p gsk3 β ser9  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p gsk3 β ser9
    Leptin mediates β -catenin activation through the crosstalk between MTA1/WNT and PI3K/AKT pathways in HTR-8/SVneo cells. (a) HTR-8/SVneo cells were treated with exogenous leptin (0 and 200 ng/ml) for 24 h, and MTA1, WNT1, <t>p-GSK3</t> β <t>(Ser9),</t> and p-AKT (Ser473) levels were detected by Western blot. Data are shown as mean ± SD; ∗ P < 0.01 vs. leptin (0 ng/ml). (b) The knockdown efficiencies of MTA1 and WNT1 were analyzed by Western blot analysis and qRT-PCR. ∗ P < 0.05 vs. control. (c) HTR-8/SVneo cells were transfected with MTA1 siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of MTA1, WNT1, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. (d) HTR-8/SVneo cells were transfected with WNT1 siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of WNT1, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. (e) The knockdown efficiencies of AKT and β -catenin were analyzed by Western blot analysis and qRT-PCR. ∗ P < 0.05 vs. control. (f) HTR-8/SVneo cells were transfected with AKT siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of AKT, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. All experiments were performed in triplicate.
    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
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    Average 96 stars, based on 1 article reviews
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    96/100 stars

    Images

    1) Product Images from "Leptin Promotes HTR-8/SVneo Cell Invasion via the Crosstalk between MTA1/WNT and PI3K/AKT Pathways"

    Article Title: Leptin Promotes HTR-8/SVneo Cell Invasion via the Crosstalk between MTA1/WNT and PI3K/AKT Pathways

    Journal: Disease Markers

    doi: 10.1155/2022/7052176

    Leptin mediates β -catenin activation through the crosstalk between MTA1/WNT and PI3K/AKT pathways in HTR-8/SVneo cells. (a) HTR-8/SVneo cells were treated with exogenous leptin (0 and 200 ng/ml) for 24 h, and MTA1, WNT1, p-GSK3 β (Ser9), and p-AKT (Ser473) levels were detected by Western blot. Data are shown as mean ± SD; ∗ P < 0.01 vs. leptin (0 ng/ml). (b) The knockdown efficiencies of MTA1 and WNT1 were analyzed by Western blot analysis and qRT-PCR. ∗ P < 0.05 vs. control. (c) HTR-8/SVneo cells were transfected with MTA1 siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of MTA1, WNT1, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. (d) HTR-8/SVneo cells were transfected with WNT1 siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of WNT1, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. (e) The knockdown efficiencies of AKT and β -catenin were analyzed by Western blot analysis and qRT-PCR. ∗ P < 0.05 vs. control. (f) HTR-8/SVneo cells were transfected with AKT siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of AKT, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. All experiments were performed in triplicate.
    Figure Legend Snippet: Leptin mediates β -catenin activation through the crosstalk between MTA1/WNT and PI3K/AKT pathways in HTR-8/SVneo cells. (a) HTR-8/SVneo cells were treated with exogenous leptin (0 and 200 ng/ml) for 24 h, and MTA1, WNT1, p-GSK3 β (Ser9), and p-AKT (Ser473) levels were detected by Western blot. Data are shown as mean ± SD; ∗ P < 0.01 vs. leptin (0 ng/ml). (b) The knockdown efficiencies of MTA1 and WNT1 were analyzed by Western blot analysis and qRT-PCR. ∗ P < 0.05 vs. control. (c) HTR-8/SVneo cells were transfected with MTA1 siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of MTA1, WNT1, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. (d) HTR-8/SVneo cells were transfected with WNT1 siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of WNT1, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. (e) The knockdown efficiencies of AKT and β -catenin were analyzed by Western blot analysis and qRT-PCR. ∗ P < 0.05 vs. control. (f) HTR-8/SVneo cells were transfected with AKT siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of AKT, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. All experiments were performed in triplicate.

    Techniques Used: Activation Assay, Western Blot, Quantitative RT-PCR, Transfection, Expressing

    p gsk3 β ser9  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p gsk3 β ser9
    Leptin mediates β -catenin activation through the crosstalk between MTA1/WNT and PI3K/AKT pathways in HTR-8/SVneo cells. (a) HTR-8/SVneo cells were treated with exogenous leptin (0 and 200 ng/ml) for 24 h, and MTA1, WNT1, <t>p-GSK3</t> β <t>(Ser9),</t> and p-AKT (Ser473) levels were detected by Western blot. Data are shown as mean ± SD; ∗ P < 0.01 vs. leptin (0 ng/ml). (b) The knockdown efficiencies of MTA1 and WNT1 were analyzed by Western blot analysis and qRT-PCR. ∗ P < 0.05 vs. control. (c) HTR-8/SVneo cells were transfected with MTA1 siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of MTA1, WNT1, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. (d) HTR-8/SVneo cells were transfected with WNT1 siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of WNT1, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. (e) The knockdown efficiencies of AKT and β -catenin were analyzed by Western blot analysis and qRT-PCR. ∗ P < 0.05 vs. control. (f) HTR-8/SVneo cells were transfected with AKT siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of AKT, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. All experiments were performed in triplicate.
    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/p gsk3 β ser9/product/Cell Signaling Technology Inc
    Average 96 stars, based on 1 article reviews
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    96/100 stars

    Images

    1) Product Images from "Leptin Promotes HTR-8/SVneo Cell Invasion via the Crosstalk between MTA1/WNT and PI3K/AKT Pathways"

    Article Title: Leptin Promotes HTR-8/SVneo Cell Invasion via the Crosstalk between MTA1/WNT and PI3K/AKT Pathways

    Journal: Disease Markers

    doi: 10.1155/2022/7052176

    Leptin mediates β -catenin activation through the crosstalk between MTA1/WNT and PI3K/AKT pathways in HTR-8/SVneo cells. (a) HTR-8/SVneo cells were treated with exogenous leptin (0 and 200 ng/ml) for 24 h, and MTA1, WNT1, p-GSK3 β (Ser9), and p-AKT (Ser473) levels were detected by Western blot. Data are shown as mean ± SD; ∗ P < 0.01 vs. leptin (0 ng/ml). (b) The knockdown efficiencies of MTA1 and WNT1 were analyzed by Western blot analysis and qRT-PCR. ∗ P < 0.05 vs. control. (c) HTR-8/SVneo cells were transfected with MTA1 siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of MTA1, WNT1, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. (d) HTR-8/SVneo cells were transfected with WNT1 siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of WNT1, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. (e) The knockdown efficiencies of AKT and β -catenin were analyzed by Western blot analysis and qRT-PCR. ∗ P < 0.05 vs. control. (f) HTR-8/SVneo cells were transfected with AKT siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of AKT, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. All experiments were performed in triplicate.
    Figure Legend Snippet: Leptin mediates β -catenin activation through the crosstalk between MTA1/WNT and PI3K/AKT pathways in HTR-8/SVneo cells. (a) HTR-8/SVneo cells were treated with exogenous leptin (0 and 200 ng/ml) for 24 h, and MTA1, WNT1, p-GSK3 β (Ser9), and p-AKT (Ser473) levels were detected by Western blot. Data are shown as mean ± SD; ∗ P < 0.01 vs. leptin (0 ng/ml). (b) The knockdown efficiencies of MTA1 and WNT1 were analyzed by Western blot analysis and qRT-PCR. ∗ P < 0.05 vs. control. (c) HTR-8/SVneo cells were transfected with MTA1 siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of MTA1, WNT1, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. (d) HTR-8/SVneo cells were transfected with WNT1 siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of WNT1, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. (e) The knockdown efficiencies of AKT and β -catenin were analyzed by Western blot analysis and qRT-PCR. ∗ P < 0.05 vs. control. (f) HTR-8/SVneo cells were transfected with AKT siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of AKT, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. All experiments were performed in triplicate.

    Techniques Used: Activation Assay, Western Blot, Quantitative RT-PCR, Transfection, Expressing

    p gsk3 β  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p gsk3 β
    Protein expression in GA muscle samples from rats treated with n-3 PUFA or vehicle for 40 days and dexamethasone or vehicle (last 10 days). Relative optical density of total Akt (tAkt) and phosphorylated Akt (P-Akt) ((a) and (c)), total <t>GSK3</t> <t>β</t> (tGSK3 β ) and phosphorylated GSK3 β (P-GSK3 β ) ((b) and (d)), and tAkt/P-Akt and tGSK3 β /P-GSK3 β ratios ((e) and (f), resp.). Bands representing tAkt, P-Akt, tGSK3, and P-GSK3 β are illustrated in (g). α -Tubulin (55 kDa) was used as control. The numbers represent the mean ± S.E.M. CT = control group ( n = 6), DX = dexamethasone group ( n = 5), n-3 = n-3 PUFA group ( n = 6), and DX + n-3 = dexamethasone + n-3 PUFA group ( n = 6). Values represent means ± S.E.M., analyzed by Student's t -test, # P < 0.05.
    P Gsk3 β, 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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    Images

    1) Product Images from "The Effects of Omega-3 Fatty Acid Supplementation on Dexamethasone-Induced Muscle Atrophy"

    Article Title: The Effects of Omega-3 Fatty Acid Supplementation on Dexamethasone-Induced Muscle Atrophy

    Journal: BioMed Research International

    doi: 10.1155/2014/961438

    Protein expression in GA muscle samples from rats treated with n-3 PUFA or vehicle for 40 days and dexamethasone or vehicle (last 10 days). Relative optical density of total Akt (tAkt) and phosphorylated Akt (P-Akt) ((a) and (c)), total GSK3 β (tGSK3 β ) and phosphorylated GSK3 β (P-GSK3 β ) ((b) and (d)), and tAkt/P-Akt and tGSK3 β /P-GSK3 β ratios ((e) and (f), resp.). Bands representing tAkt, P-Akt, tGSK3, and P-GSK3 β are illustrated in (g). α -Tubulin (55 kDa) was used as control. The numbers represent the mean ± S.E.M. CT = control group ( n = 6), DX = dexamethasone group ( n = 5), n-3 = n-3 PUFA group ( n = 6), and DX + n-3 = dexamethasone + n-3 PUFA group ( n = 6). Values represent means ± S.E.M., analyzed by Student's t -test, # P < 0.05.
    Figure Legend Snippet: Protein expression in GA muscle samples from rats treated with n-3 PUFA or vehicle for 40 days and dexamethasone or vehicle (last 10 days). Relative optical density of total Akt (tAkt) and phosphorylated Akt (P-Akt) ((a) and (c)), total GSK3 β (tGSK3 β ) and phosphorylated GSK3 β (P-GSK3 β ) ((b) and (d)), and tAkt/P-Akt and tGSK3 β /P-GSK3 β ratios ((e) and (f), resp.). Bands representing tAkt, P-Akt, tGSK3, and P-GSK3 β are illustrated in (g). α -Tubulin (55 kDa) was used as control. The numbers represent the mean ± S.E.M. CT = control group ( n = 6), DX = dexamethasone group ( n = 5), n-3 = n-3 PUFA group ( n = 6), and DX + n-3 = dexamethasone + n-3 PUFA group ( n = 6). Values represent means ± S.E.M., analyzed by Student's t -test, # P < 0.05.

    Techniques Used: Expressing

    phospho gsk3 beta ser9 position  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phospho gsk3 beta ser9 position
    NF and KF cells were treated with Wnt5a (3μg/ml) for 72 hours and equal amounts of cell lysates were analyzed for total β-catenin and phosphorylated β-catenin at Ser45/Thr41 and at Ser33/37/Thr41 positions and total <t>GSK3-β</t> and phosphorylated GSK3-β at Ser 9 position using Western blot analyses. Both NF and KF showed a significant increase (relative to β-actin; p<0.05) in the total β-catenin (Fig. A), phosphorylated β-catenin at Ser33/37/Thr41 position (Fig. C). No significant change was found in phosphorylated β-catenin at Ser45/Thr41 (Fig. B). The Western blot bands are representative for one NF and one KF case. Data represent the mean ± SD of triplicate measurements from the three NF and three KF cases.
    Phospho Gsk3 Beta Ser9 Position, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 88/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Identification and Characterization of Wnt Signaling Pathway in Keloid Pathogenesis"

    Article Title: Identification and Characterization of Wnt Signaling Pathway in Keloid Pathogenesis

    Journal: International Journal of Medical Sciences

    doi: 10.7150/ijms.5349

    NF and KF cells were treated with Wnt5a (3μg/ml) for 72 hours and equal amounts of cell lysates were analyzed for total β-catenin and phosphorylated β-catenin at Ser45/Thr41 and at Ser33/37/Thr41 positions and total GSK3-β and phosphorylated GSK3-β at Ser 9 position using Western blot analyses. Both NF and KF showed a significant increase (relative to β-actin; p<0.05) in the total β-catenin (Fig. A), phosphorylated β-catenin at Ser33/37/Thr41 position (Fig. C). No significant change was found in phosphorylated β-catenin at Ser45/Thr41 (Fig. B). The Western blot bands are representative for one NF and one KF case. Data represent the mean ± SD of triplicate measurements from the three NF and three KF cases.
    Figure Legend Snippet: NF and KF cells were treated with Wnt5a (3μg/ml) for 72 hours and equal amounts of cell lysates were analyzed for total β-catenin and phosphorylated β-catenin at Ser45/Thr41 and at Ser33/37/Thr41 positions and total GSK3-β and phosphorylated GSK3-β at Ser 9 position using Western blot analyses. Both NF and KF showed a significant increase (relative to β-actin; p<0.05) in the total β-catenin (Fig. A), phosphorylated β-catenin at Ser33/37/Thr41 position (Fig. C). No significant change was found in phosphorylated β-catenin at Ser45/Thr41 (Fig. B). The Western blot bands are representative for one NF and one KF case. Data represent the mean ± SD of triplicate measurements from the three NF and three KF cases.

    Techniques Used: Western Blot

    NF and KF cells were treated with Wnt5a (3μg/ml) for 72 hours and equal amounts of cell lysates were analyzed for total GSK3-β and phosphorylated GSK3-β at Ser 9 position using Western blot analyses. Both NF and KF showed a significant increase (relative to β-actin; p<0.05) in the phosphorylated/inactivated GSK3-β level (Fig. B). No significant change was found in total GSK3-β (Fig. A). The Western blot band bands are representative for one NF and one KF case. Data represent the mean ± SD of triplicate measurements from the three NF and three KF cases.
    Figure Legend Snippet: NF and KF cells were treated with Wnt5a (3μg/ml) for 72 hours and equal amounts of cell lysates were analyzed for total GSK3-β and phosphorylated GSK3-β at Ser 9 position using Western blot analyses. Both NF and KF showed a significant increase (relative to β-actin; p<0.05) in the phosphorylated/inactivated GSK3-β level (Fig. B). No significant change was found in total GSK3-β (Fig. A). The Western blot band bands are representative for one NF and one KF case. Data represent the mean ± SD of triplicate measurements from the three NF and three KF cases.

    Techniques Used: Western Blot

    A proposed schematic representation of Wnt5a/β-catenin signaling in keloid pathogenesis. In KF, binding of the Wnt5a to FZD receptors and LRP5/6 activates Dvl which in turn inhibits β-catenin destruction complex (APC, GSK3-β, Axin) by increased phosphorylation of GSK3-β at Ser 9 position (GSK3-β inactivation) leading to the accumulation of β-catenin in the cytoplasm and translocation into the nucleus to regulate target gene transcription in cooperation with TCF and LEF family transcription factors.
    Figure Legend Snippet: A proposed schematic representation of Wnt5a/β-catenin signaling in keloid pathogenesis. In KF, binding of the Wnt5a to FZD receptors and LRP5/6 activates Dvl which in turn inhibits β-catenin destruction complex (APC, GSK3-β, Axin) by increased phosphorylation of GSK3-β at Ser 9 position (GSK3-β inactivation) leading to the accumulation of β-catenin in the cytoplasm and translocation into the nucleus to regulate target gene transcription in cooperation with TCF and LEF family transcription factors.

    Techniques Used: Binding Assay, Translocation Assay

    anti phospho-gsk3 β (ser9)  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti phospho-gsk3 β (ser9)
    Anti Phospho Gsk3 β (Ser9), supplied by Cell Signaling Technology Inc, 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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    Average 86 stars, based on 1 article reviews
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    p gsk3 β  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p gsk3 β
    Antibody details for western immunoblotting.
    P Gsk3 β, 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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    Average 96 stars, based on 1 article reviews
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    96/100 stars

    Images

    1) Product Images from "Preserved Left Ventricular Function despite Myocardial Fibrosis and Myopathy in the Dystrophin-Deficient D2.B10-Dmd mdx /J Mouse"

    Article Title: Preserved Left Ventricular Function despite Myocardial Fibrosis and Myopathy in the Dystrophin-Deficient D2.B10-Dmd mdx /J Mouse

    Journal: Oxidative Medicine and Cellular Longevity

    doi: 10.1155/2022/5362115

    Antibody details for western immunoblotting.
    Figure Legend Snippet: Antibody details for western immunoblotting.

    Techniques Used: Western Blot, Molecular Weight

    anti phospho gsk3 β  (Cell Signaling Technology Inc)


    Bioz Verified Symbol Cell Signaling Technology Inc is a verified supplier
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    Cell Signaling Technology Inc anti phospho gsk3 β
    The effect of BZA on <t>AKT/GSK3</t> β , AMPK α , and MAPK signal pathways. The relative quantitative results of PPAR- α , P-AKT, P-GSK3 β , P-ERK, P-P38, and P-AMPK α in the four groups ( n = 6).
    Anti Phospho Gsk3 β, 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 "Bezafibrate Attenuates Pressure Overload-Induced Cardiac Hypertrophy and Fibrosis"

    Article Title: Bezafibrate Attenuates Pressure Overload-Induced Cardiac Hypertrophy and Fibrosis

    Journal: PPAR Research

    doi: 10.1155/2017/5789714

    The effect of BZA on AKT/GSK3 β , AMPK α , and MAPK signal pathways. The relative quantitative results of PPAR- α , P-AKT, P-GSK3 β , P-ERK, P-P38, and P-AMPK α in the four groups ( n = 6).
    Figure Legend Snippet: The effect of BZA on AKT/GSK3 β , AMPK α , and MAPK signal pathways. The relative quantitative results of PPAR- α , P-AKT, P-GSK3 β , P-ERK, P-P38, and P-AMPK α in the four groups ( n = 6).

    Techniques Used:

    rabbit anti phospho gsk3 ser9  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rabbit anti phospho gsk3 ser9
    Rabbit Anti Phospho Gsk3 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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    phospho gsk3 β 5558 monoclonal antibody  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phospho gsk3 β 5558 monoclonal antibody
    BHD activates NRF2 and promotes the phosphorylation of <t>AKT/GSK3</t> β during revascularization. The protein expression and quantitative analysis of NRF2 in nuclear and the phosphorylation and quantitative analysis of Akt and GSK3 β of tissue in ischemic area after 14 days of BHD treatment ( n = 4). Mean ± SD. ∗ P < 0.05, compared with HLI+NS group.
    Phospho Gsk3 β 5558 Monoclonal Antibody, 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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    Images

    1) Product Images from "Buyang Huanwu Decoction Enhances Revascularization via Akt/GSK3 β /NRF2 Pathway in Diabetic Hindlimb Ischemia"

    Article Title: Buyang Huanwu Decoction Enhances Revascularization via Akt/GSK3 β /NRF2 Pathway in Diabetic Hindlimb Ischemia

    Journal: Oxidative Medicine and Cellular Longevity

    doi: 10.1155/2021/1470829

    BHD activates NRF2 and promotes the phosphorylation of AKT/GSK3 β during revascularization. The protein expression and quantitative analysis of NRF2 in nuclear and the phosphorylation and quantitative analysis of Akt and GSK3 β of tissue in ischemic area after 14 days of BHD treatment ( n = 4). Mean ± SD. ∗ P < 0.05, compared with HLI+NS group.
    Figure Legend Snippet: BHD activates NRF2 and promotes the phosphorylation of AKT/GSK3 β during revascularization. The protein expression and quantitative analysis of NRF2 in nuclear and the phosphorylation and quantitative analysis of Akt and GSK3 β of tissue in ischemic area after 14 days of BHD treatment ( n = 4). Mean ± SD. ∗ P < 0.05, compared with HLI+NS group.

    Techniques Used: Expressing

    BHD promotes revascularization of hindlimb of HLI mice via AKT/GSK3 β /NRF2 signal pathway. (a) The mRNA expression of NRF2 after injection of Ad-NRF2-shRNA ( n = 4). (b, c) The tissue perfusion of hindlimb in HLI mice after 0, 7, and 14 days of BHD treatment ( n = 4). (d–f) The protein expression and quantitative analysis of NRF2, VEGFA, TNF- α , IL-1 β , IL-6, CAT, NQO-1, and HO-1 and the phosphorylation and quantitative analysis of Akt and GSK3 β in ischemic area after 14 days of BHD treatment ( n = 4). Mean ± SD. NS, P > 0.05; ∗ P < 0.05, compared with HLI+BHD+sh-NRF2 group.
    Figure Legend Snippet: BHD promotes revascularization of hindlimb of HLI mice via AKT/GSK3 β /NRF2 signal pathway. (a) The mRNA expression of NRF2 after injection of Ad-NRF2-shRNA ( n = 4). (b, c) The tissue perfusion of hindlimb in HLI mice after 0, 7, and 14 days of BHD treatment ( n = 4). (d–f) The protein expression and quantitative analysis of NRF2, VEGFA, TNF- α , IL-1 β , IL-6, CAT, NQO-1, and HO-1 and the phosphorylation and quantitative analysis of Akt and GSK3 β in ischemic area after 14 days of BHD treatment ( n = 4). Mean ± SD. NS, P > 0.05; ∗ P < 0.05, compared with HLI+BHD+sh-NRF2 group.

    Techniques Used: Expressing, Injection, shRNA

    BHD activates NRF2 through Akt/GSK3 β signal pathway. After injection of inhibitor, the protein expression and quantitative analysis of NRF2 in nuclear and the phosphorylation and quantitative analysis of Akt and GSK3 β in ischemic area ( n = 4). Mean ± SD. ∗ P < 0.05, compared with HLI+BHD group.
    Figure Legend Snippet: BHD activates NRF2 through Akt/GSK3 β signal pathway. After injection of inhibitor, the protein expression and quantitative analysis of NRF2 in nuclear and the phosphorylation and quantitative analysis of Akt and GSK3 β in ischemic area ( n = 4). Mean ± SD. ∗ P < 0.05, compared with HLI+BHD group.

    Techniques Used: Injection, Expressing

    anti phospho gsk3 β  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti phospho gsk3 β
    PIO protects against cardiac hypertrophy by inhibition of MAPK and <t>AKT/GSK3</t> β pathways. Representative and quantitative expression of PPAR γ , phosphorylated AKT, <t>GSK3</t> <t>β</t> , ERK, P38, and the effects of PIO in group of AB or sham with or without PIO ( n = 6). ∗ P < 0.05.
    Anti Phospho Gsk3 β, 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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    Images

    1) Product Images from "Pioglitazone Protected against Cardiac Hypertrophy via Inhibiting AKT/GSK3 β and MAPK Signaling Pathways"

    Article Title: Pioglitazone Protected against Cardiac Hypertrophy via Inhibiting AKT/GSK3 β and MAPK Signaling Pathways

    Journal: PPAR Research

    doi: 10.1155/2016/9174190

    PIO protects against cardiac hypertrophy by inhibition of MAPK and AKT/GSK3 β pathways. Representative and quantitative expression of PPAR γ , phosphorylated AKT, GSK3 β , ERK, P38, and the effects of PIO in group of AB or sham with or without PIO ( n = 6). ∗ P < 0.05.
    Figure Legend Snippet: PIO protects against cardiac hypertrophy by inhibition of MAPK and AKT/GSK3 β pathways. Representative and quantitative expression of PPAR γ , phosphorylated AKT, GSK3 β , ERK, P38, and the effects of PIO in group of AB or sham with or without PIO ( n = 6). ∗ P < 0.05.

    Techniques Used: Inhibition, Expressing

    rabbit anti phospho gsk3 β  (Cell Signaling Technology Inc)


    Bioz Verified Symbol Cell Signaling Technology Inc is a verified supplier
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    Cell Signaling Technology Inc rabbit anti phospho gsk3 β
    Rabbit Anti Phospho Gsk3 β, 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 gsk3 β ser9  (Cell Signaling Technology Inc)
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    Cell Signaling Technology Inc p gsk3 β ser9
    Leptin mediates β -catenin activation through the crosstalk between MTA1/WNT and PI3K/AKT pathways in HTR-8/SVneo cells. (a) HTR-8/SVneo cells were treated with exogenous leptin (0 and 200 ng/ml) for 24 h, and MTA1, WNT1, <t>p-GSK3</t> β <t>(Ser9),</t> and p-AKT (Ser473) levels were detected by Western blot. Data are shown as mean ± SD; ∗ P < 0.01 vs. leptin (0 ng/ml). (b) The knockdown efficiencies of MTA1 and WNT1 were analyzed by Western blot analysis and qRT-PCR. ∗ P < 0.05 vs. control. (c) HTR-8/SVneo cells were transfected with MTA1 siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of MTA1, WNT1, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. (d) HTR-8/SVneo cells were transfected with WNT1 siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of WNT1, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. (e) The knockdown efficiencies of AKT and β -catenin were analyzed by Western blot analysis and qRT-PCR. ∗ P < 0.05 vs. control. (f) HTR-8/SVneo cells were transfected with AKT siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of AKT, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. All experiments were performed in triplicate.
    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
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    p gsk3 β  (Cell Signaling Technology Inc)
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    Protein expression in GA muscle samples from rats treated with n-3 PUFA or vehicle for 40 days and dexamethasone or vehicle (last 10 days). Relative optical density of total Akt (tAkt) and phosphorylated Akt (P-Akt) ((a) and (c)), total <t>GSK3</t> <t>β</t> (tGSK3 β ) and phosphorylated GSK3 β (P-GSK3 β ) ((b) and (d)), and tAkt/P-Akt and tGSK3 β /P-GSK3 β ratios ((e) and (f), resp.). Bands representing tAkt, P-Akt, tGSK3, and P-GSK3 β are illustrated in (g). α -Tubulin (55 kDa) was used as control. The numbers represent the mean ± S.E.M. CT = control group ( n = 6), DX = dexamethasone group ( n = 5), n-3 = n-3 PUFA group ( n = 6), and DX + n-3 = dexamethasone + n-3 PUFA group ( n = 6). Values represent means ± S.E.M., analyzed by Student's t -test, # P < 0.05.
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    NF and KF cells were treated with Wnt5a (3μg/ml) for 72 hours and equal amounts of cell lysates were analyzed for total β-catenin and phosphorylated β-catenin at Ser45/Thr41 and at Ser33/37/Thr41 positions and total <t>GSK3-β</t> and phosphorylated GSK3-β at Ser 9 position using Western blot analyses. Both NF and KF showed a significant increase (relative to β-actin; p<0.05) in the total β-catenin (Fig. A), phosphorylated β-catenin at Ser33/37/Thr41 position (Fig. C). No significant change was found in phosphorylated β-catenin at Ser45/Thr41 (Fig. B). The Western blot bands are representative for one NF and one KF case. Data represent the mean ± SD of triplicate measurements from the three NF and three KF cases.
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    anti phospho-gsk3 β (ser9)  (Cell Signaling Technology Inc)
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    NF and KF cells were treated with Wnt5a (3μg/ml) for 72 hours and equal amounts of cell lysates were analyzed for total β-catenin and phosphorylated β-catenin at Ser45/Thr41 and at Ser33/37/Thr41 positions and total <t>GSK3-β</t> and phosphorylated GSK3-β at Ser 9 position using Western blot analyses. Both NF and KF showed a significant increase (relative to β-actin; p<0.05) in the total β-catenin (Fig. A), phosphorylated β-catenin at Ser33/37/Thr41 position (Fig. C). No significant change was found in phosphorylated β-catenin at Ser45/Thr41 (Fig. B). The Western blot bands are representative for one NF and one KF case. Data represent the mean ± SD of triplicate measurements from the three NF and three KF cases.
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    The effect of BZA on <t>AKT/GSK3</t> β , AMPK α , and MAPK signal pathways. The relative quantitative results of PPAR- α , P-AKT, P-GSK3 β , P-ERK, P-P38, and P-AMPK α in the four groups ( n = 6).
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    rabbit anti phospho gsk3 ser9  (Cell Signaling Technology Inc)
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    The effect of BZA on <t>AKT/GSK3</t> β , AMPK α , and MAPK signal pathways. The relative quantitative results of PPAR- α , P-AKT, P-GSK3 β , P-ERK, P-P38, and P-AMPK α in the four groups ( n = 6).
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    phospho gsk3 β 5558 monoclonal antibody  (Cell Signaling Technology Inc)
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    BHD activates NRF2 and promotes the phosphorylation of <t>AKT/GSK3</t> β during revascularization. The protein expression and quantitative analysis of NRF2 in nuclear and the phosphorylation and quantitative analysis of Akt and GSK3 β of tissue in ischemic area after 14 days of BHD treatment ( n = 4). Mean ± SD. ∗ P < 0.05, compared with HLI+NS group.
    Phospho Gsk3 β 5558 Monoclonal Antibody, 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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    BHD activates NRF2 and promotes the phosphorylation of <t>AKT/GSK3</t> β during revascularization. The protein expression and quantitative analysis of NRF2 in nuclear and the phosphorylation and quantitative analysis of Akt and GSK3 β of tissue in ischemic area after 14 days of BHD treatment ( n = 4). Mean ± SD. ∗ P < 0.05, compared with HLI+NS group.
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    Image Search Results


    Leptin mediates β -catenin activation through the crosstalk between MTA1/WNT and PI3K/AKT pathways in HTR-8/SVneo cells. (a) HTR-8/SVneo cells were treated with exogenous leptin (0 and 200 ng/ml) for 24 h, and MTA1, WNT1, p-GSK3 β (Ser9), and p-AKT (Ser473) levels were detected by Western blot. Data are shown as mean ± SD; ∗ P < 0.01 vs. leptin (0 ng/ml). (b) The knockdown efficiencies of MTA1 and WNT1 were analyzed by Western blot analysis and qRT-PCR. ∗ P < 0.05 vs. control. (c) HTR-8/SVneo cells were transfected with MTA1 siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of MTA1, WNT1, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. (d) HTR-8/SVneo cells were transfected with WNT1 siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of WNT1, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. (e) The knockdown efficiencies of AKT and β -catenin were analyzed by Western blot analysis and qRT-PCR. ∗ P < 0.05 vs. control. (f) HTR-8/SVneo cells were transfected with AKT siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of AKT, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. All experiments were performed in triplicate.

    Journal: Disease Markers

    Article Title: Leptin Promotes HTR-8/SVneo Cell Invasion via the Crosstalk between MTA1/WNT and PI3K/AKT Pathways

    doi: 10.1155/2022/7052176

    Figure Lengend Snippet: Leptin mediates β -catenin activation through the crosstalk between MTA1/WNT and PI3K/AKT pathways in HTR-8/SVneo cells. (a) HTR-8/SVneo cells were treated with exogenous leptin (0 and 200 ng/ml) for 24 h, and MTA1, WNT1, p-GSK3 β (Ser9), and p-AKT (Ser473) levels were detected by Western blot. Data are shown as mean ± SD; ∗ P < 0.01 vs. leptin (0 ng/ml). (b) The knockdown efficiencies of MTA1 and WNT1 were analyzed by Western blot analysis and qRT-PCR. ∗ P < 0.05 vs. control. (c) HTR-8/SVneo cells were transfected with MTA1 siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of MTA1, WNT1, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. (d) HTR-8/SVneo cells were transfected with WNT1 siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of WNT1, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. (e) The knockdown efficiencies of AKT and β -catenin were analyzed by Western blot analysis and qRT-PCR. ∗ P < 0.05 vs. control. (f) HTR-8/SVneo cells were transfected with AKT siRNA or scramble siRNA (Scr) in the presence or absence of 200 ng/ml leptin for 24 h, and Western blot analysis was performed to detect the expression of AKT, p-GSK3 β (Ser9), and nuclear β -catenin. ∗ P < 0.01 vs. control and # P < 0.01 vs. leptin. All experiments were performed in triplicate.

    Article Snippet: The following primary antibodies were used: MMP9 (ab76003), MTA1 (ab71153), WNT1 (ab15251), AKT (ab179463), GSK3 β (ab32391), β -catenin (ab32572), histone 3 (ab1791), β -actin (ab6276) (Abcam, USA); p-AKT (Ser473) (#4060), p-GSK3 β (Ser9) (#9322) (Cell Signaling Technology, USA).

    Techniques: Activation Assay, Western Blot, Quantitative RT-PCR, Transfection, Expressing

    Protein expression in GA muscle samples from rats treated with n-3 PUFA or vehicle for 40 days and dexamethasone or vehicle (last 10 days). Relative optical density of total Akt (tAkt) and phosphorylated Akt (P-Akt) ((a) and (c)), total GSK3 β (tGSK3 β ) and phosphorylated GSK3 β (P-GSK3 β ) ((b) and (d)), and tAkt/P-Akt and tGSK3 β /P-GSK3 β ratios ((e) and (f), resp.). Bands representing tAkt, P-Akt, tGSK3, and P-GSK3 β are illustrated in (g). α -Tubulin (55 kDa) was used as control. The numbers represent the mean ± S.E.M. CT = control group ( n = 6), DX = dexamethasone group ( n = 5), n-3 = n-3 PUFA group ( n = 6), and DX + n-3 = dexamethasone + n-3 PUFA group ( n = 6). Values represent means ± S.E.M., analyzed by Student's t -test, # P < 0.05.

    Journal: BioMed Research International

    Article Title: The Effects of Omega-3 Fatty Acid Supplementation on Dexamethasone-Induced Muscle Atrophy

    doi: 10.1155/2014/961438

    Figure Lengend Snippet: Protein expression in GA muscle samples from rats treated with n-3 PUFA or vehicle for 40 days and dexamethasone or vehicle (last 10 days). Relative optical density of total Akt (tAkt) and phosphorylated Akt (P-Akt) ((a) and (c)), total GSK3 β (tGSK3 β ) and phosphorylated GSK3 β (P-GSK3 β ) ((b) and (d)), and tAkt/P-Akt and tGSK3 β /P-GSK3 β ratios ((e) and (f), resp.). Bands representing tAkt, P-Akt, tGSK3, and P-GSK3 β are illustrated in (g). α -Tubulin (55 kDa) was used as control. The numbers represent the mean ± S.E.M. CT = control group ( n = 6), DX = dexamethasone group ( n = 5), n-3 = n-3 PUFA group ( n = 6), and DX + n-3 = dexamethasone + n-3 PUFA group ( n = 6). Values represent means ± S.E.M., analyzed by Student's t -test, # P < 0.05.

    Article Snippet: The primary antibodies used were Akt (1 : 2,000, Cell Signaling #4691), P-Akt (1 : 2,000, Cell Signaling #4060, Ser473); mTOR (1 : 500, Cell Signaling #2972), P-mTOR (1 : 500, Cell Signaling #2971, Ser2448), GSK3 β (1 : 2,000, Cell Signaling #9315), P-GSK3 β (1 : 2,000, Cell Signaling #9322, Ser9), FoXO3a (1 : 500, Cell Signaling #2497), P-FoXO3a (1 : 500, Cell Signaling #9466, Ser253), and α -tubulin (1 : 30,000, Hybridoma bank) in 5% BSA/TBS-T.

    Techniques: Expressing

    NF and KF cells were treated with Wnt5a (3μg/ml) for 72 hours and equal amounts of cell lysates were analyzed for total β-catenin and phosphorylated β-catenin at Ser45/Thr41 and at Ser33/37/Thr41 positions and total GSK3-β and phosphorylated GSK3-β at Ser 9 position using Western blot analyses. Both NF and KF showed a significant increase (relative to β-actin; p<0.05) in the total β-catenin (Fig. A), phosphorylated β-catenin at Ser33/37/Thr41 position (Fig. C). No significant change was found in phosphorylated β-catenin at Ser45/Thr41 (Fig. B). The Western blot bands are representative for one NF and one KF case. Data represent the mean ± SD of triplicate measurements from the three NF and three KF cases.

    Journal: International Journal of Medical Sciences

    Article Title: Identification and Characterization of Wnt Signaling Pathway in Keloid Pathogenesis

    doi: 10.7150/ijms.5349

    Figure Lengend Snippet: NF and KF cells were treated with Wnt5a (3μg/ml) for 72 hours and equal amounts of cell lysates were analyzed for total β-catenin and phosphorylated β-catenin at Ser45/Thr41 and at Ser33/37/Thr41 positions and total GSK3-β and phosphorylated GSK3-β at Ser 9 position using Western blot analyses. Both NF and KF showed a significant increase (relative to β-actin; p<0.05) in the total β-catenin (Fig. A), phosphorylated β-catenin at Ser33/37/Thr41 position (Fig. C). No significant change was found in phosphorylated β-catenin at Ser45/Thr41 (Fig. B). The Western blot bands are representative for one NF and one KF case. Data represent the mean ± SD of triplicate measurements from the three NF and three KF cases.

    Article Snippet: Polyclonal rabbit antibodies were against Wnt5a (Lifespan Biosciences, Seattle, WA), phospho-beta-catenin Ser33/37/Thr41 and phospho-beta-catenin Ser45/Thr41 positions, and phospho-GSK3-beta Ser9 position (Cell Signalling Technology Inc., Beverly, MA), and monoclonal mouse antibodies were against FZD4 (R&D Systems, Minneapolis, MN), ROR2 (Santa Cruz Biotechnology, Inc., LA), beta-catenin (Upstate Biotechnology, Waltham, MA), beta-actin (Sigma-Aldrich, St. Louis, MO).

    Techniques: Western Blot

    NF and KF cells were treated with Wnt5a (3μg/ml) for 72 hours and equal amounts of cell lysates were analyzed for total GSK3-β and phosphorylated GSK3-β at Ser 9 position using Western blot analyses. Both NF and KF showed a significant increase (relative to β-actin; p<0.05) in the phosphorylated/inactivated GSK3-β level (Fig. B). No significant change was found in total GSK3-β (Fig. A). The Western blot band bands are representative for one NF and one KF case. Data represent the mean ± SD of triplicate measurements from the three NF and three KF cases.

    Journal: International Journal of Medical Sciences

    Article Title: Identification and Characterization of Wnt Signaling Pathway in Keloid Pathogenesis

    doi: 10.7150/ijms.5349

    Figure Lengend Snippet: NF and KF cells were treated with Wnt5a (3μg/ml) for 72 hours and equal amounts of cell lysates were analyzed for total GSK3-β and phosphorylated GSK3-β at Ser 9 position using Western blot analyses. Both NF and KF showed a significant increase (relative to β-actin; p<0.05) in the phosphorylated/inactivated GSK3-β level (Fig. B). No significant change was found in total GSK3-β (Fig. A). The Western blot band bands are representative for one NF and one KF case. Data represent the mean ± SD of triplicate measurements from the three NF and three KF cases.

    Article Snippet: Polyclonal rabbit antibodies were against Wnt5a (Lifespan Biosciences, Seattle, WA), phospho-beta-catenin Ser33/37/Thr41 and phospho-beta-catenin Ser45/Thr41 positions, and phospho-GSK3-beta Ser9 position (Cell Signalling Technology Inc., Beverly, MA), and monoclonal mouse antibodies were against FZD4 (R&D Systems, Minneapolis, MN), ROR2 (Santa Cruz Biotechnology, Inc., LA), beta-catenin (Upstate Biotechnology, Waltham, MA), beta-actin (Sigma-Aldrich, St. Louis, MO).

    Techniques: Western Blot

    A proposed schematic representation of Wnt5a/β-catenin signaling in keloid pathogenesis. In KF, binding of the Wnt5a to FZD receptors and LRP5/6 activates Dvl which in turn inhibits β-catenin destruction complex (APC, GSK3-β, Axin) by increased phosphorylation of GSK3-β at Ser 9 position (GSK3-β inactivation) leading to the accumulation of β-catenin in the cytoplasm and translocation into the nucleus to regulate target gene transcription in cooperation with TCF and LEF family transcription factors.

    Journal: International Journal of Medical Sciences

    Article Title: Identification and Characterization of Wnt Signaling Pathway in Keloid Pathogenesis

    doi: 10.7150/ijms.5349

    Figure Lengend Snippet: A proposed schematic representation of Wnt5a/β-catenin signaling in keloid pathogenesis. In KF, binding of the Wnt5a to FZD receptors and LRP5/6 activates Dvl which in turn inhibits β-catenin destruction complex (APC, GSK3-β, Axin) by increased phosphorylation of GSK3-β at Ser 9 position (GSK3-β inactivation) leading to the accumulation of β-catenin in the cytoplasm and translocation into the nucleus to regulate target gene transcription in cooperation with TCF and LEF family transcription factors.

    Article Snippet: Polyclonal rabbit antibodies were against Wnt5a (Lifespan Biosciences, Seattle, WA), phospho-beta-catenin Ser33/37/Thr41 and phospho-beta-catenin Ser45/Thr41 positions, and phospho-GSK3-beta Ser9 position (Cell Signalling Technology Inc., Beverly, MA), and monoclonal mouse antibodies were against FZD4 (R&D Systems, Minneapolis, MN), ROR2 (Santa Cruz Biotechnology, Inc., LA), beta-catenin (Upstate Biotechnology, Waltham, MA), beta-actin (Sigma-Aldrich, St. Louis, MO).

    Techniques: Binding Assay, Translocation Assay

    The effect of BZA on AKT/GSK3 β , AMPK α , and MAPK signal pathways. The relative quantitative results of PPAR- α , P-AKT, P-GSK3 β , P-ERK, P-P38, and P-AMPK α in the four groups ( n = 6).

    Journal: PPAR Research

    Article Title: Bezafibrate Attenuates Pressure Overload-Induced Cardiac Hypertrophy and Fibrosis

    doi: 10.1155/2017/5789714

    Figure Lengend Snippet: The effect of BZA on AKT/GSK3 β , AMPK α , and MAPK signal pathways. The relative quantitative results of PPAR- α , P-AKT, P-GSK3 β , P-ERK, P-P38, and P-AMPK α in the four groups ( n = 6).

    Article Snippet: The following first antibodies were purchased from Cell Signaling Technology: anti-AKT (#4691), anti-phospho-AKT (#4060), anti-GSK3 β (#9315), anti-phospho-GSK3 β (#9323P), anti-ERK (#4695), anti-phospho-ERK (#4370P), anti-P38 (#9212P), anti-phospho-P38 (#4511P), anti-AMPK α (#2603P), and anti-phospho-AMPK α (#2535).

    Techniques:

    BHD activates NRF2 and promotes the phosphorylation of AKT/GSK3 β during revascularization. The protein expression and quantitative analysis of NRF2 in nuclear and the phosphorylation and quantitative analysis of Akt and GSK3 β of tissue in ischemic area after 14 days of BHD treatment ( n = 4). Mean ± SD. ∗ P < 0.05, compared with HLI+NS group.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Buyang Huanwu Decoction Enhances Revascularization via Akt/GSK3 β /NRF2 Pathway in Diabetic Hindlimb Ischemia

    doi: 10.1155/2021/1470829

    Figure Lengend Snippet: BHD activates NRF2 and promotes the phosphorylation of AKT/GSK3 β during revascularization. The protein expression and quantitative analysis of NRF2 in nuclear and the phosphorylation and quantitative analysis of Akt and GSK3 β of tissue in ischemic area after 14 days of BHD treatment ( n = 4). Mean ± SD. ∗ P < 0.05, compared with HLI+NS group.

    Article Snippet: BHD consists of seven herbal medicines which include Huang Qi, Dang Gui, Chi Shao, Chuan Xiong, Tao Ren, Hong Hua, and Di Long, with the ratio of 120 : 6 : 5 : 3 : 3 : 3 : 3, and the specific formulation was described previously [ ]; CD31 polyclonal antibody (ab28364) and VEGF polyclonal antibody (ab46154) were purchased from Abcam (UK); NAD(P)H dehydrogenase quinone 1 (NQO-1) polyclonal antibody (DF6437) was purchased from Affinity Biosciences (USA); heme oxygenase-1 (HO-1) polyclonal antibody (10701-1-AP), catalase polyclonal antibody (21260-1-AP), and histone H3 (17168-1-AP) were purchased from Proteintech (CHN); NRF2 monoclonal antibody (12721), Akt (4691) and phospho-Akt monoclonal antibody (4060), glycogen synthase kinase-3 beta (GSK3 β ) (12456) and phospho-GSK3 β (5558) monoclonal antibody, interleukin-6 (IL-6) monoclonal antibody (12912), interleukin-1beta (IL-1 β ) monoclonal antibody (12242), tumor necrosis factor- (TNF-) α monoclonal antibody (11948), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) monoclonal antibody (5174) were purchased from Cell Signaling Technology (USA).

    Techniques: Expressing

    BHD promotes revascularization of hindlimb of HLI mice via AKT/GSK3 β /NRF2 signal pathway. (a) The mRNA expression of NRF2 after injection of Ad-NRF2-shRNA ( n = 4). (b, c) The tissue perfusion of hindlimb in HLI mice after 0, 7, and 14 days of BHD treatment ( n = 4). (d–f) The protein expression and quantitative analysis of NRF2, VEGFA, TNF- α , IL-1 β , IL-6, CAT, NQO-1, and HO-1 and the phosphorylation and quantitative analysis of Akt and GSK3 β in ischemic area after 14 days of BHD treatment ( n = 4). Mean ± SD. NS, P > 0.05; ∗ P < 0.05, compared with HLI+BHD+sh-NRF2 group.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Buyang Huanwu Decoction Enhances Revascularization via Akt/GSK3 β /NRF2 Pathway in Diabetic Hindlimb Ischemia

    doi: 10.1155/2021/1470829

    Figure Lengend Snippet: BHD promotes revascularization of hindlimb of HLI mice via AKT/GSK3 β /NRF2 signal pathway. (a) The mRNA expression of NRF2 after injection of Ad-NRF2-shRNA ( n = 4). (b, c) The tissue perfusion of hindlimb in HLI mice after 0, 7, and 14 days of BHD treatment ( n = 4). (d–f) The protein expression and quantitative analysis of NRF2, VEGFA, TNF- α , IL-1 β , IL-6, CAT, NQO-1, and HO-1 and the phosphorylation and quantitative analysis of Akt and GSK3 β in ischemic area after 14 days of BHD treatment ( n = 4). Mean ± SD. NS, P > 0.05; ∗ P < 0.05, compared with HLI+BHD+sh-NRF2 group.

    Article Snippet: BHD consists of seven herbal medicines which include Huang Qi, Dang Gui, Chi Shao, Chuan Xiong, Tao Ren, Hong Hua, and Di Long, with the ratio of 120 : 6 : 5 : 3 : 3 : 3 : 3, and the specific formulation was described previously [ ]; CD31 polyclonal antibody (ab28364) and VEGF polyclonal antibody (ab46154) were purchased from Abcam (UK); NAD(P)H dehydrogenase quinone 1 (NQO-1) polyclonal antibody (DF6437) was purchased from Affinity Biosciences (USA); heme oxygenase-1 (HO-1) polyclonal antibody (10701-1-AP), catalase polyclonal antibody (21260-1-AP), and histone H3 (17168-1-AP) were purchased from Proteintech (CHN); NRF2 monoclonal antibody (12721), Akt (4691) and phospho-Akt monoclonal antibody (4060), glycogen synthase kinase-3 beta (GSK3 β ) (12456) and phospho-GSK3 β (5558) monoclonal antibody, interleukin-6 (IL-6) monoclonal antibody (12912), interleukin-1beta (IL-1 β ) monoclonal antibody (12242), tumor necrosis factor- (TNF-) α monoclonal antibody (11948), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) monoclonal antibody (5174) were purchased from Cell Signaling Technology (USA).

    Techniques: Expressing, Injection, shRNA

    BHD activates NRF2 through Akt/GSK3 β signal pathway. After injection of inhibitor, the protein expression and quantitative analysis of NRF2 in nuclear and the phosphorylation and quantitative analysis of Akt and GSK3 β in ischemic area ( n = 4). Mean ± SD. ∗ P < 0.05, compared with HLI+BHD group.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Buyang Huanwu Decoction Enhances Revascularization via Akt/GSK3 β /NRF2 Pathway in Diabetic Hindlimb Ischemia

    doi: 10.1155/2021/1470829

    Figure Lengend Snippet: BHD activates NRF2 through Akt/GSK3 β signal pathway. After injection of inhibitor, the protein expression and quantitative analysis of NRF2 in nuclear and the phosphorylation and quantitative analysis of Akt and GSK3 β in ischemic area ( n = 4). Mean ± SD. ∗ P < 0.05, compared with HLI+BHD group.

    Article Snippet: BHD consists of seven herbal medicines which include Huang Qi, Dang Gui, Chi Shao, Chuan Xiong, Tao Ren, Hong Hua, and Di Long, with the ratio of 120 : 6 : 5 : 3 : 3 : 3 : 3, and the specific formulation was described previously [ ]; CD31 polyclonal antibody (ab28364) and VEGF polyclonal antibody (ab46154) were purchased from Abcam (UK); NAD(P)H dehydrogenase quinone 1 (NQO-1) polyclonal antibody (DF6437) was purchased from Affinity Biosciences (USA); heme oxygenase-1 (HO-1) polyclonal antibody (10701-1-AP), catalase polyclonal antibody (21260-1-AP), and histone H3 (17168-1-AP) were purchased from Proteintech (CHN); NRF2 monoclonal antibody (12721), Akt (4691) and phospho-Akt monoclonal antibody (4060), glycogen synthase kinase-3 beta (GSK3 β ) (12456) and phospho-GSK3 β (5558) monoclonal antibody, interleukin-6 (IL-6) monoclonal antibody (12912), interleukin-1beta (IL-1 β ) monoclonal antibody (12242), tumor necrosis factor- (TNF-) α monoclonal antibody (11948), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) monoclonal antibody (5174) were purchased from Cell Signaling Technology (USA).

    Techniques: Injection, Expressing