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AhR activates the <t>PI3K/AKT</t> pathway <t>through</t> <t>RAB3D.</t> (A, B) RAB3D was knocked down in PC-3M cells, and the expression of AhR was analyzed by Real-time PCR (A) and Western blotting (B). One-way ANOVA, *** P < 0.001, shRAB3D vs. shNC. n = 3. (C) RAB3D was knocked down in AhR-overexpressing PC-3M cells, and the expression of AhR and RAB3D at the mRNA level was measured. One-way ANOVA, *** P < 0.001, AhR vs. Control, shRAB3D vs. shNC. n = 3. (D, E) Analyses of p-PI3K (D) and p-AKT (E) protein levels in PC-3M cells after AhR was overexpressed and RAB3D was knocked down. One-way ANOVA, ** P < 0.01, *** P < 0.001, AhR vs. Control, shRAB3D vs. shNC. n = 3. (F) Measurement of LD formation after AhR overexpression and RAB3D knockdown. Scale bar, 50 μm, 400×. One-way ANOVA, *** P < 0.001, AhR vs. Control; ** P < 0.01, shRAB3D vs. shNC. n = 3. (G) Caspase 3 content in PC-3M cells. One-way ANOVA, **P < 0.01, AhR vs. Control; *P < 0.05, shRAB3D vs. shNC. n = 3.
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Antibodies in this study.

Journal: Journal of Biochemical and Molecular Toxicology

Article Title: Eupatilin Alleviates Acute Myocardial Ischemia‐Reperfusion Injury in Rats via the Akt/GSK‐3β Pathway by Targeting COXs

doi: 10.1002/jbt.71111

Figure Lengend Snippet: Antibodies in this study.

Article Snippet: Phospho‐Akt1 (S473) , AP0140 , WB: 1:800 , Abclonal.

Techniques:

Effects of eupatilin on the COX‐mediated Akt/GSK pathway in OGD/R‐induced H9c2 cells. The levels of COX1 (A), COX2 (B), phosphorylated Akt1 (S473), and phosphorylated GSK‐3β (S9) proteins (C) were measured by Western blotting. (D) The interaction between eupatilin and COXs was predicted using molecular docking. n = 6, * p < 0.05, ** p < 0.01.

Journal: Journal of Biochemical and Molecular Toxicology

Article Title: Eupatilin Alleviates Acute Myocardial Ischemia‐Reperfusion Injury in Rats via the Akt/GSK‐3β Pathway by Targeting COXs

doi: 10.1002/jbt.71111

Figure Lengend Snippet: Effects of eupatilin on the COX‐mediated Akt/GSK pathway in OGD/R‐induced H9c2 cells. The levels of COX1 (A), COX2 (B), phosphorylated Akt1 (S473), and phosphorylated GSK‐3β (S9) proteins (C) were measured by Western blotting. (D) The interaction between eupatilin and COXs was predicted using molecular docking. n = 6, * p < 0.05, ** p < 0.01.

Article Snippet: Phospho‐Akt1 (S473) , AP0140 , WB: 1:800 , Abclonal.

Techniques: Western Blot, Docking Assay

Eupatilin treatment upregulated the Akt/GSK pathway via COXs in OGD/R‐induced H9c2 cells. Levels of COX1 (A), COX2 (B), p‐Akt1 (S473)/Akt1, and p‐GSK‐3β (S9)/GSK‐3β (C) proteins were measured by western blotting. n = 6, * p < 0.05, ** p < 0.01.

Journal: Journal of Biochemical and Molecular Toxicology

Article Title: Eupatilin Alleviates Acute Myocardial Ischemia‐Reperfusion Injury in Rats via the Akt/GSK‐3β Pathway by Targeting COXs

doi: 10.1002/jbt.71111

Figure Lengend Snippet: Eupatilin treatment upregulated the Akt/GSK pathway via COXs in OGD/R‐induced H9c2 cells. Levels of COX1 (A), COX2 (B), p‐Akt1 (S473)/Akt1, and p‐GSK‐3β (S9)/GSK‐3β (C) proteins were measured by western blotting. n = 6, * p < 0.05, ** p < 0.01.

Article Snippet: Phospho‐Akt1 (S473) , AP0140 , WB: 1:800 , Abclonal.

Techniques: Western Blot

Eupatilin inhibited the COXs and upregulated the Akt/GSK pathway in MIRI‐induced rats. The levels of COX1 (A), COX2 (B), p‐Akt1 (S473)/Akt1, and p‐GSK‐3β (S9)/GSK‐3β (C) proteins were measured by Western blotting. n = 6, * p < 0.05, ** p < 0.01.

Journal: Journal of Biochemical and Molecular Toxicology

Article Title: Eupatilin Alleviates Acute Myocardial Ischemia‐Reperfusion Injury in Rats via the Akt/GSK‐3β Pathway by Targeting COXs

doi: 10.1002/jbt.71111

Figure Lengend Snippet: Eupatilin inhibited the COXs and upregulated the Akt/GSK pathway in MIRI‐induced rats. The levels of COX1 (A), COX2 (B), p‐Akt1 (S473)/Akt1, and p‐GSK‐3β (S9)/GSK‐3β (C) proteins were measured by Western blotting. n = 6, * p < 0.05, ** p < 0.01.

Article Snippet: Phospho‐Akt1 (S473) , AP0140 , WB: 1:800 , Abclonal.

Techniques: Western Blot

AhR activates the PI3K/AKT pathway through RAB3D. (A, B) RAB3D was knocked down in PC-3M cells, and the expression of AhR was analyzed by Real-time PCR (A) and Western blotting (B). One-way ANOVA, *** P < 0.001, shRAB3D vs. shNC. n = 3. (C) RAB3D was knocked down in AhR-overexpressing PC-3M cells, and the expression of AhR and RAB3D at the mRNA level was measured. One-way ANOVA, *** P < 0.001, AhR vs. Control, shRAB3D vs. shNC. n = 3. (D, E) Analyses of p-PI3K (D) and p-AKT (E) protein levels in PC-3M cells after AhR was overexpressed and RAB3D was knocked down. One-way ANOVA, ** P < 0.01, *** P < 0.001, AhR vs. Control, shRAB3D vs. shNC. n = 3. (F) Measurement of LD formation after AhR overexpression and RAB3D knockdown. Scale bar, 50 μm, 400×. One-way ANOVA, *** P < 0.001, AhR vs. Control; ** P < 0.01, shRAB3D vs. shNC. n = 3. (G) Caspase 3 content in PC-3M cells. One-way ANOVA, **P < 0.01, AhR vs. Control; *P < 0.05, shRAB3D vs. shNC. n = 3.

Journal: American Journal of Cancer Research

Article Title: Aryl hydrocarbon receptor-dependent lipid droplet accumulation supports redox homeostasis in hypoxia-induced PCa cells

doi: 10.62347/HYGZ1071

Figure Lengend Snippet: AhR activates the PI3K/AKT pathway through RAB3D. (A, B) RAB3D was knocked down in PC-3M cells, and the expression of AhR was analyzed by Real-time PCR (A) and Western blotting (B). One-way ANOVA, *** P < 0.001, shRAB3D vs. shNC. n = 3. (C) RAB3D was knocked down in AhR-overexpressing PC-3M cells, and the expression of AhR and RAB3D at the mRNA level was measured. One-way ANOVA, *** P < 0.001, AhR vs. Control, shRAB3D vs. shNC. n = 3. (D, E) Analyses of p-PI3K (D) and p-AKT (E) protein levels in PC-3M cells after AhR was overexpressed and RAB3D was knocked down. One-way ANOVA, ** P < 0.01, *** P < 0.001, AhR vs. Control, shRAB3D vs. shNC. n = 3. (F) Measurement of LD formation after AhR overexpression and RAB3D knockdown. Scale bar, 50 μm, 400×. One-way ANOVA, *** P < 0.001, AhR vs. Control; ** P < 0.01, shRAB3D vs. shNC. n = 3. (G) Caspase 3 content in PC-3M cells. One-way ANOVA, **P < 0.01, AhR vs. Control; *P < 0.05, shRAB3D vs. shNC. n = 3.

Article Snippet: The primary antibodies were as follows: AhR (1:1000, Thermo Fisher Scientific Inc., Cat. No. MA1-513, Pittsburgh, PA, USA), DGAT2 (1:1000, ABclonal Biotechnology Co., Ltd., Cat. No. A13891, Wuhan, China), p-PI3K (1:500, ABclonal Biotechnology Co., Ltd., Cat. No. AP0427), PI3K (1:500, ABclonal Biotechnology Co., Ltd., Cat. No. A4992), p-AKT (1:500, ABclonal Biotechnology Co., Ltd., Cat. No. AP0637), AKT (1:500, ABclonal Biotechnology Co., Ltd., Cat. No. A22412), RAB3D (1:500, ABclonal Biotechnology Co., Ltd., Cat. No. A10390), CYLD (1:500, proteintech, Cat. No. 11110-1-AP), Histone H3 (1:80000, ABclonal Biotechnology Co., Ltd., Cat. No. AC070), and β-actin (1:20000, 1:500, ABclonal Biotechnology Co., Ltd., Cat. No. AC038).

Techniques: Expressing, Real-time Polymerase Chain Reaction, Western Blot, Control, Over Expression, Knockdown