nqo-1 antibody (a180) Search Results


nqo1  (Novus Biologicals)
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Novus Biologicals nqo1
a Starburst plot showing the correlation of differences in promoter methylation and expression between the hepatoblastoma clusters F versus E1/E2. The only gene with absolute methylation difference ≥ 0.25 and absolute log2-fold expression change ≥ 2.5 is <t>NQO1</t> , indicated in red. b Correlation between the methylation of probe cg26598152 and NQO1 expression. Rs represents Spearman’s correlation coefficient. c , d Dose–response curves of HepG2 cells exposed to various concentrations of doxorubicin (DOX) after NQO1 inhibition (red) or negative control treatment (black). NQO1 was inhibited by using siRNA ( c ) or dicoumarol ( d ). Horizontal bars and whiskers at the bottom indicate EC 50 values with 95% confidence intervals. e , f Enhancement of DOX cytotoxicity by NQO1 inhibition in HepG2 cells. NQO1 was inhibited using siRNA ( e ) or dicoumarol ( f ). The luminescence intensities representing the cell viability are compared between the conditions with and without NQO1 inhibition using the unpaired Student’s t test.
Nqo1, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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a Starburst plot showing the correlation of differences in promoter methylation and expression between the hepatoblastoma clusters F versus E1/E2. The only gene with absolute methylation difference ≥ 0.25 and absolute log2-fold expression change ≥ 2.5 is NQO1 , indicated in red. b Correlation between the methylation of probe cg26598152 and NQO1 expression. Rs represents Spearman’s correlation coefficient. c , d Dose–response curves of HepG2 cells exposed to various concentrations of doxorubicin (DOX) after NQO1 inhibition (red) or negative control treatment (black). NQO1 was inhibited by using siRNA ( c ) or dicoumarol ( d ). Horizontal bars and whiskers at the bottom indicate EC 50 values with 95% confidence intervals. e , f Enhancement of DOX cytotoxicity by NQO1 inhibition in HepG2 cells. NQO1 was inhibited using siRNA ( e ) or dicoumarol ( f ). The luminescence intensities representing the cell viability are compared between the conditions with and without NQO1 inhibition using the unpaired Student’s t test.

Journal: NPJ Precision Oncology

Article Title: Integrated multiomics analysis of hepatoblastoma unravels its heterogeneity and provides novel druggable targets

doi: 10.1038/s41698-020-0125-y

Figure Lengend Snippet: a Starburst plot showing the correlation of differences in promoter methylation and expression between the hepatoblastoma clusters F versus E1/E2. The only gene with absolute methylation difference ≥ 0.25 and absolute log2-fold expression change ≥ 2.5 is NQO1 , indicated in red. b Correlation between the methylation of probe cg26598152 and NQO1 expression. Rs represents Spearman’s correlation coefficient. c , d Dose–response curves of HepG2 cells exposed to various concentrations of doxorubicin (DOX) after NQO1 inhibition (red) or negative control treatment (black). NQO1 was inhibited by using siRNA ( c ) or dicoumarol ( d ). Horizontal bars and whiskers at the bottom indicate EC 50 values with 95% confidence intervals. e , f Enhancement of DOX cytotoxicity by NQO1 inhibition in HepG2 cells. NQO1 was inhibited using siRNA ( e ) or dicoumarol ( f ). The luminescence intensities representing the cell viability are compared between the conditions with and without NQO1 inhibition using the unpaired Student’s t test.

Article Snippet: Whole-cell lysates were analyzed by western blotting using antibodies against alpha-tubulin (ab7291; Abcam), NQO1 (NB200-209; Novus Biologicals), and ODC1 (GTX101521; GeneTex) at the concentrations of 1/10,000, 1/1666, and 1/1000, respectively.

Techniques: Methylation, Expressing, Inhibition, Negative Control

a Schematic presentation of ODC1 stabilization by NQO1. b Volcano plot displaying genes that are differentially expressed between the hepatoblastoma clusters F versus E1/E2. Each gene is plotted with log2-fold expression change on x -axis and negative log10 false discovery rate (FDR) q value on y -axis. Genes with absolute log2-fold change > 2 and an FDR q value of <1.0 × 10 −7 are shown in orange. NQO1 and ODC1 are shown in red. c Kaplan–Meier survival curves for overall survival according to ODC1 expression. d ODC1 FPKM in hepatoblastoma samples and cell lines. e , f Cell proliferation assay to assess the effect of ODC1 inhibition on HepG2 cells. ODC1 was inhibited using siRNA ( e ) or difluoromethylornithine (DFMO; f ). Error bars indicate SD of triplicate experiments. Cell viabilities on day 4 are compared between the conditions using the unpaired Student’s t test. g – i Ethynyl deoxyuridine (EdU) assay using HepG2 cells treated with PBS, dicoumarol, DFMO, and negative control/ NQO1 / ODC1 siRNA. The ratio of EdU-positive cells per total Hoechst-positive cells are compared among the conditions using the unpaired Student’s t test. Scale bar represents 100 μm.

Journal: NPJ Precision Oncology

Article Title: Integrated multiomics analysis of hepatoblastoma unravels its heterogeneity and provides novel druggable targets

doi: 10.1038/s41698-020-0125-y

Figure Lengend Snippet: a Schematic presentation of ODC1 stabilization by NQO1. b Volcano plot displaying genes that are differentially expressed between the hepatoblastoma clusters F versus E1/E2. Each gene is plotted with log2-fold expression change on x -axis and negative log10 false discovery rate (FDR) q value on y -axis. Genes with absolute log2-fold change > 2 and an FDR q value of <1.0 × 10 −7 are shown in orange. NQO1 and ODC1 are shown in red. c Kaplan–Meier survival curves for overall survival according to ODC1 expression. d ODC1 FPKM in hepatoblastoma samples and cell lines. e , f Cell proliferation assay to assess the effect of ODC1 inhibition on HepG2 cells. ODC1 was inhibited using siRNA ( e ) or difluoromethylornithine (DFMO; f ). Error bars indicate SD of triplicate experiments. Cell viabilities on day 4 are compared between the conditions using the unpaired Student’s t test. g – i Ethynyl deoxyuridine (EdU) assay using HepG2 cells treated with PBS, dicoumarol, DFMO, and negative control/ NQO1 / ODC1 siRNA. The ratio of EdU-positive cells per total Hoechst-positive cells are compared among the conditions using the unpaired Student’s t test. Scale bar represents 100 μm.

Article Snippet: Whole-cell lysates were analyzed by western blotting using antibodies against alpha-tubulin (ab7291; Abcam), NQO1 (NB200-209; Novus Biologicals), and ODC1 (GTX101521; GeneTex) at the concentrations of 1/10,000, 1/1666, and 1/1000, respectively.

Techniques: Expressing, Proliferation Assay, Inhibition, EdU Assay, Negative Control

All hepatoblastoma cells are commonly derived from immature hepatocytes with aberrant activation of the Wnt signaling pathway, whereas heterogeneity among cases arises from the diversity of the differentiation stage of the origins. Clusters E1/E2 are derived from liver progenitor cells at an earlier differentiation stage and consequently harbor hypermethylation of HNF4A/CEBPA-binding regions that leads to expression profiles mimicking fetal liver, which explain the poorly differentiated pathology and aggressive cell proliferation. In addition, clusters E1/E2 highly express NQO1 due to promoter hypomethylation, which induces chemoresistance. Cluster F arises from hepatoblasts at a relatively mature stage, harbors genetic features that are opposite of those observed in clusters E1/E2, and represents good prognosis.

Journal: NPJ Precision Oncology

Article Title: Integrated multiomics analysis of hepatoblastoma unravels its heterogeneity and provides novel druggable targets

doi: 10.1038/s41698-020-0125-y

Figure Lengend Snippet: All hepatoblastoma cells are commonly derived from immature hepatocytes with aberrant activation of the Wnt signaling pathway, whereas heterogeneity among cases arises from the diversity of the differentiation stage of the origins. Clusters E1/E2 are derived from liver progenitor cells at an earlier differentiation stage and consequently harbor hypermethylation of HNF4A/CEBPA-binding regions that leads to expression profiles mimicking fetal liver, which explain the poorly differentiated pathology and aggressive cell proliferation. In addition, clusters E1/E2 highly express NQO1 due to promoter hypomethylation, which induces chemoresistance. Cluster F arises from hepatoblasts at a relatively mature stage, harbors genetic features that are opposite of those observed in clusters E1/E2, and represents good prognosis.

Article Snippet: Whole-cell lysates were analyzed by western blotting using antibodies against alpha-tubulin (ab7291; Abcam), NQO1 (NB200-209; Novus Biologicals), and ODC1 (GTX101521; GeneTex) at the concentrations of 1/10,000, 1/1666, and 1/1000, respectively.

Techniques: Derivative Assay, Activation Assay, Binding Assay, Expressing