tudca chemical chaperone targetmol t2532 Search Results


tudca  (TargetMol)
94
TargetMol tudca
Fig. 3. Cuproptosis provoked ER stress responses to induce ICD (A) GSEA analysis of the transcriptome sequencing data of HCT116 cells and SW620 cells after cuproptosis. (B) GSEA analysis of GOBP regulation of response to ER stress for HCT116 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in HCT116 genes. ER stress-related genes were labeled in figure. (D) GSEA analysis of GOBP regulation of response to ER stress for SW620 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in SW620 genes. ER stress-related genes were labeled in figure. (F–G) Western blotting analysis of CHOP, EIF2A, PERK and GADD34 expression in HCT116 cells (F) and MC38 cells (G) after different treatments. (H–I) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (H) and MC38 cells (I) after treatment with NAC, Elesclomol-Cu2+ and Disulfiram-Cu2+. (J–K) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (J) and MC38 cells (K) after treatment with 4-PBA, <t>TUDCA</t> and Elesclomol-Cu2+. Statistical significance: *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001 vs the control group.
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Fig. 3. Cuproptosis provoked ER stress responses to induce ICD (A) GSEA analysis of the transcriptome sequencing data of HCT116 cells and SW620 cells after cuproptosis. (B) GSEA analysis of GOBP regulation of response to ER stress for HCT116 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in HCT116 genes. ER stress-related genes were labeled in figure. (D) GSEA analysis of GOBP regulation of response to ER stress for SW620 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in SW620 genes. ER stress-related genes were labeled in figure. (F–G) Western blotting analysis of CHOP, EIF2A, PERK and GADD34 expression in HCT116 cells (F) and MC38 cells (G) after different treatments. (H–I) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (H) and MC38 cells (I) after treatment with NAC, Elesclomol-Cu2+ and Disulfiram-Cu2+. (J–K) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (J) and MC38 cells (K) after treatment with 4-PBA, <t>TUDCA</t> and Elesclomol-Cu2+. Statistical significance: *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001 vs the control group.
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Fig. 3. Cuproptosis provoked ER stress responses to induce ICD (A) GSEA analysis of the transcriptome sequencing data of HCT116 cells and SW620 cells after cuproptosis. (B) GSEA analysis of GOBP regulation of response to ER stress for HCT116 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in HCT116 genes. ER stress-related genes were labeled in figure. (D) GSEA analysis of GOBP regulation of response to ER stress for SW620 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in SW620 genes. ER stress-related genes were labeled in figure. (F–G) Western blotting analysis of CHOP, EIF2A, PERK and GADD34 expression in HCT116 cells (F) and MC38 cells (G) after different treatments. (H–I) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (H) and MC38 cells (I) after treatment with NAC, Elesclomol-Cu2+ and Disulfiram-Cu2+. (J–K) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (J) and MC38 cells (K) after treatment with 4-PBA, <t>TUDCA</t> and Elesclomol-Cu2+. Statistical significance: *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001 vs the control group.
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cycloheximide (chx  (GlpBio Technology Inc)
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Fig. 3. Cuproptosis provoked ER stress responses to induce ICD (A) GSEA analysis of the transcriptome sequencing data of HCT116 cells and SW620 cells after cuproptosis. (B) GSEA analysis of GOBP regulation of response to ER stress for HCT116 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in HCT116 genes. ER stress-related genes were labeled in figure. (D) GSEA analysis of GOBP regulation of response to ER stress for SW620 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in SW620 genes. ER stress-related genes were labeled in figure. (F–G) Western blotting analysis of CHOP, EIF2A, PERK and GADD34 expression in HCT116 cells (F) and MC38 cells (G) after different treatments. (H–I) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (H) and MC38 cells (I) after treatment with NAC, Elesclomol-Cu2+ and Disulfiram-Cu2+. (J–K) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (J) and MC38 cells (K) after treatment with 4-PBA, <t>TUDCA</t> and Elesclomol-Cu2+. Statistical significance: *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001 vs the control group.
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3 ig  (Proteintech)
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Fig. 3. Cuproptosis provoked ER stress responses to induce ICD (A) GSEA analysis of the transcriptome sequencing data of HCT116 cells and SW620 cells after cuproptosis. (B) GSEA analysis of GOBP regulation of response to ER stress for HCT116 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in HCT116 genes. ER stress-related genes were labeled in figure. (D) GSEA analysis of GOBP regulation of response to ER stress for SW620 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in SW620 genes. ER stress-related genes were labeled in figure. (F–G) Western blotting analysis of CHOP, EIF2A, PERK and GADD34 expression in HCT116 cells (F) and MC38 cells (G) after different treatments. (H–I) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (H) and MC38 cells (I) after treatment with NAC, Elesclomol-Cu2+ and Disulfiram-Cu2+. (J–K) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (J) and MC38 cells (K) after treatment with 4-PBA, <t>TUDCA</t> and Elesclomol-Cu2+. Statistical significance: *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001 vs the control group.
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1 ig  (Proteintech)
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Proteintech 1 ig
Fig. 3. Cuproptosis provoked ER stress responses to induce ICD (A) GSEA analysis of the transcriptome sequencing data of HCT116 cells and SW620 cells after cuproptosis. (B) GSEA analysis of GOBP regulation of response to ER stress for HCT116 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in HCT116 genes. ER stress-related genes were labeled in figure. (D) GSEA analysis of GOBP regulation of response to ER stress for SW620 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in SW620 genes. ER stress-related genes were labeled in figure. (F–G) Western blotting analysis of CHOP, EIF2A, PERK and GADD34 expression in HCT116 cells (F) and MC38 cells (G) after different treatments. (H–I) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (H) and MC38 cells (I) after treatment with NAC, Elesclomol-Cu2+ and Disulfiram-Cu2+. (J–K) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (J) and MC38 cells (K) after treatment with 4-PBA, <t>TUDCA</t> and Elesclomol-Cu2+. Statistical significance: *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001 vs the control group.
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12929s  (Cell Signaling Technology Inc)
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Cell Signaling Technology Inc 12929s
Fig. 3. Cuproptosis provoked ER stress responses to induce ICD (A) GSEA analysis of the transcriptome sequencing data of HCT116 cells and SW620 cells after cuproptosis. (B) GSEA analysis of GOBP regulation of response to ER stress for HCT116 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in HCT116 genes. ER stress-related genes were labeled in figure. (D) GSEA analysis of GOBP regulation of response to ER stress for SW620 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in SW620 genes. ER stress-related genes were labeled in figure. (F–G) Western blotting analysis of CHOP, EIF2A, PERK and GADD34 expression in HCT116 cells (F) and MC38 cells (G) after different treatments. (H–I) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (H) and MC38 cells (I) after treatment with NAC, Elesclomol-Cu2+ and Disulfiram-Cu2+. (J–K) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (J) and MC38 cells (K) after treatment with 4-PBA, <t>TUDCA</t> and Elesclomol-Cu2+. Statistical significance: *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001 vs the control group.
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5356s  (Cell Signaling Technology Inc)
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Cell Signaling Technology Inc 5356s
Fig. 3. Cuproptosis provoked ER stress responses to induce ICD (A) GSEA analysis of the transcriptome sequencing data of HCT116 cells and SW620 cells after cuproptosis. (B) GSEA analysis of GOBP regulation of response to ER stress for HCT116 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in HCT116 genes. ER stress-related genes were labeled in figure. (D) GSEA analysis of GOBP regulation of response to ER stress for SW620 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in SW620 genes. ER stress-related genes were labeled in figure. (F–G) Western blotting analysis of CHOP, EIF2A, PERK and GADD34 expression in HCT116 cells (F) and MC38 cells (G) after different treatments. (H–I) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (H) and MC38 cells (I) after treatment with NAC, Elesclomol-Cu2+ and Disulfiram-Cu2+. (J–K) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (J) and MC38 cells (K) after treatment with 4-PBA, <t>TUDCA</t> and Elesclomol-Cu2+. Statistical significance: *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001 vs the control group.
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sapk jnk cell signaling technology  (Cell Signaling Technology Inc)
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Cell Signaling Technology Inc sapk jnk cell signaling technology
Fig. 3. Cuproptosis provoked ER stress responses to induce ICD (A) GSEA analysis of the transcriptome sequencing data of HCT116 cells and SW620 cells after cuproptosis. (B) GSEA analysis of GOBP regulation of response to ER stress for HCT116 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in HCT116 genes. ER stress-related genes were labeled in figure. (D) GSEA analysis of GOBP regulation of response to ER stress for SW620 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in SW620 genes. ER stress-related genes were labeled in figure. (F–G) Western blotting analysis of CHOP, EIF2A, PERK and GADD34 expression in HCT116 cells (F) and MC38 cells (G) after different treatments. (H–I) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (H) and MC38 cells (I) after treatment with NAC, Elesclomol-Cu2+ and Disulfiram-Cu2+. (J–K) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (J) and MC38 cells (K) after treatment with 4-PBA, <t>TUDCA</t> and Elesclomol-Cu2+. Statistical significance: *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001 vs the control group.
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p sapk jnk thr183 tyr185 cell signaling technology  (Cell Signaling Technology Inc)
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Fig. 3. Cuproptosis provoked ER stress responses to induce ICD (A) GSEA analysis of the transcriptome sequencing data of HCT116 cells and SW620 cells after cuproptosis. (B) GSEA analysis of GOBP regulation of response to ER stress for HCT116 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in HCT116 genes. ER stress-related genes were labeled in figure. (D) GSEA analysis of GOBP regulation of response to ER stress for SW620 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in SW620 genes. ER stress-related genes were labeled in figure. (F–G) Western blotting analysis of CHOP, EIF2A, PERK and GADD34 expression in HCT116 cells (F) and MC38 cells (G) after different treatments. (H–I) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (H) and MC38 cells (I) after treatment with NAC, Elesclomol-Cu2+ and Disulfiram-Cu2+. (J–K) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (J) and MC38 cells (K) after treatment with 4-PBA, <t>TUDCA</t> and Elesclomol-Cu2+. Statistical significance: *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001 vs the control group.
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Fig. 3. Cuproptosis provoked ER stress responses to induce ICD (A) GSEA analysis of the transcriptome sequencing data of HCT116 cells and SW620 cells after cuproptosis. (B) GSEA analysis of GOBP regulation of response to ER stress for HCT116 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in HCT116 genes. ER stress-related genes were labeled in figure. (D) GSEA analysis of GOBP regulation of response to ER stress for SW620 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in SW620 genes. ER stress-related genes were labeled in figure. (F–G) Western blotting analysis of CHOP, EIF2A, PERK and GADD34 expression in HCT116 cells (F) and MC38 cells (G) after different treatments. (H–I) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (H) and MC38 cells (I) after treatment with NAC, Elesclomol-Cu2+ and Disulfiram-Cu2+. (J–K) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (J) and MC38 cells (K) after treatment with 4-PBA, TUDCA and Elesclomol-Cu2+. Statistical significance: *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001 vs the control group.

Journal: Biomaterials

Article Title: Immunogenic cuproptosis in cancer immunotherapy via an in situ cuproptosis-inducing system.

doi: 10.1016/j.biomaterials.2025.123201

Figure Lengend Snippet: Fig. 3. Cuproptosis provoked ER stress responses to induce ICD (A) GSEA analysis of the transcriptome sequencing data of HCT116 cells and SW620 cells after cuproptosis. (B) GSEA analysis of GOBP regulation of response to ER stress for HCT116 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in HCT116 genes. ER stress-related genes were labeled in figure. (D) GSEA analysis of GOBP regulation of response to ER stress for SW620 cells after cuproptosis. (C) DEG analysis showed the upregulated and down-regulated genes after cuproptosis in SW620 genes. ER stress-related genes were labeled in figure. (F–G) Western blotting analysis of CHOP, EIF2A, PERK and GADD34 expression in HCT116 cells (F) and MC38 cells (G) after different treatments. (H–I) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (H) and MC38 cells (I) after treatment with NAC, Elesclomol-Cu2+ and Disulfiram-Cu2+. (J–K) Western blotting analysis of CHOP, EIF2A, PERK, GADD34, HSP90, HSP70 and CRT expression in HCT116 cells (J) and MC38 cells (K) after treatment with 4-PBA, TUDCA and Elesclomol-Cu2+. Statistical significance: *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001 vs the control group.

Article Snippet: Elesclomol, Fer-1, Z-Vad-FMK, NEC-1, Imiquimod, and Mitomycin C were acquired from Selleck Chemicals (Shanghai, China), while Disulfiram, 4-PBA and TUDCA were obtained from TargetMol (Boston, USA).

Techniques: Sequencing, Labeling, Western Blot, Expressing, Control