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Merck & Co cpt camp
Cpt Camp, supplied by Merck & Co, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Emodin inhibits the survival of upper urinary tract urothelial carcinoma Cells by inhibiting PKA signaling. The cells were divided into four groups. Con group, cells were treated with 10 nM BZ alone for 48 h; Emodin group, cells were pretreated with 50 μ M emodin for 1 h, followed by the addition of 10 nM BZ for <t>48</t> <t>h;</t> <t>Sp-8-CPT-cAMPS</t> group, cells were pretreated with 10 μ M Sp-8-CPT-cAMPS for 1 h, followed by the addition of 10 nM BZ for 48 h; and Emodin + Sp-8-CPT-cAMPS group, cells were pretreated with a combination of 10 μ M Sp-8-CPT-cAMPS and 50 μ M emodin for 1 h, followed by the addition of 10 nM BZ for 48 h. Western blotting analysis showing the PKA and COX2 expression levels in (A) BFTC909 and (B) UM-UC-14 cells treated as aforementioned. The PGE2 levels in (C) BFTC909 and (D) UM-UC-14 cells treated as aforementioned. Cell Counting Kit-8 assays indicating the viability of (E) BFTC909 and (F) UM-UC-14 cells treated as aforementioned. * P<0.05, ** P<0.01, *** P<0.001 vs. Con; # P<0.05, ## P<0.01, ### P<0.001 vs. emodin. BZ, benzidine; Con, control; COX2, cyclooxygenase 2; PGE2, prostaglandin E2; PKA, protein kinase A.
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Journal: iScience

Article Title: Adenylate cyclase 10 promotes brown adipose tissue thermogenesis

doi: 10.1016/j.isci.2025.111833

Figure Lengend Snippet:

Article Snippet: Brown adipocytes were treated with 5 μΜ AG-221, 1 mM acetazolamide (Sigma), 10 μΜ KH7 (MedChemExpress), 50 μΜ LRE1 (MedChemExpress), 10 μΜ H89 (Selleckchem), 10 μΜ (R)-CE3F4 (MedChemExpress), 100 μΜ 8-CPT-2Me-cAMP (Tocris), 10 μΜ CPI-613 (Cayman), 1 μΜ CL316,243 (MedChemExpress), 1 μΜ isoproterenol (Sigma) or respective controls as indicated in the figure legends.

Techniques: Recombinant, Transfection, cAMP Assay, Activity Assay, Software

Emodin inhibits the survival of upper urinary tract urothelial carcinoma Cells by inhibiting PKA signaling. The cells were divided into four groups. Con group, cells were treated with 10 nM BZ alone for 48 h; Emodin group, cells were pretreated with 50 μ M emodin for 1 h, followed by the addition of 10 nM BZ for 48 h; Sp-8-CPT-cAMPS group, cells were pretreated with 10 μ M Sp-8-CPT-cAMPS for 1 h, followed by the addition of 10 nM BZ for 48 h; and Emodin + Sp-8-CPT-cAMPS group, cells were pretreated with a combination of 10 μ M Sp-8-CPT-cAMPS and 50 μ M emodin for 1 h, followed by the addition of 10 nM BZ for 48 h. Western blotting analysis showing the PKA and COX2 expression levels in (A) BFTC909 and (B) UM-UC-14 cells treated as aforementioned. The PGE2 levels in (C) BFTC909 and (D) UM-UC-14 cells treated as aforementioned. Cell Counting Kit-8 assays indicating the viability of (E) BFTC909 and (F) UM-UC-14 cells treated as aforementioned. * P<0.05, ** P<0.01, *** P<0.001 vs. Con; # P<0.05, ## P<0.01, ### P<0.001 vs. emodin. BZ, benzidine; Con, control; COX2, cyclooxygenase 2; PGE2, prostaglandin E2; PKA, protein kinase A.

Journal: International Journal of Oncology

Article Title: Emodin inhibits benzidine-enhanced survival and migration of upper urinary tract urothelial carcinoma cells by targeting the PKA/COX2 signaling pathway

doi: 10.3892/ijo.2024.5691

Figure Lengend Snippet: Emodin inhibits the survival of upper urinary tract urothelial carcinoma Cells by inhibiting PKA signaling. The cells were divided into four groups. Con group, cells were treated with 10 nM BZ alone for 48 h; Emodin group, cells were pretreated with 50 μ M emodin for 1 h, followed by the addition of 10 nM BZ for 48 h; Sp-8-CPT-cAMPS group, cells were pretreated with 10 μ M Sp-8-CPT-cAMPS for 1 h, followed by the addition of 10 nM BZ for 48 h; and Emodin + Sp-8-CPT-cAMPS group, cells were pretreated with a combination of 10 μ M Sp-8-CPT-cAMPS and 50 μ M emodin for 1 h, followed by the addition of 10 nM BZ for 48 h. Western blotting analysis showing the PKA and COX2 expression levels in (A) BFTC909 and (B) UM-UC-14 cells treated as aforementioned. The PGE2 levels in (C) BFTC909 and (D) UM-UC-14 cells treated as aforementioned. Cell Counting Kit-8 assays indicating the viability of (E) BFTC909 and (F) UM-UC-14 cells treated as aforementioned. * P<0.05, ** P<0.01, *** P<0.001 vs. Con; # P<0.05, ## P<0.01, ### P<0.001 vs. emodin. BZ, benzidine; Con, control; COX2, cyclooxygenase 2; PGE2, prostaglandin E2; PKA, protein kinase A.

Article Snippet: The cells were divided into four groups for treatment: i) Control (Con) group, cells were treated with 10 nM BZ alone for 48 h; ii) emodin group, cells were pretreated with 50 μ M emodin for 1 h, followed by the addition of 10 nM BZ for 48 h; iii) Sp-8-CPT-cAMPS group, cells were pretreated with 10 μ M Sp-8-CPT-cAMPS (cat. no. HY-120994B; MedChemExpress) for 1 h, followed by the addition of 10 nM BZ for 48 h; and iv) emodin + Sp-8-CPT-cAMPS group, cells were pretreated with a combination of 10 μ M Sp-8-CPT-cAMPS and 50 μ M emodin for 1 h, followed by the addition of 10 nM BZ for 48 h. Then, the cells were collected for further assay.

Techniques: Western Blot, Expressing, Cell Counting, Control

Effects of emodin and Sp-8-CPT-cAMPS on MMP9 and VEGF expression and cell migration in BFTC909 and UM-UC-14 cells. The cells were divided into four groups. Con group, cells were treated with 10 nM BZ alone for 48 h; Emodin group, cells were pretreated with 50 μ M emodin for 1 h, followed by the addition of 10 nM BZ for 48 h; Sp-8-CPT-cAMPS group, cells were pretreated with 10 μ M Sp-8-CPT-cAMPS for 1 h, followed by the addition of 10 nM BZ for 48 h; and Emodin + Sp-8-CPT-cAMPS group, cells were pretreated with a combination of 10 μ M Sp-8-CPT-cAMPS and 50 μ M emodin for 1 h, followed by the addition of 10 nM BZ for 48 h. MMP9 and VEGF levels in (A) BFTC909 and (B) UM-UC-14 cells treated as aforementioned. Transwell assay results of (C) BFTC909 and (D) UM-UC-14 cells treated as aforementioned. * P<0.05, ** P<0.01, *** P<0.001 vs. Con; # P<0.05, ## P<0.01, ### P<0.001 vs. emodin. BZ, benzidine; Con, control; MMP9, matrix metalloproteinase 9; VEGF, vascular endothelial growth factor.

Journal: International Journal of Oncology

Article Title: Emodin inhibits benzidine-enhanced survival and migration of upper urinary tract urothelial carcinoma cells by targeting the PKA/COX2 signaling pathway

doi: 10.3892/ijo.2024.5691

Figure Lengend Snippet: Effects of emodin and Sp-8-CPT-cAMPS on MMP9 and VEGF expression and cell migration in BFTC909 and UM-UC-14 cells. The cells were divided into four groups. Con group, cells were treated with 10 nM BZ alone for 48 h; Emodin group, cells were pretreated with 50 μ M emodin for 1 h, followed by the addition of 10 nM BZ for 48 h; Sp-8-CPT-cAMPS group, cells were pretreated with 10 μ M Sp-8-CPT-cAMPS for 1 h, followed by the addition of 10 nM BZ for 48 h; and Emodin + Sp-8-CPT-cAMPS group, cells were pretreated with a combination of 10 μ M Sp-8-CPT-cAMPS and 50 μ M emodin for 1 h, followed by the addition of 10 nM BZ for 48 h. MMP9 and VEGF levels in (A) BFTC909 and (B) UM-UC-14 cells treated as aforementioned. Transwell assay results of (C) BFTC909 and (D) UM-UC-14 cells treated as aforementioned. * P<0.05, ** P<0.01, *** P<0.001 vs. Con; # P<0.05, ## P<0.01, ### P<0.001 vs. emodin. BZ, benzidine; Con, control; MMP9, matrix metalloproteinase 9; VEGF, vascular endothelial growth factor.

Article Snippet: The cells were divided into four groups for treatment: i) Control (Con) group, cells were treated with 10 nM BZ alone for 48 h; ii) emodin group, cells were pretreated with 50 μ M emodin for 1 h, followed by the addition of 10 nM BZ for 48 h; iii) Sp-8-CPT-cAMPS group, cells were pretreated with 10 μ M Sp-8-CPT-cAMPS (cat. no. HY-120994B; MedChemExpress) for 1 h, followed by the addition of 10 nM BZ for 48 h; and iv) emodin + Sp-8-CPT-cAMPS group, cells were pretreated with a combination of 10 μ M Sp-8-CPT-cAMPS and 50 μ M emodin for 1 h, followed by the addition of 10 nM BZ for 48 h. Then, the cells were collected for further assay.

Techniques: Expressing, Migration, Transwell Assay, Control