2023年9月1日 · FDX1 KO resulted in the suppression of lipid metabolism and cell cycle–related genes and the induction of stress-related gene signatures that include hypoxia-induced genes (NOP53, PDK1, BACH1, BNIP3L, BNIP3, CDKN1B, and more), ER stress-related genes (USP25, PPP1R15A, HSPA1A, DNAJB9 and more), and integrated stress response (ISR) genes such ...

2024年1月22日 · To generate Fdx1-KO murine cells, two single-guide RNA (sgRNA) expression vectors pSpCas9(BB)–2A-Puro-sgFdx1-1 and pSpCas9(BB)–2A-Puro-sgFdx1-2 were used to remove initiation codon in exon 1 and create frame shift deletions.

通过免疫荧光也证明了，elesclomol处理显著诱导产生DLAT 小的聚集体（foci），而这种foci在FDX1 KO和脂酰化缺陷细胞中减少(图5F至H)。 Fig. 5. Copper directly binds and promotes the oligomerization of lipoylated DLAT

2022年12月22日 · We therefore tested if gentle overexpression of FDX2 could functionally complement lipoate deficiency in FDX1 KO cells. We analyzed growth and lipoate production of control and FDX1 KO cells that were simultaneously overexpressing GFP, FDX2, or a guide-resistant FDX1 complementary DNA (cDNA) (Fig. S5, A and B).

研究人员发现铜离子积累主要通过调控 fdx1 来介导铜死亡。 一方面，fdx1 将 cu2+ 还原成更具毒性的 cu+，可促使 tca 循环中硫辛酰化蛋白异常寡聚化，另一方面，fdx1 导致 fe-s 簇蛋白的不稳定。

通过敲除Fdx1基因exon 2，建立Fdx1基因敲除小鼠模型。 *使用本品系发表的文献需注明: Fdx1-KO mice (Cat. NO. NM-KO-232941) were purchased from Shanghai Model Organisms Center, Inc..

2024年12月1日 · Engineered lplA restored lipoylation in all tested lipoylation null cell models, mimicking defects in mitochondrial fatty acid synthesis (MECR KO), Fe–S cluster biosynthesis (BOLA3 KO), and specific lipoylation-regulating enzymes (FDX1 [ferredoxin 1], LIAS [lipoyl synthase], and LIPT1 [lipoyl (octanoyl) transferase 1] KOs).

CRISPR/Cas9 to induce FDX1 loss-of-function (we will term FDX1 KO) and controlled for off-target effects by over-expressing FDX1 in the FDX1 loss-of-function cells (KO+OE). These experiments were conducted in ABC1 (lung), HEK293 T (kidney), and K562 (myeloid) cell lines to ensure the representation of multiple cell lineages in our study. In all

FDX1 or lipoyl synthase KO cells, lipoylation in these same cells is not rescued, arguing against an alternative biosynthetic route or salvage pathway for lipoate in hypoxia. Our work re-veals the divergent roles of FDX1 and FDX2 in mitochondria, identifies a role for FDX1 in lipoate synthesis, and suggests that

We found that the intracellular levels of both cholesterol and TAGs were significantly upregulated in FDX1-KO HCT116 cells compared to isogenic control cells (Figure 4E and F), confirming aberrant lipid metabolism upon loss of FDX1.