eIF2 alpha Antibody - #AF6087

Figure 7. Effect of A22 on ameliorating apoptosis, ER stress, inflammation, metabolic syndrome, and fibrogenesis in HF diet-fed mice. (A) Effect of A22 on BCL-2 gene transcription. (B) Effect of A22 on BAX gene transcription. (C) Effect of A22 on expressions of apoptosis-related proteins in liver. The extracted proteins from the liver were immunoblotted with specific antibodies, and quantified based on the loading control of ACTIN. (D) Effect of A22 on ER stress. The UPR proteins (IRE-1, PERK, elF-2 and CHOP) were analyzed by using western Blot. (E) Effect of A22 on expressions of inflammatory factors. (F) Effect of A22 on expressions of fibrogenic proteins.

Fig. 5 SPI1 activates the UPRmt via PERK and inhibits chondrocyte senescence rather than by activating GCN2. a Protein expression of SPI1, PERK, p16INK4A, p21, GLB1, GCN2, eIF2α, p-eIF2α, ATF5, HSP60, LONP1 and ClpP was detected by WB in chondrocytes with SPI1 overexpression in model groups. The ratio of p-eIF2α to eIF2α is shown. b Gene expression changes of SPI1, PERK, CDKN2A, CDKN1A, GLB1, GCN2, eIF2α, ATF5, HSP60, LONP1 and ClpP was detected by RT-qPCR in chondrocytes with SPI1 overexpression in model groups. c Protein expression of SPI1, PERK, p16INK4A, p21, GLB1, GCN2, eIF2α, p-eIF2α and ATF5 were detected by WB in chondrocytes with SPI1 inhibition in model groups. The ratio of p-eIF2α to eIF2α is shown. d Gene expression changes of SPI1, PERK, CDKN2A, CDKN1A, GLB1, GCN2, eIF2α and ATF5 were detected by RT-qPCR in chondrocytes with SPI1 inhibition in model groups. The cell sample size is n = 4. Experiments were independently repeated three times. The data were expressed as mean ± SD. *P 

Fig. 5 BA triggers breast cancer cells apoptosis via ER stress-mediated pathway. a MCF-7 and MDA-MB-231 cells were treated with the indicated concentrations of BA for 24 h, and the protein levels of ER stress-associated signals were stimulated by BA in a dose-dependent manner, including GRP78, p-PERK/PERK, p-eIF2α/eIF2α, CHOP, and caspase-12. b MCF-7 and MDA-MB-231 cells were treated with BA alone or in combination with taxol for 24 h, the expression levels of GRP78, p-PERK/PERK, p-eIF2α/eIF2α, CHOP, and caspase-12 were also significantly upregulated following drug administration, especially in the co-treatment group, indicating the ER stress-mediated apoptosis pathway was aggravatedly activated by drug combination.

FIGURE 5 | PA treatment attenuated HFD-induced VLDLR expression in rats. (A) Representative immunoreactive bands of eIF2α, p-eIF2α, ATF4, and VLDLR

Figure 2. 5-MTP mitigated ERS-mediated apoptosis in mice exposed to renal I/R injury. (A) The DEGs between renal I/R injury and sham mice (GSE212678). The dotted line indicates the threshold for DEGs, with blue and red dots representing genes with low and high expression in renal I/R injury mice, respectively. (B) GO and KEGG enrichment analyses of DEGs. (C) Representative images of WB assays are shown. (D) The relative protein expression level of ATF6 was determined via normalization to that of GAPDH, and the Sham group was set as the baseline (value of 1). (E–G) The relative phosphorylation levels of PERK, IRE1α, and eIF2α were detected by measuring the ratio of phosphorylated to total proteins, and the Sham group was set as the baseline (value of 1). (H) The relative levels of expression of ERS-mediated apoptosis proteins (ATF4, CHOP, and DR5) in kidney tissues were evaluated and normalized to those of GAPDH, and the Sham group was set as the baseline (value of 1). (I) Relative fluorescence intensity of CHOP (red). (J) Quantification of the TUNEL staining results. (K) CHOP expression in renal tissues was visualized by conducting IF staining (×400, scale bar: 40 μm). (L) Representative TUNEL staining (green) of renal tissues (×400, scale bar: 40 μm). The data are presented as the mean ± SD and evaluated by conducting one-way ANOVA and the Bonferroni correction for multiple comparisons, n = 5 for each group; *P < 0.05, **P < 0.01, and ***P < 0.001.