anti p gsk 3β  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti p gsk 3β
    Western blotting and quantitative analyses of β-catenin, p-β-catenin Ser33/37/Thr41 , <t>p-GSK-3β</t> Ser9 , GSK-3β, AKT, and p-AKT ser473 protein levels in H157 cells with or without HORMAD1 expression ( A ) and in NC and HORMAD1 KO H650 cells ( B ). α-tubulin was used as the loading control. C Western blotting and quantitative analyses of p-GSK-3β Ser9 , GSK-3β, p-β-catenin Ser33/37/Thr41 , and β-catenin protein levels in NC and HORMAD1 KO H650 cells after 24 h of treatment with 20 mM LiCl. α-tubulin was used as the loading control. D Western blotting and quantitative analyses of p-AKT ser473 , AKT, p-GSK-3β Ser9 , GSK-3β, p-β-catenin Ser33/37 Thr41 , and β-catenin protein levels in H157 cells with or without HORMAD1 expression after 24 h of treatment with 10 μM MK-2206. α-tubulin was used as the loading control. E .TOP-Flash/FOP-Flash luciferase reporter assay of β-catenin transcriptional activity in H157 cells with or without HORMAD1 expression after 24 h of treatment with 10 μM MK-2206. All histograms representing indicated the results of three independent experiments. Mean ± SEM from three independent experiments are shown. ** p < 0.01; *** p < 0.001; ns, not significant.
    Anti P Gsk 3β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "The cancer/testis antigen HORMAD1 mediates epithelial–mesenchymal transition to promote tumor growth and metastasis by activating the Wnt/β-catenin signaling pathway in lung cancer"

    Article Title: The cancer/testis antigen HORMAD1 mediates epithelial–mesenchymal transition to promote tumor growth and metastasis by activating the Wnt/β-catenin signaling pathway in lung cancer

    Journal: Cell Death Discovery

    doi: 10.1038/s41420-022-00946-1

    Western blotting and quantitative analyses of β-catenin, p-β-catenin Ser33/37/Thr41 , p-GSK-3β Ser9 , GSK-3β, AKT, and p-AKT ser473 protein levels in H157 cells with or without HORMAD1 expression ( A ) and in NC and HORMAD1 KO H650 cells ( B ). α-tubulin was used as the loading control. C Western blotting and quantitative analyses of p-GSK-3β Ser9 , GSK-3β, p-β-catenin Ser33/37/Thr41 , and β-catenin protein levels in NC and HORMAD1 KO H650 cells after 24 h of treatment with 20 mM LiCl. α-tubulin was used as the loading control. D Western blotting and quantitative analyses of p-AKT ser473 , AKT, p-GSK-3β Ser9 , GSK-3β, p-β-catenin Ser33/37 Thr41 , and β-catenin protein levels in H157 cells with or without HORMAD1 expression after 24 h of treatment with 10 μM MK-2206. α-tubulin was used as the loading control. E .TOP-Flash/FOP-Flash luciferase reporter assay of β-catenin transcriptional activity in H157 cells with or without HORMAD1 expression after 24 h of treatment with 10 μM MK-2206. All histograms representing indicated the results of three independent experiments. Mean ± SEM from three independent experiments are shown. ** p < 0.01; *** p < 0.001; ns, not significant.
    Figure Legend Snippet: Western blotting and quantitative analyses of β-catenin, p-β-catenin Ser33/37/Thr41 , p-GSK-3β Ser9 , GSK-3β, AKT, and p-AKT ser473 protein levels in H157 cells with or without HORMAD1 expression ( A ) and in NC and HORMAD1 KO H650 cells ( B ). α-tubulin was used as the loading control. C Western blotting and quantitative analyses of p-GSK-3β Ser9 , GSK-3β, p-β-catenin Ser33/37/Thr41 , and β-catenin protein levels in NC and HORMAD1 KO H650 cells after 24 h of treatment with 20 mM LiCl. α-tubulin was used as the loading control. D Western blotting and quantitative analyses of p-AKT ser473 , AKT, p-GSK-3β Ser9 , GSK-3β, p-β-catenin Ser33/37 Thr41 , and β-catenin protein levels in H157 cells with or without HORMAD1 expression after 24 h of treatment with 10 μM MK-2206. α-tubulin was used as the loading control. E .TOP-Flash/FOP-Flash luciferase reporter assay of β-catenin transcriptional activity in H157 cells with or without HORMAD1 expression after 24 h of treatment with 10 μM MK-2206. All histograms representing indicated the results of three independent experiments. Mean ± SEM from three independent experiments are shown. ** p < 0.01; *** p < 0.001; ns, not significant.

    Techniques Used: Western Blot, Expressing, Luciferase, Reporter Assay, Activity Assay

    A Western blotting and quantitative analyses of nuclear β-catenin, p-β-catenin Ser33/37/Thr41 , p-GSK-3β Ser9 , and GSK-3β protein levels in H157 cells with or without HORMAD1 expression after 24 h of treatment with 15 μM XAV939. α-tubulin and Lamin B1 were used as the loading controls. B Western blotting and quantitative analyses of nuclear β-catenin, p-β-catenin Ser33/37/Thr41 , p-GSK-3β Ser9 , and GSK-3β protein levels in NC and HORMAD1 KO H650 cells after 24 h of treatment with 6 μM CHIR99021. α-tubulin and Lamin B1 were used as the loading controls. C Immunofluorescence staining analyses of the subcellular β-catenin localization in H157 cells with or without HORMAD1 expression after 24 h of treatment with 15 μM XAV939; scale bars are 100 μm. D Immunofluorescence staining analyses of subcellular β-catenin localization in NC and HORMAD1 KO H650 cells after 24 h of treatment with 6 μM CHIR99021, scale bars are 100 μm. E Western blotting and quantitative analyses of E-cadherin, N-cadherin, Vimentin, and ZEB-1 protein levels in H157 cells with or without HORMAD1 after 24 h of 15 μM XAV-939 treatment. α-tubulin was used as the loading control. F Western blotting and quantitative analyses of E-cadherin, N-cadherin, Vimentin, and ZEB-1 protein levels in H650 NC and HORMAD1 KO cells after 24 h of treatment with 6 μM CHIR99021. α-tubulin was used as the loading control. G . The migration and invasion of H157 cells with or without HORMAD1 expression were examined after 24 h of treatment with 15 μM XAV939. H The migration and invasion of NC and HORMAD1 KO H650 cells were examined after 24 h of treatment with 6 μM CHIR99021. All histograms representing indicated the results of three independent experiments. Mean ± SEM from three independent experiments are shown. ** p < 0.01; *** p < 0.001; ns, not significant.
    Figure Legend Snippet: A Western blotting and quantitative analyses of nuclear β-catenin, p-β-catenin Ser33/37/Thr41 , p-GSK-3β Ser9 , and GSK-3β protein levels in H157 cells with or without HORMAD1 expression after 24 h of treatment with 15 μM XAV939. α-tubulin and Lamin B1 were used as the loading controls. B Western blotting and quantitative analyses of nuclear β-catenin, p-β-catenin Ser33/37/Thr41 , p-GSK-3β Ser9 , and GSK-3β protein levels in NC and HORMAD1 KO H650 cells after 24 h of treatment with 6 μM CHIR99021. α-tubulin and Lamin B1 were used as the loading controls. C Immunofluorescence staining analyses of the subcellular β-catenin localization in H157 cells with or without HORMAD1 expression after 24 h of treatment with 15 μM XAV939; scale bars are 100 μm. D Immunofluorescence staining analyses of subcellular β-catenin localization in NC and HORMAD1 KO H650 cells after 24 h of treatment with 6 μM CHIR99021, scale bars are 100 μm. E Western blotting and quantitative analyses of E-cadherin, N-cadherin, Vimentin, and ZEB-1 protein levels in H157 cells with or without HORMAD1 after 24 h of 15 μM XAV-939 treatment. α-tubulin was used as the loading control. F Western blotting and quantitative analyses of E-cadherin, N-cadherin, Vimentin, and ZEB-1 protein levels in H650 NC and HORMAD1 KO cells after 24 h of treatment with 6 μM CHIR99021. α-tubulin was used as the loading control. G . The migration and invasion of H157 cells with or without HORMAD1 expression were examined after 24 h of treatment with 15 μM XAV939. H The migration and invasion of NC and HORMAD1 KO H650 cells were examined after 24 h of treatment with 6 μM CHIR99021. All histograms representing indicated the results of three independent experiments. Mean ± SEM from three independent experiments are shown. ** p < 0.01; *** p < 0.001; ns, not significant.

    Techniques Used: Western Blot, Expressing, Immunofluorescence, Staining, Migration

    Aberrant HORMAD1 expression suppresses the degradation of cytosolic β-catenin and promotes nuclear β-catenin accumulation by regulating AKT/GSK-3β signaling to activate the Wnt/β-catenin pathway, accompanied with upregulation of downstream target genes and induction of EMT to promote tumor growth and metastasis in lung cancer.
    Figure Legend Snippet: Aberrant HORMAD1 expression suppresses the degradation of cytosolic β-catenin and promotes nuclear β-catenin accumulation by regulating AKT/GSK-3β signaling to activate the Wnt/β-catenin pathway, accompanied with upregulation of downstream target genes and induction of EMT to promote tumor growth and metastasis in lung cancer.

    Techniques Used: Expressing

    anti p gsk 3β ser9  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti p gsk 3β ser9
    Anti P Gsk 3β Ser9, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti p gsk 3β ser9  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti p gsk 3β ser9
    Hyperoside regulation of the <t>PHLPP2-AKT-GSK-3β</t> signaling pathway in liver L02 cells. (A) Western blots. The cytoplasmic HO-1, p-GSK-3β, p-AKT, and PHLPP2 were analyzed using western blotting in liver L02 cells after treated with t-BHP. (B) Representative blots of cytoplasmic and nuclear Nrf2. (C) Quantification data of HO-1, cytoplasmic Nrf2, nuclear Nrf2, p-Nrf2 (S40), p-GSK-3β, p-AKT (S473), and PHLPP2. These western blots were quantified by using Image J Software and the data are expressed as mean and standard deviation (SD) and statistically analyzed by ANOVA. a P < 0.05 vs. Control, b P < 0.05 vs. Morin, c P < 0.05 vs. Hyp for 1 h, and d P < 0.05 vs. Hyp for 3 h.
    Anti P Gsk 3β Ser9, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti p gsk 3β ser9/product/Cell Signaling Technology Inc
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    1) Product Images from "Hyperoside Protected Against Oxidative Stress-Induced Liver Injury via the PHLPP2-AKT-GSK-3β Signaling Pathway In Vivo and In Vitro"

    Article Title: Hyperoside Protected Against Oxidative Stress-Induced Liver Injury via the PHLPP2-AKT-GSK-3β Signaling Pathway In Vivo and In Vitro

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2020.01065

    Hyperoside regulation of the PHLPP2-AKT-GSK-3β signaling pathway in liver L02 cells. (A) Western blots. The cytoplasmic HO-1, p-GSK-3β, p-AKT, and PHLPP2 were analyzed using western blotting in liver L02 cells after treated with t-BHP. (B) Representative blots of cytoplasmic and nuclear Nrf2. (C) Quantification data of HO-1, cytoplasmic Nrf2, nuclear Nrf2, p-Nrf2 (S40), p-GSK-3β, p-AKT (S473), and PHLPP2. These western blots were quantified by using Image J Software and the data are expressed as mean and standard deviation (SD) and statistically analyzed by ANOVA. a P < 0.05 vs. Control, b P < 0.05 vs. Morin, c P < 0.05 vs. Hyp for 1 h, and d P < 0.05 vs. Hyp for 3 h.
    Figure Legend Snippet: Hyperoside regulation of the PHLPP2-AKT-GSK-3β signaling pathway in liver L02 cells. (A) Western blots. The cytoplasmic HO-1, p-GSK-3β, p-AKT, and PHLPP2 were analyzed using western blotting in liver L02 cells after treated with t-BHP. (B) Representative blots of cytoplasmic and nuclear Nrf2. (C) Quantification data of HO-1, cytoplasmic Nrf2, nuclear Nrf2, p-Nrf2 (S40), p-GSK-3β, p-AKT (S473), and PHLPP2. These western blots were quantified by using Image J Software and the data are expressed as mean and standard deviation (SD) and statistically analyzed by ANOVA. a P < 0.05 vs. Control, b P < 0.05 vs. Morin, c P < 0.05 vs. Hyp for 1 h, and d P < 0.05 vs. Hyp for 3 h.

    Techniques Used: Western Blot, Software, Standard Deviation

    Hyperoside regulation of the PHLPP2-AKT-GSK-3β signaling pathway in t-BHP-treated liver L02 cells. (A) Western blots. The cytoplasmic and nuclear HO-1, Nrf2, p-GSK-3β, p-AKT, and PHLPP2 levels were assessed using western blotting in t-BHP-treated liver L02 cells. (B) Representative quantification data of HO-1, cytoplasmic Nrf2, nuclear Nrf2, p-Nrf2(S40), cytoplasmic p-Fyn, nuclear p-Fyn, p-GSK-3β, p-AKT, and PHLPP2. These Western blots were quantified by using Image J Software and the data are expressed as mean and standard deviation (SD) and statistically analyzed by ANOVA. a P < 0.05 vs. Control, b P < 0.05 vs. Morin, c P < 0.05 vs. Hyp for 6 h, and d P < 0.05 vs. t-BHP.
    Figure Legend Snippet: Hyperoside regulation of the PHLPP2-AKT-GSK-3β signaling pathway in t-BHP-treated liver L02 cells. (A) Western blots. The cytoplasmic and nuclear HO-1, Nrf2, p-GSK-3β, p-AKT, and PHLPP2 levels were assessed using western blotting in t-BHP-treated liver L02 cells. (B) Representative quantification data of HO-1, cytoplasmic Nrf2, nuclear Nrf2, p-Nrf2(S40), cytoplasmic p-Fyn, nuclear p-Fyn, p-GSK-3β, p-AKT, and PHLPP2. These Western blots were quantified by using Image J Software and the data are expressed as mean and standard deviation (SD) and statistically analyzed by ANOVA. a P < 0.05 vs. Control, b P < 0.05 vs. Morin, c P < 0.05 vs. Hyp for 6 h, and d P < 0.05 vs. t-BHP.

    Techniques Used: Western Blot, Software, Standard Deviation

    Enhancement of Hyperoside-regulated PHLPP2-AKT-GSK-3β signaling pathway after knockdown of PHLPP2 expression in liver L02 cells. (A) Western blots. Levels of these different proteins were analyzed using western blotting in L02 liver cells after PHLPP2 siRNA1 transfection with or without t-BHP treatment. (B) Quantified data on PHLPP2 expression after PHLPP2 siRNA transfection (Left: protein expression; Right: mRNA expression). a P < 0.05 vs. the control, b P < 0.05 vs. the negative control, c P < 0.05 vs. PHLPP2 siRNA1, d P < 0.05 vs. PHLPP2 siRNA2. (C) Representative blots. (D) Representative quantification data on HO-1, nuclear Nrf2, cytoplasmic p-Fyn, nuclear p-Fyn, p-GSK-3β, p-AKT, and PHLPP2. These western blots were quantified by using Image J Software and the data are expressed as mean and standard deviation (SD) and statistically analyzed by ANOVA. a P < 0.05 vs. Control, b P < 0.05 vs. Hyp for 6 h, c P < 0.05 vs. PHLPP2 siRNA, d P < 0.05 vs. the t-BHP treatment, and e P < 0.05 vs. PHLPP2 siRNA + Hyp.
    Figure Legend Snippet: Enhancement of Hyperoside-regulated PHLPP2-AKT-GSK-3β signaling pathway after knockdown of PHLPP2 expression in liver L02 cells. (A) Western blots. Levels of these different proteins were analyzed using western blotting in L02 liver cells after PHLPP2 siRNA1 transfection with or without t-BHP treatment. (B) Quantified data on PHLPP2 expression after PHLPP2 siRNA transfection (Left: protein expression; Right: mRNA expression). a P < 0.05 vs. the control, b P < 0.05 vs. the negative control, c P < 0.05 vs. PHLPP2 siRNA1, d P < 0.05 vs. PHLPP2 siRNA2. (C) Representative blots. (D) Representative quantification data on HO-1, nuclear Nrf2, cytoplasmic p-Fyn, nuclear p-Fyn, p-GSK-3β, p-AKT, and PHLPP2. These western blots were quantified by using Image J Software and the data are expressed as mean and standard deviation (SD) and statistically analyzed by ANOVA. a P < 0.05 vs. Control, b P < 0.05 vs. Hyp for 6 h, c P < 0.05 vs. PHLPP2 siRNA, d P < 0.05 vs. the t-BHP treatment, and e P < 0.05 vs. PHLPP2 siRNA + Hyp.

    Techniques Used: Expressing, Western Blot, Transfection, Negative Control, Software, Standard Deviation

    Hyperoside regulation of the PHLPP2-AKT-GSK-3β signaling pathway in CCl4-injured rat liver. (A) Western blots. Levels of cytoplasmic and nuclear p-GSK-3β and p-AKT proteins were assessed using western blotting in CCl4-injured rat liver tissues. (B) Representative quantification data on p-GSK-3β, p-AKT (S473), p-AKT (The308), and PHLPP2. These western blots were quantified by using Image J Software and the data are expressed as mean and standard deviation (SD) and statistically analyzed by the ANOVA. a P < 0.05 vs. Control, b P < 0.05 vs. CCl4, c P < 0.05 vs. Hyp (60 mg/kg), d P < 0.05 vs. Hyp(15 mg/kg + CCl4), e P < 0.05 vs. Hyp(30 mg/kg + CCl4), and f P < 0.05 vs. Hyp(60 mg/kg + CCl4).
    Figure Legend Snippet: Hyperoside regulation of the PHLPP2-AKT-GSK-3β signaling pathway in CCl4-injured rat liver. (A) Western blots. Levels of cytoplasmic and nuclear p-GSK-3β and p-AKT proteins were assessed using western blotting in CCl4-injured rat liver tissues. (B) Representative quantification data on p-GSK-3β, p-AKT (S473), p-AKT (The308), and PHLPP2. These western blots were quantified by using Image J Software and the data are expressed as mean and standard deviation (SD) and statistically analyzed by the ANOVA. a P < 0.05 vs. Control, b P < 0.05 vs. CCl4, c P < 0.05 vs. Hyp (60 mg/kg), d P < 0.05 vs. Hyp(15 mg/kg + CCl4), e P < 0.05 vs. Hyp(30 mg/kg + CCl4), and f P < 0.05 vs. Hyp(60 mg/kg + CCl4).

    Techniques Used: Western Blot, Software, Standard Deviation

    A schematic illustrating the mechanisms involved in the protection of hyperoside against oxidative liver stress. Hyperoside was able to down regulate PHLPP2 expression in liver cells treated with t-BHP and in CCl4-injured rat liver to induce AKT phosphorylation and inactivate GSK-3β (Ser9), and thereby, reduced Fyn phosphorylation, and nuclear translocation. The phosphorylation of Nrf2 at S40 site was probably involved in Hyp-mediated regulation of Fyn kinase, likely through nuclear translocation for HO-1 transcription and translation. The dashed line highlights that this is a strong suggestion and has not been completely proven with experiment.
    Figure Legend Snippet: A schematic illustrating the mechanisms involved in the protection of hyperoside against oxidative liver stress. Hyperoside was able to down regulate PHLPP2 expression in liver cells treated with t-BHP and in CCl4-injured rat liver to induce AKT phosphorylation and inactivate GSK-3β (Ser9), and thereby, reduced Fyn phosphorylation, and nuclear translocation. The phosphorylation of Nrf2 at S40 site was probably involved in Hyp-mediated regulation of Fyn kinase, likely through nuclear translocation for HO-1 transcription and translation. The dashed line highlights that this is a strong suggestion and has not been completely proven with experiment.

    Techniques Used: Expressing, Translocation Assay

    anti p gsk 3β ser9  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti p gsk 3β ser9
    Anti P Gsk 3β Ser9, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti p gsk 3β ser9  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti p gsk 3β ser9
    Anti P Gsk 3β Ser9, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti p gsk 3β ser9/product/Cell Signaling Technology Inc
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    anti p gsk 3β ser9  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
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    Cell Signaling Technology Inc anti p gsk 3β ser9
    Anti P Gsk 3β Ser9, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    p gsk 3β  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p gsk 3β
    The effect of Alsterpaullone (Als) against MPP + -induced cytotoxicity and inactivation of Wnt signaling. (A) Cells were treated with a range of MPP + concentrations (0–2,000 μM) for 24 h, and MTT assay was used to detect the cell viability. (B) Various concentrations of Als (0–2.0 μM) were added for 24 h before MPP + treatment (500 μM). Cell viability was evaluated using the MTT assay (the means ± SEM; n = 3; * p < 0.05, ** p < 0.01). (C) Cells were treated as described in (B) and Western blot was conducted in the different groups. (D–F) Relative amounts of β-catenin/actin, c-Myc/actin and p-glycogen synthase kinase <t>3β</t> <t>(GSK-3β;</t> <t>ser9)/GSK-3β</t> were analyzed (the means ± SEM; n = 3; * p < 0.05, ** p < 0.01).
    P Gsk 3β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "GSK-3β Inhibitor Alsterpaullone Attenuates MPP + -Induced Cell Damage in a c-Myc-Dependent Manner in SH-SY5Y Cells"

    Article Title: GSK-3β Inhibitor Alsterpaullone Attenuates MPP + -Induced Cell Damage in a c-Myc-Dependent Manner in SH-SY5Y Cells

    Journal: Frontiers in Cellular Neuroscience

    doi: 10.3389/fncel.2018.00283

    The effect of Alsterpaullone (Als) against MPP + -induced cytotoxicity and inactivation of Wnt signaling. (A) Cells were treated with a range of MPP + concentrations (0–2,000 μM) for 24 h, and MTT assay was used to detect the cell viability. (B) Various concentrations of Als (0–2.0 μM) were added for 24 h before MPP + treatment (500 μM). Cell viability was evaluated using the MTT assay (the means ± SEM; n = 3; * p < 0.05, ** p < 0.01). (C) Cells were treated as described in (B) and Western blot was conducted in the different groups. (D–F) Relative amounts of β-catenin/actin, c-Myc/actin and p-glycogen synthase kinase 3β (GSK-3β; ser9)/GSK-3β were analyzed (the means ± SEM; n = 3; * p < 0.05, ** p < 0.01).
    Figure Legend Snippet: The effect of Alsterpaullone (Als) against MPP + -induced cytotoxicity and inactivation of Wnt signaling. (A) Cells were treated with a range of MPP + concentrations (0–2,000 μM) for 24 h, and MTT assay was used to detect the cell viability. (B) Various concentrations of Als (0–2.0 μM) were added for 24 h before MPP + treatment (500 μM). Cell viability was evaluated using the MTT assay (the means ± SEM; n = 3; * p < 0.05, ** p < 0.01). (C) Cells were treated as described in (B) and Western blot was conducted in the different groups. (D–F) Relative amounts of β-catenin/actin, c-Myc/actin and p-glycogen synthase kinase 3β (GSK-3β; ser9)/GSK-3β were analyzed (the means ± SEM; n = 3; * p < 0.05, ** p < 0.01).

    Techniques Used: MTT Assay, Western Blot

    Als effectively rescued c-Myc from the MPP + -induced decline via Wnt signaling. (A) Cells transfected with pcDNA3.0-β-catenin were treated with MPP + (500 μM) for 24 h. Western blot was conducted in the Control, MPP + and MPP + +β-catenin groups. (B) Relative amounts of β-catenin/actin, c-Myc/actin and p- GSK-3β (ser9)/GSK-3β level were quantified (the means ± SEM; n = 3; * p < 0.05, ** p < 0.01). (C) Cells transfected with β-catenin siRNA were treated with MPP + (500 μM) for 24 h. Western blot was conducted in the Control siRNA, MPP + and β-catenin siRNA groups. (D) The ratios of β-catenin/actin, c-Myc/actin and p-GSK-3β(ser9)/GSK-3β were analyzed (the means ± SEM; n = 3; * p < 0.05, ** p < 0.01). (E) Cells transfected with pcDNA3.0 or pcDNA3.0-β-catenin were pretreated with Als for 24 h before MPP + treatment. Western blot was conducted in different groups. (F) Quantification graphs of the ratios of β-catenin/actin, c-Myc/actin and p-GSK-3β (ser9)/GSK-3β (the means ± SEM; n = 3; * p < 0.05, ** p < 0.01). (G) Cells transfected with control siRNA or β-catenin siRNA were pretreated with Als for 24 h before MPP + treatment and Western blot was conducted in different groups. (H) Quantification graphs indicating the ratios of β-catenin/actin, c-Myc/actin and p-GSK-3β(ser9)/GSK-3β (the means ± SEM; n = 3; * p < 0.05, ** p < 0.01).
    Figure Legend Snippet: Als effectively rescued c-Myc from the MPP + -induced decline via Wnt signaling. (A) Cells transfected with pcDNA3.0-β-catenin were treated with MPP + (500 μM) for 24 h. Western blot was conducted in the Control, MPP + and MPP + +β-catenin groups. (B) Relative amounts of β-catenin/actin, c-Myc/actin and p- GSK-3β (ser9)/GSK-3β level were quantified (the means ± SEM; n = 3; * p < 0.05, ** p < 0.01). (C) Cells transfected with β-catenin siRNA were treated with MPP + (500 μM) for 24 h. Western blot was conducted in the Control siRNA, MPP + and β-catenin siRNA groups. (D) The ratios of β-catenin/actin, c-Myc/actin and p-GSK-3β(ser9)/GSK-3β were analyzed (the means ± SEM; n = 3; * p < 0.05, ** p < 0.01). (E) Cells transfected with pcDNA3.0 or pcDNA3.0-β-catenin were pretreated with Als for 24 h before MPP + treatment. Western blot was conducted in different groups. (F) Quantification graphs of the ratios of β-catenin/actin, c-Myc/actin and p-GSK-3β (ser9)/GSK-3β (the means ± SEM; n = 3; * p < 0.05, ** p < 0.01). (G) Cells transfected with control siRNA or β-catenin siRNA were pretreated with Als for 24 h before MPP + treatment and Western blot was conducted in different groups. (H) Quantification graphs indicating the ratios of β-catenin/actin, c-Myc/actin and p-GSK-3β(ser9)/GSK-3β (the means ± SEM; n = 3; * p < 0.05, ** p < 0.01).

    Techniques Used: Transfection, Western Blot

    anti p gsk 3β ser9  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
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    Cell Signaling Technology Inc anti p gsk 3β ser9
    NDRG2 represses Skp2 transcription via the suppression of β-catenin. a NDRG2 overexpression decreased the total and nuclear β-catenin expression. β-Actin and Lamin B served as internal controls. b, c HT29 cells were transfected with pcDNA3.1 or pcDNA3.1-NDRG2-overexpressing construct. b NDRG2 attenuated the induction of TCF/LEF activity following LiCl treatment or Wnt-3a expression. c, d The amount of TCF bound to the Skp2 promoter was determined by ChIP following NDRG2 overexpression c or knockdown d . e Levels of the indicated proteins were determined by western blotting in HT29 cells. f , g Levels of the indicated proteins f or Skp2 mRNA g were determined in HT29 cells treated for 24 h with the indicated concentrations of Chir99021. h Immunofluorescent staining and intensity quanification of <t>p-GSK-3β</t> and SKP2 were performed in intestinal epithelium from 2-month WT or NDRG2-/- mice. i Schematic representation of NDRG2 deletion mutants. The full length of NDRG2 contains NH2-terminal region, NDR domain (containing a putative α/β hydrolase fold), and carboxyl-terminal region. NDRG2 deletion mutants without NH2-terminal half (ΔN) or carboxyl-terminal half (ΔC) were generated as indicated. All constructs were tagged with FLAG. j , k We overexpressed full-length NDRG2, NDRG2ΔN, and NDRG2ΔC using relative expressing lentivirus in HT29 cells. The AKP activity i and indicated proteins j were determined, respectively
    Anti P Gsk 3β Ser9, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "NDRG2 facilitates colorectal cancer differentiation through the regulation of Skp2-p21/p27 axis"

    Article Title: NDRG2 facilitates colorectal cancer differentiation through the regulation of Skp2-p21/p27 axis

    Journal: Oncogene

    doi: 10.1038/s41388-017-0118-7

    NDRG2 represses Skp2 transcription via the suppression of β-catenin. a NDRG2 overexpression decreased the total and nuclear β-catenin expression. β-Actin and Lamin B served as internal controls. b, c HT29 cells were transfected with pcDNA3.1 or pcDNA3.1-NDRG2-overexpressing construct. b NDRG2 attenuated the induction of TCF/LEF activity following LiCl treatment or Wnt-3a expression. c, d The amount of TCF bound to the Skp2 promoter was determined by ChIP following NDRG2 overexpression c or knockdown d . e Levels of the indicated proteins were determined by western blotting in HT29 cells. f , g Levels of the indicated proteins f or Skp2 mRNA g were determined in HT29 cells treated for 24 h with the indicated concentrations of Chir99021. h Immunofluorescent staining and intensity quanification of p-GSK-3β and SKP2 were performed in intestinal epithelium from 2-month WT or NDRG2-/- mice. i Schematic representation of NDRG2 deletion mutants. The full length of NDRG2 contains NH2-terminal region, NDR domain (containing a putative α/β hydrolase fold), and carboxyl-terminal region. NDRG2 deletion mutants without NH2-terminal half (ΔN) or carboxyl-terminal half (ΔC) were generated as indicated. All constructs were tagged with FLAG. j , k We overexpressed full-length NDRG2, NDRG2ΔN, and NDRG2ΔC using relative expressing lentivirus in HT29 cells. The AKP activity i and indicated proteins j were determined, respectively
    Figure Legend Snippet: NDRG2 represses Skp2 transcription via the suppression of β-catenin. a NDRG2 overexpression decreased the total and nuclear β-catenin expression. β-Actin and Lamin B served as internal controls. b, c HT29 cells were transfected with pcDNA3.1 or pcDNA3.1-NDRG2-overexpressing construct. b NDRG2 attenuated the induction of TCF/LEF activity following LiCl treatment or Wnt-3a expression. c, d The amount of TCF bound to the Skp2 promoter was determined by ChIP following NDRG2 overexpression c or knockdown d . e Levels of the indicated proteins were determined by western blotting in HT29 cells. f , g Levels of the indicated proteins f or Skp2 mRNA g were determined in HT29 cells treated for 24 h with the indicated concentrations of Chir99021. h Immunofluorescent staining and intensity quanification of p-GSK-3β and SKP2 were performed in intestinal epithelium from 2-month WT or NDRG2-/- mice. i Schematic representation of NDRG2 deletion mutants. The full length of NDRG2 contains NH2-terminal region, NDR domain (containing a putative α/β hydrolase fold), and carboxyl-terminal region. NDRG2 deletion mutants without NH2-terminal half (ΔN) or carboxyl-terminal half (ΔC) were generated as indicated. All constructs were tagged with FLAG. j , k We overexpressed full-length NDRG2, NDRG2ΔN, and NDRG2ΔC using relative expressing lentivirus in HT29 cells. The AKP activity i and indicated proteins j were determined, respectively

    Techniques Used: Over Expression, Expressing, Transfection, Construct, Activity Assay, Western Blot, Staining, Generated

    rabbit anti p gsk 3β  (Cell Signaling Technology Inc)


    Bioz Manufacturer Symbol Cell Signaling Technology Inc manufactures this product  
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    Cell Signaling Technology Inc rabbit anti p gsk 3β
    Rabbit Anti P Gsk 3β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti p gsk 3β/product/Cell Signaling Technology Inc
    Average 96 stars, based on 1 article reviews
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    anti p gsk3 β ser9  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti p gsk3 β ser9
    Effect of PI3K/Akt-GSK-3 β signaling on EMT in FUT4 -overexpressing cells. ( a – c ) The cells were treated with 25 μ M of the specific <t>GSK3</t> β inhibitor SB415286 for 48 h. ( a ) The cellular protein levels of Snail and cyclin D were determined by western blot analysis. ( b ) The conditioned media were collected, and MMP-9 activities were determined by gelatin zymography. ( c ) Cell migratory activity was determined by wound-healing assay. Quantitative data are presented as the mean (±S.D.) percentage of migration distance ( n =10). ( d – f ) Cells were transfected with empty pcDNA3.1 vector or pcDNA3.1- FUT4, then treated with 20 μ M of PI3K inhibitor LY294002 for 24 h. ( d ) Total proteins were subjected to western blot analysis using phosphorylated Akt, GSK-3 β and Snail antibodies as described in Materials and Methods. ( e ) The secreted activity of MMP-9 was detected by gelatin zymography. ( f ) Cell migratory activity was determined using the wound-healing assay. Quantitative data are presented as the mean (±S.D.) percentage of migration distance ( n =10). *Indicates a significant difference compared with the respective control ( P <0.05). # Indicates a significant difference compared with MCF-7 cells ( P <0.05)
    Anti P Gsk3 β Ser9, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti p gsk3 β ser9/product/Cell Signaling Technology Inc
    Average 96 stars, based on 1 article reviews
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    1) Product Images from "Role of fucosyltransferase IV in epithelial–mesenchymal transition in breast cancer cells"

    Article Title: Role of fucosyltransferase IV in epithelial–mesenchymal transition in breast cancer cells

    Journal: Cell Death & Disease

    doi: 10.1038/cddis.2013.241

    Effect of PI3K/Akt-GSK-3 β signaling on EMT in FUT4 -overexpressing cells. ( a – c ) The cells were treated with 25 μ M of the specific GSK3 β inhibitor SB415286 for 48 h. ( a ) The cellular protein levels of Snail and cyclin D were determined by western blot analysis. ( b ) The conditioned media were collected, and MMP-9 activities were determined by gelatin zymography. ( c ) Cell migratory activity was determined by wound-healing assay. Quantitative data are presented as the mean (±S.D.) percentage of migration distance ( n =10). ( d – f ) Cells were transfected with empty pcDNA3.1 vector or pcDNA3.1- FUT4, then treated with 20 μ M of PI3K inhibitor LY294002 for 24 h. ( d ) Total proteins were subjected to western blot analysis using phosphorylated Akt, GSK-3 β and Snail antibodies as described in Materials and Methods. ( e ) The secreted activity of MMP-9 was detected by gelatin zymography. ( f ) Cell migratory activity was determined using the wound-healing assay. Quantitative data are presented as the mean (±S.D.) percentage of migration distance ( n =10). *Indicates a significant difference compared with the respective control ( P <0.05). # Indicates a significant difference compared with MCF-7 cells ( P <0.05)
    Figure Legend Snippet: Effect of PI3K/Akt-GSK-3 β signaling on EMT in FUT4 -overexpressing cells. ( a – c ) The cells were treated with 25 μ M of the specific GSK3 β inhibitor SB415286 for 48 h. ( a ) The cellular protein levels of Snail and cyclin D were determined by western blot analysis. ( b ) The conditioned media were collected, and MMP-9 activities were determined by gelatin zymography. ( c ) Cell migratory activity was determined by wound-healing assay. Quantitative data are presented as the mean (±S.D.) percentage of migration distance ( n =10). ( d – f ) Cells were transfected with empty pcDNA3.1 vector or pcDNA3.1- FUT4, then treated with 20 μ M of PI3K inhibitor LY294002 for 24 h. ( d ) Total proteins were subjected to western blot analysis using phosphorylated Akt, GSK-3 β and Snail antibodies as described in Materials and Methods. ( e ) The secreted activity of MMP-9 was detected by gelatin zymography. ( f ) Cell migratory activity was determined using the wound-healing assay. Quantitative data are presented as the mean (±S.D.) percentage of migration distance ( n =10). *Indicates a significant difference compared with the respective control ( P <0.05). # Indicates a significant difference compared with MCF-7 cells ( P <0.05)

    Techniques Used: Western Blot, Zymography, Activity Assay, Wound Healing Assay, Migration, Transfection, Plasmid Preparation

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