AIFM2 Antibody - #DF8636

Fig. 9 OA drives the transcriptional regulator Nrf2 to upregulate GPX4 and FSP1. A: An illustrative diagram of the proposed model delineating the mechanisms of FSP1-mediated regulation of ferroptosis in EBI following SAH. B: Western blot data illustrate the levels of NQO1, FSP1, and HO-1 in the brain cortex after SAH. C: Quantification of CoQ10 among the three groups. OA increased the expression of CoQ10 (n = 3). D: Quantification of HO-1 among the three groups. OA increased the expression of HO-1 (n = 3). E: Quantification of FSP1 among the three groups. OA increased the expression of FSP1 (n = 3). F: Representative views of immunofluorescence staining of FSP1. Scale bar = 50 μm. G: Quantitative analysis of the of FSP1 (n = 3). H: Western blot data show that OA fosters the protein levels of FSP1, and Nrf2 knockout does not prevent the OA-induced escalation in GPX4 levels after SAH (n = 3)

Fig. 9 OA drives the transcriptional regulator Nrf2 to upregulate GPX4 and FSP1. A: An illustrative diagram of the proposed model delineating the mechanisms of FSP1-mediated regulation of ferroptosis in EBI following SAH. B: Western blot data illustrate the levels of NQO1, FSP1, and HO-1 in the brain cortex after SAH. C: Quantification of CoQ10 among the three groups. OA increased the expression of CoQ10 (n = 3). D: Quantification of HO-1 among the three groups. OA increased the expression of HO-1 (n = 3). E: Quantification of FSP1 among the three groups. OA increased the expression of FSP1 (n = 3). F: Representative views of immunofluorescence staining of FSP1. Scale bar = 50 μm. G: Quantitative analysis of the of FSP1 (n = 3). H: Western blot data show that OA fosters the protein levels of FSP1, and Nrf2 knockout does not prevent the OA-induced escalation in GPX4 levels after SAH (n = 3)

Fig. 4: P. merdae and FMN treatment inhibit MPTP-induced ferroptosis. A, B PTGS2 mRNA levels in the STR of P. merdae- and FMN-treated mice following MPTP administration. C, D Representative western blots and quantification of PTGS2, GPX4, ACSL4 and FSP1 protein levels in the STR. E, F Intracellular Fe2+ levels in the indicated groups of mice (n = 6). G, H Malondialdehyde (MDA) levels were measured in P. merdae- and FMN-treated mice (n = 6). I, J Glutathione (GSH) levels were determined (n = 6). K–N Cells were pretreated with 10 μM FMN and 10 mM Fer-1 for 2 h before MPP+ (1 mM) exposure. K Cell viability was evaluated. L MDA levels were measured. M GSH levels were determined. N Representative western blots and quantification of PTGS2, GPX4, ACSL4 and FSP1 protein levels in cells. Data are presented as mean ± SD (n = 3–6). Statistical significance was determined using one-way ANOVA followed by Tukey’s test (*p 

Figure 5 Knockdown of circ0060467 promotes ferroptosis in HCC. (A) Western blotting was performed to determine the expression levels of AIFM2, GPX4 and β-Actin. (B) Expression status of AIFM2 and GPX4 in hematoxylin-eosin-stained sections of harvested xenograft tumors. (C) Glutathione (GSH)/oxidized GSH (GSSG) ratio was determined with a GSH/GSSG Quantification Kit.

Fig. 5 LINC02587 silencing inhibits the CoQ-FSP1 pathway. (A) KEGG pathway enrichment in the si-NC and si-LINC02587-ii groups. (B) Volcano map of differentially expressed Ferroptosis-related genes.(C) Hierarchical clustering heatmap of differentially expressed Ferroptosis-related genes.(D) qRT-PCR was carried out to analyse the relative expression of Ferroptosis-related genes in the si-NC and si-LINC02587-ii groups. (E) Western blot analysis of CoQ10B, FSP1 in U87 and LN229 cells transfected with si-NC or si-LINC02587. (F) Changes in GSH levels in cells after iFSP1 and si-LINC02587-ii intervention.Data are expressed as the mean ± SD.*P