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Merck & Co cuso 4
Cuso 4, 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
https://www.bioz.com/product/cuso+4/cuso4/pmc12929513-69-21-5
Average 86 stars, based on 1 article reviews
cuso 4 - by Bioz Stars, 2026-09
86/100 stars

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Article Title: Fabrication of Cu@Ag core-shell/nafion/polyalizarin: Applications to simultaneous electrocatalytic oxidation and reduction of nitrite in water samples
Article Snippet: Ascorbic acid, Nafion, ethanol, alizarin yellow R, polyvinylpyrrolidone, NaNO 2 ,CuSO 4 , HCl, NaOH, Na 2 HPO 4, AgNO 3 , NaH 2 PO 4 , KI, KIO 3 , Na 3 PO 4 , and alumina were purchased from Merck.

Article Title: Stick–slip behaviour on Au(111) with adsorption of copper and sulfate
Article Snippet: The solutions were made of ultrapure H 2 SO 4 (Merck, suprapure), CuSO 4 (Merck, >99%, p.a.) and high purity water (millipore, toc < 3 ppb, 18 .

Article Title: Structural and biochemical analysis of ligand binding in yeast Niemann–Pick type C1–related protein
Article Snippet: The final concentrations of click reagents in sample tubes were 80 μM CuSO 4 (Merck), 3 μM TBTA (Merck), 3 μM AF647-picolyl azide (Jena Bioscience), and 80 μM ascorbic acid (Merck).

Article Title: Manufacturing of Living Building Materials With Calcifying Cyanobacteria
Article Snippet: CuSO 4 ·5H 2 O (Merck, CAS: 7758-99-8) 16.

Concentration Assay:

Article Title: The sterol transporter STARD3 transports sphingosine at ER-lysosome contact sites
Article Snippet: .. Final concentration of click reagents in tubes was 80 μM CuSO 4 (Merck), 3 μM TBTA (Merck), 3 μM Picolyl-Alexa647-Azide (Jena Bioscience) and 80 μM ascorbic acid (Merck). ..

Maltodextrin:

Article Title: Native oleaginous yeasts Rhodotorula mucilaginosa and Solicoccozyma gelidoterrea : a sustainable biotechnological alternative for lipid production with potential application in diets for farmed fish
Article Snippet: .. All compounds were purchased from Merck and prepared at standard working concentrations commonly used in yeast phenotypic profiling: Caffeine (0.5 mM), CuSO 4 (0.2 mM), DTT (2 mM), ethanol at 8%, 9%, and 10% (v/v), fructose (2% w/v), G418 (200 μg/mL), galactose (2% w/v), glycerol (2% v/v), hydrogen peroxide (H 2 O 2 , 2 mM), KCl (0.5 M), lactose (2% w/v), maltodextrin (2% w/v), maltose (2% w/v), methanol (8% v/v), NaCl (1 M), p-coumaric acid (0.5 mM), raffinose (2% w/v), sucrose (2% w/v), SDS (0.01% w/v), sorbitol (1 M), and xylose (2% w/v). ..

Staining:

Article Title: Impaired TGFβ Signaling in Plaque-Associated Microglia
Article Snippet: .. To reduce lipofuscin autofluorescence, sections were finally treated with a solution of 35 mM CuSO 4 in 50 mM ammonium acetate buffer (pH 5), both were purchased from Merck EMSURE, Darmstadt, Germany for 1 h after antibody staining and washed afterwards with PBS to remove any residues of CuSO 4 . ..



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Multivariate analysis of RNA sequencing data. The GSE107323 dataset includes <t>HepG2</t> and HepG2 ATP7B-KO cells that were treated with 0.5mmol/l CuCl 2 for 6–24 h. Mean gene counts > 30 were used for analysis. a Principal component analysis was performed with the following settings for standard deviation: p = 0.005 and q = 0,01788 (FDR). b Thus, 2,142 genes were hierarchically clustered via a multivariance analysis visualised in a heatmap. c Genes were analysed by functional annotation analysis for biological processes by the DAVID tool and showed high EASE scores in genes involved in autophagy ( p = 1.1E-7), lipid metabolism ( p = 3.0E-6) and stress response ( p = 8,6E-5). Volcano plots were generated to compare the CuCl 2 -dependent gene regulation, indicating d 7,722 gene alterations in HepG2 cells and e 7,241 gene alterations in HepG2 ATP7B-KO cells. sig, significant; ut, untreated; t, treated
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Multivariate analysis of RNA sequencing data. The GSE107323 dataset includes HepG2 and HepG2 ATP7B-KO cells that were treated with 0.5mmol/l CuCl 2 for 6–24 h. Mean gene counts > 30 were used for analysis. a Principal component analysis was performed with the following settings for standard deviation: p = 0.005 and q = 0,01788 (FDR). b Thus, 2,142 genes were hierarchically clustered via a multivariance analysis visualised in a heatmap. c Genes were analysed by functional annotation analysis for biological processes by the DAVID tool and showed high EASE scores in genes involved in autophagy ( p = 1.1E-7), lipid metabolism ( p = 3.0E-6) and stress response ( p = 8,6E-5). Volcano plots were generated to compare the CuCl 2 -dependent gene regulation, indicating d 7,722 gene alterations in HepG2 cells and e 7,241 gene alterations in HepG2 ATP7B-KO cells. sig, significant; ut, untreated; t, treated

Journal: Molecular and Cellular Biochemistry

Article Title: High copper levels induce oxidative stress and inflammatory processes in a cell culture model of Wilson’s disease

doi: 10.1007/s11010-026-05481-6

Figure Lengend Snippet: Multivariate analysis of RNA sequencing data. The GSE107323 dataset includes HepG2 and HepG2 ATP7B-KO cells that were treated with 0.5mmol/l CuCl 2 for 6–24 h. Mean gene counts > 30 were used for analysis. a Principal component analysis was performed with the following settings for standard deviation: p = 0.005 and q = 0,01788 (FDR). b Thus, 2,142 genes were hierarchically clustered via a multivariance analysis visualised in a heatmap. c Genes were analysed by functional annotation analysis for biological processes by the DAVID tool and showed high EASE scores in genes involved in autophagy ( p = 1.1E-7), lipid metabolism ( p = 3.0E-6) and stress response ( p = 8,6E-5). Volcano plots were generated to compare the CuCl 2 -dependent gene regulation, indicating d 7,722 gene alterations in HepG2 cells and e 7,241 gene alterations in HepG2 ATP7B-KO cells. sig, significant; ut, untreated; t, treated

Article Snippet: Cell viability of CuCl 2 (Merck) or CuSO 4 (Merck) -treated HepG2 and HepG2 ATP7B-KO cells was measurement by cell counting assay (CCK-8, Sigma-Aldrich).

Techniques: RNA Sequencing, Standard Deviation, Functional Assay, Generated

CuCl 2 -dependent gene expression of autophagy-associated genes. HepG2 and HepG2 ATP7B-KO cells were treated with 0.2–1.2.2mmol/l CuCl 2 or CuSO 4 for 6–24 h. Cell viability was measured after a CuCl 2 and b CuSO 4 treatment via a CCK-8 assay and normalised to that of the untreated control (mean ± SD; n = 4 (CuCl 2 ), n = 5 (CuSO 4 )). RNA from HepG2 and HepG2 ATP7B-KO cells treated with CuCl 2 and untreated PHH (Ctrl and WD) was extracted, and the expression of autophagy-related genes ( c , GABARALP1 ; d , HSP90AA1 ; e , LAMTOR3 ; f , PLOD2 ; g , PRAGC ; h , UBC ) was measured via two-step qRT‒PCR (mean ± SD; n = 3 (HepG2 and HepG2 ATP7B-KO), n = 4 (PHH Ctrl), n = 2 (PHH WD). The data represent copy numbers normalised to 100,000 copies of the reference gene GAPDH . The effect of CuCl 2 concentrations in HepG2 or HepG2 ATP7B-KO cells (* p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001) and differences between HepG2 and HepG2 ATP7B-KO cells after 6–24 h (# p < 0.05; ## p < 0.01; ### p < 0.001; ####; p < 0.0001) were measured by two-way ANOVA tests and Tukey’s multiple comparison tests. Differences in gene expression between PHH Ctrl and WD cells were tested by an unpaired t-test (× p < 0.05; ×× p < 0.01). Ctrl control, PHH primary human hepatocytes, WD Wilson’s disease

Journal: Molecular and Cellular Biochemistry

Article Title: High copper levels induce oxidative stress and inflammatory processes in a cell culture model of Wilson’s disease

doi: 10.1007/s11010-026-05481-6

Figure Lengend Snippet: CuCl 2 -dependent gene expression of autophagy-associated genes. HepG2 and HepG2 ATP7B-KO cells were treated with 0.2–1.2.2mmol/l CuCl 2 or CuSO 4 for 6–24 h. Cell viability was measured after a CuCl 2 and b CuSO 4 treatment via a CCK-8 assay and normalised to that of the untreated control (mean ± SD; n = 4 (CuCl 2 ), n = 5 (CuSO 4 )). RNA from HepG2 and HepG2 ATP7B-KO cells treated with CuCl 2 and untreated PHH (Ctrl and WD) was extracted, and the expression of autophagy-related genes ( c , GABARALP1 ; d , HSP90AA1 ; e , LAMTOR3 ; f , PLOD2 ; g , PRAGC ; h , UBC ) was measured via two-step qRT‒PCR (mean ± SD; n = 3 (HepG2 and HepG2 ATP7B-KO), n = 4 (PHH Ctrl), n = 2 (PHH WD). The data represent copy numbers normalised to 100,000 copies of the reference gene GAPDH . The effect of CuCl 2 concentrations in HepG2 or HepG2 ATP7B-KO cells (* p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001) and differences between HepG2 and HepG2 ATP7B-KO cells after 6–24 h (# p < 0.05; ## p < 0.01; ### p < 0.001; ####; p < 0.0001) were measured by two-way ANOVA tests and Tukey’s multiple comparison tests. Differences in gene expression between PHH Ctrl and WD cells were tested by an unpaired t-test (× p < 0.05; ×× p < 0.01). Ctrl control, PHH primary human hepatocytes, WD Wilson’s disease

Article Snippet: Cell viability of CuCl 2 (Merck) or CuSO 4 (Merck) -treated HepG2 and HepG2 ATP7B-KO cells was measurement by cell counting assay (CCK-8, Sigma-Aldrich).

Techniques: Gene Expression, CCK-8 Assay, Control, Expressing, Comparison

Copper induces oxidative stress and H 2 O 2 production. HepG2 and HepG2 ATP7B-KO cells were treated with 0.2–0.6mmol/l CuCl 2 for 6–24 h. RNA from HepG2 and HepG2 ATP7B-KO cells and PHH (Ctrl and WD) was extracted, and the gene expression of oxidated stress-related genes ( a , HMOX1 ; b , DNAJB1 ; c , GADD45B ) was measured via two-step qRT-PCR. The data represent copy numbers normalised to 100,000 copies of the reference gene GAPDH (mean ± SD; n = 3 (HepG2), n = 4 (PHH Ctrl), n = 2 (PHH WD)). d The GSH/GSSG ratios of HepG2 and HepG2 ATP7B-KO cells were measured via the GSH/GSSG-Glo™ assay (means ± SDs; n = 3). e H 2 O 2 levels in HepG2 and HepG2 ATP7B-KO cells were measured by luminescence via the ROS-Glo™ H 2 O 2 assay (mean ± SD; n = 3). The effect of CuCl 2 concentrations in HepG2 or HepG2 ATP7B-KO cells (* p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001) and differences between HepG2 and HepG2 ATP7B-KO cells after 6–24 h (# p < 0.05; ## p < 0.01; ### p < 0.001; ####; p < 0.0001) were measured by two two-way ANOVA tests and a Tukey’s multiple comparison tests. Differences in gene expression between PHH Ctrl and WD cells was tested by an unpaired t-test (× p < 0.05; ×× p < 0.01). Ctrl control, PHH primary human hepatocytes, WD Wilson’s disease

Journal: Molecular and Cellular Biochemistry

Article Title: High copper levels induce oxidative stress and inflammatory processes in a cell culture model of Wilson’s disease

doi: 10.1007/s11010-026-05481-6

Figure Lengend Snippet: Copper induces oxidative stress and H 2 O 2 production. HepG2 and HepG2 ATP7B-KO cells were treated with 0.2–0.6mmol/l CuCl 2 for 6–24 h. RNA from HepG2 and HepG2 ATP7B-KO cells and PHH (Ctrl and WD) was extracted, and the gene expression of oxidated stress-related genes ( a , HMOX1 ; b , DNAJB1 ; c , GADD45B ) was measured via two-step qRT-PCR. The data represent copy numbers normalised to 100,000 copies of the reference gene GAPDH (mean ± SD; n = 3 (HepG2), n = 4 (PHH Ctrl), n = 2 (PHH WD)). d The GSH/GSSG ratios of HepG2 and HepG2 ATP7B-KO cells were measured via the GSH/GSSG-Glo™ assay (means ± SDs; n = 3). e H 2 O 2 levels in HepG2 and HepG2 ATP7B-KO cells were measured by luminescence via the ROS-Glo™ H 2 O 2 assay (mean ± SD; n = 3). The effect of CuCl 2 concentrations in HepG2 or HepG2 ATP7B-KO cells (* p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001) and differences between HepG2 and HepG2 ATP7B-KO cells after 6–24 h (# p < 0.05; ## p < 0.01; ### p < 0.001; ####; p < 0.0001) were measured by two two-way ANOVA tests and a Tukey’s multiple comparison tests. Differences in gene expression between PHH Ctrl and WD cells was tested by an unpaired t-test (× p < 0.05; ×× p < 0.01). Ctrl control, PHH primary human hepatocytes, WD Wilson’s disease

Article Snippet: Cell viability of CuCl 2 (Merck) or CuSO 4 (Merck) -treated HepG2 and HepG2 ATP7B-KO cells was measurement by cell counting assay (CCK-8, Sigma-Aldrich).

Techniques: Gene Expression, Quantitative RT-PCR, Glo Assay, Comparison, Control

Copper induces NFKB- and AP1-related inflammatory responses. HepG2 and HepG2 ATP7B-KO cells were treated with 0.2-0.2.6mmol/l CuCl 2 for 6 and 24 h. RNA from HepG2 and HepG2 ATP7B-KO cells and untreated PHH (Ctrl and WD) was extracted, and the gene expression of genes related to NFKB and AP1 ( a , FOS ; b , PLA2G2A ; c , JUN; d , JUNB ) was measured via two-step qRT‒PCR (mean ± SD; n = 3 (HepG2), n = 4 (PHH Ctrl), n = 2 (PHH WD)). Supernatants from HepG2 and HepG2 ATP7B-KO cells treated with CuCl 2 were collected, and various cytokine levels ( e , IL1B; f , TNF; g , IL8; h , GM-CSF) were measured via the LEGENDplex™ Assay (mean ± SD, n = 3). HepG2 and HepG2 ATP7B-KO cells were transfected with luciferase-based reporter plasmids pAP1-Luc ( i , j ), pNFKB-Luc ( k , l ) and pTA-Luc as a control and incubated with CuCl 2 . Measurement of NFKB and AP1 promoter activity was performed via a luciferase reporter assay (means ± SDs, n = 3). The effect of CuCl 2 concentrations in HepG2 or HepG2 ATP7B-KO cells (* p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001) and differences between HepG2 and HepG2 ATP7B-KO cells after 6–24 h (# p < 0.05; ## p < 0.01; ### p < 0.001; #### p < 0.0001) were measured by two-way ANOVA tests and Tukey’s multiple comparison tests. Differences in gene expression between PHH Ctrl and WD cells were tested by an unpaired t-test (× p < 0.05; ×× p < 0.01; ×××× p < 0.0001). Ctrl control, ns not significant, PHH primary human hepatocytes, WD Wilson’s disease

Journal: Molecular and Cellular Biochemistry

Article Title: High copper levels induce oxidative stress and inflammatory processes in a cell culture model of Wilson’s disease

doi: 10.1007/s11010-026-05481-6

Figure Lengend Snippet: Copper induces NFKB- and AP1-related inflammatory responses. HepG2 and HepG2 ATP7B-KO cells were treated with 0.2-0.2.6mmol/l CuCl 2 for 6 and 24 h. RNA from HepG2 and HepG2 ATP7B-KO cells and untreated PHH (Ctrl and WD) was extracted, and the gene expression of genes related to NFKB and AP1 ( a , FOS ; b , PLA2G2A ; c , JUN; d , JUNB ) was measured via two-step qRT‒PCR (mean ± SD; n = 3 (HepG2), n = 4 (PHH Ctrl), n = 2 (PHH WD)). Supernatants from HepG2 and HepG2 ATP7B-KO cells treated with CuCl 2 were collected, and various cytokine levels ( e , IL1B; f , TNF; g , IL8; h , GM-CSF) were measured via the LEGENDplex™ Assay (mean ± SD, n = 3). HepG2 and HepG2 ATP7B-KO cells were transfected with luciferase-based reporter plasmids pAP1-Luc ( i , j ), pNFKB-Luc ( k , l ) and pTA-Luc as a control and incubated with CuCl 2 . Measurement of NFKB and AP1 promoter activity was performed via a luciferase reporter assay (means ± SDs, n = 3). The effect of CuCl 2 concentrations in HepG2 or HepG2 ATP7B-KO cells (* p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001) and differences between HepG2 and HepG2 ATP7B-KO cells after 6–24 h (# p < 0.05; ## p < 0.01; ### p < 0.001; #### p < 0.0001) were measured by two-way ANOVA tests and Tukey’s multiple comparison tests. Differences in gene expression between PHH Ctrl and WD cells were tested by an unpaired t-test (× p < 0.05; ×× p < 0.01; ×××× p < 0.0001). Ctrl control, ns not significant, PHH primary human hepatocytes, WD Wilson’s disease

Article Snippet: Cell viability of CuCl 2 (Merck) or CuSO 4 (Merck) -treated HepG2 and HepG2 ATP7B-KO cells was measurement by cell counting assay (CCK-8, Sigma-Aldrich).

Techniques: Gene Expression, Transfection, Luciferase, Control, Incubation, Activity Assay, Reporter Assay, Comparison