XBP1 Antibody - #AF5110

a Schematic representation of the unfolded protein response pathways. Expression of GRP78, ATF6, CHOP, phospho-IRE1α (p-IRE1α), XBP1, phospho-PERK (p-PERK), phospho-eIF2α (p-eIF2α) and ATF4 was determined by western blotting. Molm13 (b) or (c) MV4-11 cells were treated with HPA-12 (80 µM), Creno (6 µM) or their combination for 48 h. Protein expression levels of GRP78 (d), ATF6 (e) and CHOP (f) in (b, c). n = 3 independent experiments. Effects of the ERS inhibitor 4-PBA on the viability of Molm13 (g) and MV4-11 (h) cells. n = 3 independent experiments. Representative flow plots of annexin V/PI staining of Molm13 (i) and MV4-11 (j) cells in (g, h). k, l Statistical analysis of the number of apoptotic cells in (i, j). n = 3 independent experiments. The data are presented as the means ± SDs, and differences were compared by 2-tailed Student’s t tests. Multiple groups were analyzed with one-way ANOVA. ns: not significant, *P 

Figure.6. |Effects of BSSEE (0.5, 1 and 2 mL/kg) on the expression of hepatic (A) XBP1, (B) phospho-IKK alpha/beta (Thr 183+Tyr 185), (C) phospho-JNK1/2/3 (Ser180/181) and (D) phospho-IRS1 (Ser 307).

FIGURE 3 The effect of regulating the expression of ASIC1a on ERS in copper-treated HSC-T6 cells (A) Western blotting analysis and densitometric quantification of GRP78, and XBP1 protein levels in HSCs treated with PcTX-1; (B) mRNA levels of GRP78, and XBP1 in HSCs treated with PcTX-1 (C) Western blotting analysis and densitometric quantification of GRP78, XBP1 protein levels in HSCs transfected with ASIC1a-siRNA; (D) mRNA levels of GRP78, XBP1 in HSCs transfected with ASIC1a-siRNA. Statistical analyses were performed using t-test. Data are expressed as the mean ± SEM (n = 4). * p < 0.05, **p < 0.01 vs. Control group; # p < 0.05, ## p < 0.01 vs. CuSO4 group.

FIGURE 7 | PA treatment attenuated HFD-induced MTP reduction in rats. (A) Representative immunoreactive bands of XBP1, PDI, and MTP

FIGURE 5 ACLY inhibitor triggers ER stress and activates p‐eIF2α/ATF4/CHOP axis in vitro. Western blot analysis of (A) ER stress‐related proteins (p‐eIF2α, eIF2α, ATF4 and CHOP) and (B) UPR signal transduction molecules (p‐PERK, PERK, p‐IRE1α, IRE1α and sXBP1) in HepG2 cells after administration of BMS‐303141. ATF4p‐eIF2α, eIF2α were activated 3 h post‐treatment; CHOP was activated 8 h post‐treatment. (* P < .05, ** P < .01 and *** P < .001, compared with control group) (C) Western blot analysis of protein expression after ATF4 knockdown. (D) Annexin V‐FITC/PI double staining was performed to determine the apoptosis rate of HepG2 cells after ATF4 knockdown via flow cytometry. (* P < .05, ** P < .01 and *** P < .001, compared with con siRNA group). All experiments were repeated 3 times

Figure 5 Anti-OX40L inhibits TLR7-mediated differentiation of ASCs and antibody production through the regulation of the SPIB-BLIMP1-XBP1 axis. (A) Representative flow cytometry diagrams and statistical analysis of the percentages of naïve B cells, memory B cells, plasmablast cells, plasma cells, and ASCs (CD44hi CD138+) in the splenic B cells stimulated by R848 and IL-4. (B) The levels of IgG1, IgG2b, IgG3, IgA, and IgM from the splenic B-cell supernatant. (C) Regulation of key transcription factors related to B-cell proliferation and differentiation after anti-OX40L treatment. Horizontal bars represent the mean ± SEM. n = 4 in NC group: IgG isotype control; n = 4 in anti-OX40L-L group (1 µg/mL); n = 4 in anti-OX40L-M group (10 µg/mL); n = 4 in anti-OX40L-H group (100 µg/mL). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.