipoylation synthase (LIAS): encoding iron–sulfur enzyme that belongs to the biotin and lipoic acid