p-gsk3β Search Results


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  • 96
    Cell Signaling Technology Inc phosphorylated gsk3β ser9 p gsk3β
    Western blot analysis of pan and phosphorylated Akt and <t>GSK3β</t> in myocardium from WT and Akt2 knockout (AKO) mice treated with LPS (4 mg/kg, i.p.) or saline for 4 hrs. A: Pan Akt; B: Pan GSK3β; C: Phosphorylated Akt (pAkt); D: Phosphorylated
    Phosphorylated Gsk3β Ser9 P Gsk3β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc phosphorylated gsk3β p gsk3β
    ACTN4 sustains CSCs properties by promoting β-catenin stabilization. (A) The expressions of ACTN4 and β-catenin pathway signaling were elevated in the sorted ALDEFLUOR-positive and CD44 + /CD24 − cells; (B) ACTN4 knockdown in CSCs resulted in decreased β-catenin and <t>p-AKT/GSK3β</t> expressions; (C) a. the immunofluorescence assay showed the co-localization of ACTN4 and β-catenin was mainly located in the cytosol (arrowheads); b. the immunoprecipitation assay revealed the direct molecular interaction between β-catenin and ACTN4; (D) Breast CSCs were transfected with shACTN4, treated with CHX (10 μg/ml), and MG132 (10 μM) for the indicated time and immunoblotted, and the results showed that ACTN4 silencing could promote β-catenin proteasome degradation. A quantitative measurement was conducted to further analyze with Image J (** P
    Phosphorylated Gsk3β P Gsk3β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 88/100, based on 220 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Abcam p gsk3β
    ITCZ attenuates hepatic gluconeogenesis. HepG2 cells were treated with different concentrations of ITCZ (0, 5, 10 or 50 µg/ml) for 6 h in flasks or 6-well plates. (A) Western blot analysis was performed to detect the expression and phosphorylation level of <t>GSK3β.</t> Representative blots and corresponding densitometric analysis are shown. (B) HepG2 cells were seeded in 6-well plates, incubated with ITCZ at the indicated concentrations, and glucose production was evaluated by a Glucose Assay kit. (C) The mRNA expression levels of PGC-1α, PEPCK and G6Pase were analyzed by reverse-transcription quantitative polymerase chain reaction analysis. (D) The protein expression levels of PGC-1α, PEPCK and G6Pase were analyzed by western blot. A series of representative images are shown. GAPDH served as an internal control. The above experiments were performed in triplicate and values are expressed as the mean ± standard deviation. *P
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    Epitomics p gsk3β
    ITCZ attenuates hepatic gluconeogenesis. HepG2 cells were treated with different concentrations of ITCZ (0, 5, 10 or 50 µg/ml) for 6 h in flasks or 6-well plates. (A) Western blot analysis was performed to detect the expression and phosphorylation level of <t>GSK3β.</t> Representative blots and corresponding densitometric analysis are shown. (B) HepG2 cells were seeded in 6-well plates, incubated with ITCZ at the indicated concentrations, and glucose production was evaluated by a Glucose Assay kit. (C) The mRNA expression levels of PGC-1α, PEPCK and G6Pase were analyzed by reverse-transcription quantitative polymerase chain reaction analysis. (D) The protein expression levels of PGC-1α, PEPCK and G6Pase were analyzed by western blot. A series of representative images are shown. GAPDH served as an internal control. The above experiments were performed in triplicate and values are expressed as the mean ± standard deviation. *P
    P Gsk3β, supplied by Epitomics, used in various techniques. Bioz Stars score: 93/100, based on 81 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc protcol p gsk3β
    ITCZ attenuates hepatic gluconeogenesis. HepG2 cells were treated with different concentrations of ITCZ (0, 5, 10 or 50 µg/ml) for 6 h in flasks or 6-well plates. (A) Western blot analysis was performed to detect the expression and phosphorylation level of <t>GSK3β.</t> Representative blots and corresponding densitometric analysis are shown. (B) HepG2 cells were seeded in 6-well plates, incubated with ITCZ at the indicated concentrations, and glucose production was evaluated by a Glucose Assay kit. (C) The mRNA expression levels of PGC-1α, PEPCK and G6Pase were analyzed by reverse-transcription quantitative polymerase chain reaction analysis. (D) The protein expression levels of PGC-1α, PEPCK and G6Pase were analyzed by western blot. A series of representative images are shown. GAPDH served as an internal control. The above experiments were performed in triplicate and values are expressed as the mean ± standard deviation. *P
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    Cell Signaling Technology Inc p gsk3β ser9
    β-Adrenergic GSK3 inactivation is PKA dependent. ( a ) The PKA consensus sites around Ser21 and <t>Ser9</t> in GSK3α and <t>GSK3β,</t> respectively, are conserved in various species. ( b ) Immunoblot analysis of total and phosphorylated GSK3α and GSK3β in immortalized brown adipocytes treated with 40 μM H89 for 1 h before stimulation with 0.1 μM ISO for additional 15 min. Some of the cells were stimulated with 100 μM 6-MB-cAMP (6-MB) for 15 min. ( c ) Immunoblot analysis of total and phosphorylated GSK3α and GSK3β as well as phosphorylated HSL (Ser660) in iBAT from AdipoQ -caPKA and wild-type mice housed at room temperature. ( d ) Medium glycerol of immortalized brown adipocytes pre-treated with 10 μM SB216763 for 1 h before stimulation with 0.1 μM for 24 h. ( e ) Immunoblot analysis of phosphorylated and total HSL (Ser660), CREB (Ser133) and phosphorylated PKA substrates in immortalized brown adipocytes pre-treated with 10 μM SB216763 for 1 h before stimulation with 0.1 μM ISO for 1 h. Vinculin (tissues) or TFIIB (cells) serves as loading control. Data presented as mean of means +SEM (n = 4). Statistical significance was determined by two-way ANOVA with repeated measures and Tukey’s post hoc test for multiple comparisons. *p
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    Cell Signaling Technology Inc 1000 p gsk3β
    β-Adrenergic GSK3 inactivation is PKA dependent. ( a ) The PKA consensus sites around Ser21 and <t>Ser9</t> in GSK3α and <t>GSK3β,</t> respectively, are conserved in various species. ( b ) Immunoblot analysis of total and phosphorylated GSK3α and GSK3β in immortalized brown adipocytes treated with 40 μM H89 for 1 h before stimulation with 0.1 μM ISO for additional 15 min. Some of the cells were stimulated with 100 μM 6-MB-cAMP (6-MB) for 15 min. ( c ) Immunoblot analysis of total and phosphorylated GSK3α and GSK3β as well as phosphorylated HSL (Ser660) in iBAT from AdipoQ -caPKA and wild-type mice housed at room temperature. ( d ) Medium glycerol of immortalized brown adipocytes pre-treated with 10 μM SB216763 for 1 h before stimulation with 0.1 μM for 24 h. ( e ) Immunoblot analysis of phosphorylated and total HSL (Ser660), CREB (Ser133) and phosphorylated PKA substrates in immortalized brown adipocytes pre-treated with 10 μM SB216763 for 1 h before stimulation with 0.1 μM ISO for 1 h. Vinculin (tissues) or TFIIB (cells) serves as loading control. Data presented as mean of means +SEM (n = 4). Statistical significance was determined by two-way ANOVA with repeated measures and Tukey’s post hoc test for multiple comparisons. *p
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    Santa Cruz Biotechnology p gsk3β ser9
    Immunostaining for <t>P-GSK3β-Ser9.</t> A. Dysplasia from Gal3 +/+ mice presenting a specific nuclear expression. (B and C) Carcinoma from Gal3 +/+ mice. As in the dysplasia, a nuclear expression inside tumor cells was observed. D. Dysplastic lesion from
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    Cell Signaling Technology Inc p gsk3β thr390
    Immunostaining for <t>P-GSK3β-Ser9.</t> A. Dysplasia from Gal3 +/+ mice presenting a specific nuclear expression. (B and C) Carcinoma from Gal3 +/+ mice. As in the dysplasia, a nuclear expression inside tumor cells was observed. D. Dysplastic lesion from
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    Cell Signaling Technology Inc p gsk3β ser9 5b3
    Immunostaining for <t>P-GSK3β-Ser9.</t> A. Dysplasia from Gal3 +/+ mice presenting a specific nuclear expression. (B and C) Carcinoma from Gal3 +/+ mice. As in the dysplasia, a nuclear expression inside tumor cells was observed. D. Dysplastic lesion from
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    Santa Cruz Biotechnology anti p gsk3β
    Immunostaining for <t>P-GSK3β-Ser9.</t> A. Dysplasia from Gal3 +/+ mice presenting a specific nuclear expression. (B and C) Carcinoma from Gal3 +/+ mice. As in the dysplasia, a nuclear expression inside tumor cells was observed. D. Dysplastic lesion from
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    Santa Cruz Biotechnology p gsk3β
    PAK7 inhibits the degradation of β-catenin via phosphorylating <t>GSK3β.</t> A, PAK7 knockdown suppressed p-GSK3β (S9) expression. pEGFP-β-catenin was transfected into HEK293T cells along with siR-PAK7 or negative control. Forty-eight hours after transfection, cells were harvested for western blotting analysis to detect the expression of PAK7, GFP-β-catenin, GSK3β, p-GSK3β. B, PAK7 knockdown inhibited β-catenin mediated transcriptional activity of TCF. HEK293T cells were cotransfected with siR-PAK7 or siR-NC, pEGFP-β-catenin, TOP flash (TOP) or FOP flash (FOP), and Renilla. 48 h after transfection, cells were harvested for luciferase activity assay. C, Inhibiting proteasomes degradation by MG132 reverses the effect of PAK7 knockdown on β-catenin degradation. HEK293T cells were cotransfected with pEGFP-β-catenin and siR-PAK7 or siR-NC. Forty-four hours after transfection, the cells were treated with 30μM MG132. Cells were harvested 4 hours later and subjected to western blotting analysis to detect the expression of GFP-β-catenin and PAK7. D, Inhibiting GSK3β activity by Licl reduced β-catenin expression inhibition by PAK7 knockdown. siR-PAK7 or siR-NC was transfected into MDA-MB-231 cells. 36 hours after transfection, the cells were treated with 30 mM Licl for 12 hours and then harvested for western blotting analysis to detect the expression of GFP-β-catenin, p-GSK3β (S9) and PAK7. E, siR-PAK7 or siR-NC was transfected into MDA-MB-231 cells. 36 hours after transfection, the cells were treated with 30 mM Licl for 12 hours and harvested for luciferase activity assay. F, MDA-MB-231 cells were transfected with flag-NC and flag-PAK7, treated with Licl for 48 hours and harvested for western blot assay.
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    Affinity Biosciences p gsk3β
    PAK7 inhibits the degradation of β-catenin via phosphorylating <t>GSK3β.</t> A, PAK7 knockdown suppressed p-GSK3β (S9) expression. pEGFP-β-catenin was transfected into HEK293T cells along with siR-PAK7 or negative control. Forty-eight hours after transfection, cells were harvested for western blotting analysis to detect the expression of PAK7, GFP-β-catenin, GSK3β, p-GSK3β. B, PAK7 knockdown inhibited β-catenin mediated transcriptional activity of TCF. HEK293T cells were cotransfected with siR-PAK7 or siR-NC, pEGFP-β-catenin, TOP flash (TOP) or FOP flash (FOP), and Renilla. 48 h after transfection, cells were harvested for luciferase activity assay. C, Inhibiting proteasomes degradation by MG132 reverses the effect of PAK7 knockdown on β-catenin degradation. HEK293T cells were cotransfected with pEGFP-β-catenin and siR-PAK7 or siR-NC. Forty-four hours after transfection, the cells were treated with 30μM MG132. Cells were harvested 4 hours later and subjected to western blotting analysis to detect the expression of GFP-β-catenin and PAK7. D, Inhibiting GSK3β activity by Licl reduced β-catenin expression inhibition by PAK7 knockdown. siR-PAK7 or siR-NC was transfected into MDA-MB-231 cells. 36 hours after transfection, the cells were treated with 30 mM Licl for 12 hours and then harvested for western blotting analysis to detect the expression of GFP-β-catenin, p-GSK3β (S9) and PAK7. E, siR-PAK7 or siR-NC was transfected into MDA-MB-231 cells. 36 hours after transfection, the cells were treated with 30 mM Licl for 12 hours and harvested for luciferase activity assay. F, MDA-MB-231 cells were transfected with flag-NC and flag-PAK7, treated with Licl for 48 hours and harvested for western blot assay.
    P Gsk3β, supplied by Affinity Biosciences, used in various techniques. Bioz Stars score: 91/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Thermo Fisher p gsk3β
    Effect of CBL on neuropathological alterations in <t>Tau/GSK3β</t> bigenic mice. (A) Immunohistochemical analysis of dendritic pathology as evidenced by MAP2 immunoreactivity in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. Boxes in upper panels are represented at higher magnification in the lower panels. (B) Quantitative analysis of MAP2 immunoreactivity in the CA1 region of the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (C) Quantitative analysis of MAP2 immunoreactivity in the molecular layer (ML) of the dentate gyrus of the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (D) Immunohistochemical analysis neuronal density as evidenced by NeuN immunoreactivity in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. Boxes in upper panels are represented at higher magnification in the lower panels. (E) Quantitative analysis of NeuN immunoreactivity in the CA1 region of the hippocampus the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (F) Quantitative analysis of NeuN immunoreactivity in the molecular layer of the dentate gyrus of the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (A, D) Scale bar in upper panels = 250 μm, in lower panels = 50 μm. (B, C, E, F) Error bars represent mean ± SEM (n = 6 per group, 6 m/o). *Indicates a significant difference (p
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    Becton Dickinson anti p gsk3β
    Effect of CBL on neuropathological alterations in <t>Tau/GSK3β</t> bigenic mice. (A) Immunohistochemical analysis of dendritic pathology as evidenced by MAP2 immunoreactivity in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. Boxes in upper panels are represented at higher magnification in the lower panels. (B) Quantitative analysis of MAP2 immunoreactivity in the CA1 region of the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (C) Quantitative analysis of MAP2 immunoreactivity in the molecular layer (ML) of the dentate gyrus of the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (D) Immunohistochemical analysis neuronal density as evidenced by NeuN immunoreactivity in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. Boxes in upper panels are represented at higher magnification in the lower panels. (E) Quantitative analysis of NeuN immunoreactivity in the CA1 region of the hippocampus the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (F) Quantitative analysis of NeuN immunoreactivity in the molecular layer of the dentate gyrus of the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (A, D) Scale bar in upper panels = 250 μm, in lower panels = 50 μm. (B, C, E, F) Error bars represent mean ± SEM (n = 6 per group, 6 m/o). *Indicates a significant difference (p
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    Enzo Biochem p gsk3β
    Effect of CBL on neuropathological alterations in <t>Tau/GSK3β</t> bigenic mice. (A) Immunohistochemical analysis of dendritic pathology as evidenced by MAP2 immunoreactivity in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. Boxes in upper panels are represented at higher magnification in the lower panels. (B) Quantitative analysis of MAP2 immunoreactivity in the CA1 region of the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (C) Quantitative analysis of MAP2 immunoreactivity in the molecular layer (ML) of the dentate gyrus of the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (D) Immunohistochemical analysis neuronal density as evidenced by NeuN immunoreactivity in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. Boxes in upper panels are represented at higher magnification in the lower panels. (E) Quantitative analysis of NeuN immunoreactivity in the CA1 region of the hippocampus the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (F) Quantitative analysis of NeuN immunoreactivity in the molecular layer of the dentate gyrus of the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (A, D) Scale bar in upper panels = 250 μm, in lower panels = 50 μm. (B, C, E, F) Error bars represent mean ± SEM (n = 6 per group, 6 m/o). *Indicates a significant difference (p
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    Bioworld Antibodies p gsk3β
    (A) By western blot analysis, ILK silencing combined with hyperthermia could inhibit the proteins level of p-Akt, <t>p-GSK3β</t> and p-HSF1, and promote the expression of Bax protein (P
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    Merck KGaA p gsk3β tyr216
    (A) By western blot analysis, ILK silencing combined with hyperthermia could inhibit the proteins level of p-Akt, <t>p-GSK3β</t> and p-HSF1, and promote the expression of Bax protein (P
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    Santa Cruz Biotechnology mouse phosphorylated gsk3β p gsk3β antibody
    (A) By western blot analysis, ILK silencing combined with hyperthermia could inhibit the proteins level of p-Akt, <t>p-GSK3β</t> and p-HSF1, and promote the expression of Bax protein (P
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    Image Search Results


    Western blot analysis of pan and phosphorylated Akt and GSK3β in myocardium from WT and Akt2 knockout (AKO) mice treated with LPS (4 mg/kg, i.p.) or saline for 4 hrs. A: Pan Akt; B: Pan GSK3β; C: Phosphorylated Akt (pAkt); D: Phosphorylated

    Journal: Journal of molecular and cellular cardiology

    Article Title: Ablation of Akt2 Protects against Lipopolysaccharide-Induced Cardiac Dysfunction: Role of Akt Ubiquitination E3 Ligase TRAF6

    doi: 10.1016/j.yjmcc.2014.04.020

    Figure Lengend Snippet: Western blot analysis of pan and phosphorylated Akt and GSK3β in myocardium from WT and Akt2 knockout (AKO) mice treated with LPS (4 mg/kg, i.p.) or saline for 4 hrs. A: Pan Akt; B: Pan GSK3β; C: Phosphorylated Akt (pAkt); D: Phosphorylated

    Article Snippet: Membranes were blocked with 5% milk in TBS-T, and were incubated overnight at 4°C with anti-cleaved Caspase-3 (1:1,000, #9664, Cell Signaling Technology, Danvers, MA), anti-Caspase-12 (1:1,000, #2202 Cell Signaling), anti-TNF-α (1:1,000, #3707, Cell Signaling), anti-TLR4 (1:1,000, #2219, Cell Signaling), anti-ALDH2 (1:1,000, kindly provided by the late Dr. Henry Weiner, Purdue University, West Lafayette, IN), anti-TRAF6 (1:1000, #ab33915, Abcam, Cambridge, MA), anti-Ubiquitin (1:1,000, #ab7780, Abcam, Cambridge, MA), anti-Akt (1:1,000, #9272, Cell Signaling), anti-Akt1 (1:1,000, #2967, Cell Signaling), anti-Akt2 (1:1,000, #2962, Cell Signaling), anti-Akt3 (1:1,000, #3788, Cell Signaling), anti-phosphorylated Akt (pAkt, Ser473, 1:1,000, #4058, Cell Signaling), anti-GSK3β (1:1,000, #9315, Cell Signaling), anti-phosphorylated GSK3β (pGSK3β, Ser9, 1:1,000, #9323, Cell Signaling), anti-ERK (1:1,000, #9102, Cell Signaling), anti-phosphorylated ERK (pERK, Thr202/Tyr204, 1:1,000, #4377, Cell Signaling), anti-p38 (1:1,000, #9212, Cell Signaling), anti-phosphorylated (pp38, Thr180/Tyr182, 1:1,000, #9211, Cell Signaling), anti-IКB (1:1,000, #9242, Cell Signaling), anti-phosphorylated IКB (pIКB, Ser32, 1:1,000, #2859, Cell Signaling) and anti-GAPDH (1:1,000, loading control, #2118, Cell Signaling) antibodies.

    Techniques: Western Blot, Knock-Out, Mouse Assay

    ACTN4 sustains CSCs properties by promoting β-catenin stabilization. (A) The expressions of ACTN4 and β-catenin pathway signaling were elevated in the sorted ALDEFLUOR-positive and CD44 + /CD24 − cells; (B) ACTN4 knockdown in CSCs resulted in decreased β-catenin and p-AKT/GSK3β expressions; (C) a. the immunofluorescence assay showed the co-localization of ACTN4 and β-catenin was mainly located in the cytosol (arrowheads); b. the immunoprecipitation assay revealed the direct molecular interaction between β-catenin and ACTN4; (D) Breast CSCs were transfected with shACTN4, treated with CHX (10 μg/ml), and MG132 (10 μM) for the indicated time and immunoblotted, and the results showed that ACTN4 silencing could promote β-catenin proteasome degradation. A quantitative measurement was conducted to further analyze with Image J (** P

    Journal: Journal of Experimental & Clinical Cancer Research : CR

    Article Title: Direct inhibition of ACTN4 by ellagic acid limits breast cancer metastasis via regulation of β-catenin stabilization in cancer stem cells

    doi: 10.1186/s13046-017-0635-9

    Figure Lengend Snippet: ACTN4 sustains CSCs properties by promoting β-catenin stabilization. (A) The expressions of ACTN4 and β-catenin pathway signaling were elevated in the sorted ALDEFLUOR-positive and CD44 + /CD24 − cells; (B) ACTN4 knockdown in CSCs resulted in decreased β-catenin and p-AKT/GSK3β expressions; (C) a. the immunofluorescence assay showed the co-localization of ACTN4 and β-catenin was mainly located in the cytosol (arrowheads); b. the immunoprecipitation assay revealed the direct molecular interaction between β-catenin and ACTN4; (D) Breast CSCs were transfected with shACTN4, treated with CHX (10 μg/ml), and MG132 (10 μM) for the indicated time and immunoblotted, and the results showed that ACTN4 silencing could promote β-catenin proteasome degradation. A quantitative measurement was conducted to further analyze with Image J (** P

    Article Snippet: Antibodies for western blotting included ACTN4 (Abcam, Cambridge, USA), vimentin, E-cadherin (Abclonal, Cambridge, MA, USA), β-catenin, p -β-catenin (Ser33/37/Thr41), Akt, p -Akt (Ser473), GSK3β, p -GSK3β (Ser9), lamin B, β-actin (Cell Signaling Technology, MA, USA) as well as secondary anti-rabbit or anti-mouse antibodies.

    Techniques: Immunofluorescence, Immunoprecipitation, Transfection

    ITCZ attenuates hepatic gluconeogenesis. HepG2 cells were treated with different concentrations of ITCZ (0, 5, 10 or 50 µg/ml) for 6 h in flasks or 6-well plates. (A) Western blot analysis was performed to detect the expression and phosphorylation level of GSK3β. Representative blots and corresponding densitometric analysis are shown. (B) HepG2 cells were seeded in 6-well plates, incubated with ITCZ at the indicated concentrations, and glucose production was evaluated by a Glucose Assay kit. (C) The mRNA expression levels of PGC-1α, PEPCK and G6Pase were analyzed by reverse-transcription quantitative polymerase chain reaction analysis. (D) The protein expression levels of PGC-1α, PEPCK and G6Pase were analyzed by western blot. A series of representative images are shown. GAPDH served as an internal control. The above experiments were performed in triplicate and values are expressed as the mean ± standard deviation. *P

    Journal: Experimental and Therapeutic Medicine

    Article Title: Itraconazole attenuates hepatic gluconeogenesis and promotes glucose uptake by regulating AMPK pathway

    doi: 10.3892/etm.2017.5602

    Figure Lengend Snippet: ITCZ attenuates hepatic gluconeogenesis. HepG2 cells were treated with different concentrations of ITCZ (0, 5, 10 or 50 µg/ml) for 6 h in flasks or 6-well plates. (A) Western blot analysis was performed to detect the expression and phosphorylation level of GSK3β. Representative blots and corresponding densitometric analysis are shown. (B) HepG2 cells were seeded in 6-well plates, incubated with ITCZ at the indicated concentrations, and glucose production was evaluated by a Glucose Assay kit. (C) The mRNA expression levels of PGC-1α, PEPCK and G6Pase were analyzed by reverse-transcription quantitative polymerase chain reaction analysis. (D) The protein expression levels of PGC-1α, PEPCK and G6Pase were analyzed by western blot. A series of representative images are shown. GAPDH served as an internal control. The above experiments were performed in triplicate and values are expressed as the mean ± standard deviation. *P

    Article Snippet: After blocking with 5% non-fat milk for 1 h, the membranes were probed with primary antibodies against AMPK-α1 (ab32047), phosphorylated (p)-AMPK (phospho S487) (ab131357), GSK3β (ab32391) (all diluted at 1:5,000; Abcam, Cambridge, MA, USA), p-GSK3β (ab75745), PGC-1α (ab54481) (both diluted at 1:1,000; Abcam), PEPCK (sc-377027) (diluted at 1:100; Santa Cruz Biotechnology, Inc., Dallas, TX, USA), G-6-Pase (ab83690) (diluted at 1:250; Abcam) and GLUT4 (ab654) (diluted at 1:2,500; Abcam) at 4°C overnight, and subsequently incubated with the corresponding secondary horseradish peroxidase-conjugated anti-rabbit (ab6721) or anti-mouse (ab6785) immunoglobulin G antibodies (1:5,000 dilution; Beyotime Institute of Biotechnology, Inc.) at 37°C for 45 min. Unbound antibodies in each step were washed with Tris-buffered saline containing Tween-20 four times.

    Techniques: Western Blot, Expressing, Incubation, Glucose Assay, Pyrolysis Gas Chromatography, Real-time Polymerase Chain Reaction, Standard Deviation

    β-Adrenergic GSK3 inactivation is PKA dependent. ( a ) The PKA consensus sites around Ser21 and Ser9 in GSK3α and GSK3β, respectively, are conserved in various species. ( b ) Immunoblot analysis of total and phosphorylated GSK3α and GSK3β in immortalized brown adipocytes treated with 40 μM H89 for 1 h before stimulation with 0.1 μM ISO for additional 15 min. Some of the cells were stimulated with 100 μM 6-MB-cAMP (6-MB) for 15 min. ( c ) Immunoblot analysis of total and phosphorylated GSK3α and GSK3β as well as phosphorylated HSL (Ser660) in iBAT from AdipoQ -caPKA and wild-type mice housed at room temperature. ( d ) Medium glycerol of immortalized brown adipocytes pre-treated with 10 μM SB216763 for 1 h before stimulation with 0.1 μM for 24 h. ( e ) Immunoblot analysis of phosphorylated and total HSL (Ser660), CREB (Ser133) and phosphorylated PKA substrates in immortalized brown adipocytes pre-treated with 10 μM SB216763 for 1 h before stimulation with 0.1 μM ISO for 1 h. Vinculin (tissues) or TFIIB (cells) serves as loading control. Data presented as mean of means +SEM (n = 4). Statistical significance was determined by two-way ANOVA with repeated measures and Tukey’s post hoc test for multiple comparisons. *p

    Journal: Scientific Reports

    Article Title: GSK3 is a negative regulator of the thermogenic program in brown adipocytes

    doi: 10.1038/s41598-018-21795-y

    Figure Lengend Snippet: β-Adrenergic GSK3 inactivation is PKA dependent. ( a ) The PKA consensus sites around Ser21 and Ser9 in GSK3α and GSK3β, respectively, are conserved in various species. ( b ) Immunoblot analysis of total and phosphorylated GSK3α and GSK3β in immortalized brown adipocytes treated with 40 μM H89 for 1 h before stimulation with 0.1 μM ISO for additional 15 min. Some of the cells were stimulated with 100 μM 6-MB-cAMP (6-MB) for 15 min. ( c ) Immunoblot analysis of total and phosphorylated GSK3α and GSK3β as well as phosphorylated HSL (Ser660) in iBAT from AdipoQ -caPKA and wild-type mice housed at room temperature. ( d ) Medium glycerol of immortalized brown adipocytes pre-treated with 10 μM SB216763 for 1 h before stimulation with 0.1 μM for 24 h. ( e ) Immunoblot analysis of phosphorylated and total HSL (Ser660), CREB (Ser133) and phosphorylated PKA substrates in immortalized brown adipocytes pre-treated with 10 μM SB216763 for 1 h before stimulation with 0.1 μM ISO for 1 h. Vinculin (tissues) or TFIIB (cells) serves as loading control. Data presented as mean of means +SEM (n = 4). Statistical significance was determined by two-way ANOVA with repeated measures and Tukey’s post hoc test for multiple comparisons. *p

    Article Snippet: Primary antibodies used were: CREB (#9192), p-CREB (Ser133) (#9198), GSK3α (#4337), p-GSK3α (Ser21) (#9316), GSK3β (#12456), p-GSK3β (Ser9) (#5558), p38 MAPK (#9212), p-p38 MAPK (Thr180/Tyr182) (#9211), MKK3 (#8535), MKK6 (#8550), p-MKK3/6 (Ser189/Ser207) (#12280), ATF2 (#9226), p-ATF2 (Thr71) (#5112), HSL (#4107), p-HSL (Ser660) (#4126), Phospho-(Ser/Thr) PKA substrate (#9621) (all from Cell Signaling Technology), TFIIB (#sc-225) (Santa Cruz Biotechnology), Vinculin (#V9264) (Sigma-Aldrich), UCP1 (#10983) (Abcam) and HA (#11583816001) (Roche).

    Techniques: Mouse Assay

    Immunostaining for P-GSK3β-Ser9. A. Dysplasia from Gal3 +/+ mice presenting a specific nuclear expression. (B and C) Carcinoma from Gal3 +/+ mice. As in the dysplasia, a nuclear expression inside tumor cells was observed. D. Dysplastic lesion from

    Journal: International Journal of Clinical and Experimental Pathology

    Article Title: The inactive form of glycogen synthase kinase-3? is associated with the development of carcinomas in galectin-3 wild-type mice, but not in galectin-3-deficient mice

    doi:

    Figure Lengend Snippet: Immunostaining for P-GSK3β-Ser9. A. Dysplasia from Gal3 +/+ mice presenting a specific nuclear expression. (B and C) Carcinoma from Gal3 +/+ mice. As in the dysplasia, a nuclear expression inside tumor cells was observed. D. Dysplastic lesion from

    Article Snippet: A standard streptavidin-biotin peroxidase method using a polyclonal antibody to P-GSK3β-Ser9 (Santa Cruz Biotechnology, USA; catalog number # sc-11757) was performed to evaluate its expression in the dysplasias and carcinomas from both groups of mice.

    Techniques: Immunostaining, Mouse Assay, Expressing

    Mean index of cells positive for P-GSK3β-Ser9. (A and B) Comparative analysis between dysplasias and carcinomas developed in Gal3 +/+ and Gal3 -/- mice. C. Comparative analysis between dysplasias and carcinomas from Gal3 +/+ mice. D. Comparative

    Journal: International Journal of Clinical and Experimental Pathology

    Article Title: The inactive form of glycogen synthase kinase-3? is associated with the development of carcinomas in galectin-3 wild-type mice, but not in galectin-3-deficient mice

    doi:

    Figure Lengend Snippet: Mean index of cells positive for P-GSK3β-Ser9. (A and B) Comparative analysis between dysplasias and carcinomas developed in Gal3 +/+ and Gal3 -/- mice. C. Comparative analysis between dysplasias and carcinomas from Gal3 +/+ mice. D. Comparative

    Article Snippet: A standard streptavidin-biotin peroxidase method using a polyclonal antibody to P-GSK3β-Ser9 (Santa Cruz Biotechnology, USA; catalog number # sc-11757) was performed to evaluate its expression in the dysplasias and carcinomas from both groups of mice.

    Techniques: Mouse Assay

    PAK7 inhibits the degradation of β-catenin via phosphorylating GSK3β. A, PAK7 knockdown suppressed p-GSK3β (S9) expression. pEGFP-β-catenin was transfected into HEK293T cells along with siR-PAK7 or negative control. Forty-eight hours after transfection, cells were harvested for western blotting analysis to detect the expression of PAK7, GFP-β-catenin, GSK3β, p-GSK3β. B, PAK7 knockdown inhibited β-catenin mediated transcriptional activity of TCF. HEK293T cells were cotransfected with siR-PAK7 or siR-NC, pEGFP-β-catenin, TOP flash (TOP) or FOP flash (FOP), and Renilla. 48 h after transfection, cells were harvested for luciferase activity assay. C, Inhibiting proteasomes degradation by MG132 reverses the effect of PAK7 knockdown on β-catenin degradation. HEK293T cells were cotransfected with pEGFP-β-catenin and siR-PAK7 or siR-NC. Forty-four hours after transfection, the cells were treated with 30μM MG132. Cells were harvested 4 hours later and subjected to western blotting analysis to detect the expression of GFP-β-catenin and PAK7. D, Inhibiting GSK3β activity by Licl reduced β-catenin expression inhibition by PAK7 knockdown. siR-PAK7 or siR-NC was transfected into MDA-MB-231 cells. 36 hours after transfection, the cells were treated with 30 mM Licl for 12 hours and then harvested for western blotting analysis to detect the expression of GFP-β-catenin, p-GSK3β (S9) and PAK7. E, siR-PAK7 or siR-NC was transfected into MDA-MB-231 cells. 36 hours after transfection, the cells were treated with 30 mM Licl for 12 hours and harvested for luciferase activity assay. F, MDA-MB-231 cells were transfected with flag-NC and flag-PAK7, treated with Licl for 48 hours and harvested for western blot assay.

    Journal: Journal of Cancer

    Article Title: P21-activated kinase 7 (PAK7) interacts with and activates Wnt/β-catenin signaling pathway in breast cancer

    doi: 10.7150/jca.24934

    Figure Lengend Snippet: PAK7 inhibits the degradation of β-catenin via phosphorylating GSK3β. A, PAK7 knockdown suppressed p-GSK3β (S9) expression. pEGFP-β-catenin was transfected into HEK293T cells along with siR-PAK7 or negative control. Forty-eight hours after transfection, cells were harvested for western blotting analysis to detect the expression of PAK7, GFP-β-catenin, GSK3β, p-GSK3β. B, PAK7 knockdown inhibited β-catenin mediated transcriptional activity of TCF. HEK293T cells were cotransfected with siR-PAK7 or siR-NC, pEGFP-β-catenin, TOP flash (TOP) or FOP flash (FOP), and Renilla. 48 h after transfection, cells were harvested for luciferase activity assay. C, Inhibiting proteasomes degradation by MG132 reverses the effect of PAK7 knockdown on β-catenin degradation. HEK293T cells were cotransfected with pEGFP-β-catenin and siR-PAK7 or siR-NC. Forty-four hours after transfection, the cells were treated with 30μM MG132. Cells were harvested 4 hours later and subjected to western blotting analysis to detect the expression of GFP-β-catenin and PAK7. D, Inhibiting GSK3β activity by Licl reduced β-catenin expression inhibition by PAK7 knockdown. siR-PAK7 or siR-NC was transfected into MDA-MB-231 cells. 36 hours after transfection, the cells were treated with 30 mM Licl for 12 hours and then harvested for western blotting analysis to detect the expression of GFP-β-catenin, p-GSK3β (S9) and PAK7. E, siR-PAK7 or siR-NC was transfected into MDA-MB-231 cells. 36 hours after transfection, the cells were treated with 30 mM Licl for 12 hours and harvested for luciferase activity assay. F, MDA-MB-231 cells were transfected with flag-NC and flag-PAK7, treated with Licl for 48 hours and harvested for western blot assay.

    Article Snippet: The membranes were blocked with Tris-buffered saline containing 5% nonfat milk for 2 h, then probed with primary antibodies of target protein, including PAK7, flag, GSK3β, p-GSK3β, β-catenin, p-β-catenin, c-myc, cyclin D1 and GAPDH at 4℃ overnight, followed by incubation with horseradish peroxidase (HRP)-linked secondary antibodies (1:5000, Santa Cruz Biotechnology, Santa Cruz, CA) for 1 h at room temperature, and detected by ECL reagents (Pierce).

    Techniques: Expressing, Transfection, Negative Control, Western Blot, Activity Assay, Luciferase, Inhibition, Multiple Displacement Amplification

    PAK7 activates Wnt/β-catenin signaling pathway in breast cancer cells. A, The effect of transfecting with flag-PAK7 overexpression plasmid or flag-NC negative control vector on the protein levels of flag-PAK7, β-catenin, p-β-catenin (S33/S37/T41), GSK3β, p-GSK3β(S9), c-myc, cyclin D1 and β-catenin (nucleus), c-myc (nucleus) in MCF-7 cells. B, The effect of transfecting with small interfering RNA of PAK7 (siR-PAK7) or negative control (siR-NC) vector on the protein levels of flag-PAK7, β-catenin, p-β-catenin (S33/S37/T41), GSK3β, p-GSK3β(S9), c-myc, cyclin D1 and β-catenin (nucleus), c-myc (nucleus) in MDA-MB-231 cells. C, PAK7 overexpression increases the activity of Wnt/β-catenin signaling pathway which was detected by TOP/FOP flash assay in MCF-7 cells. D, PAK7 knockdown inhibits the activity of Wnt/β-catenin signaling pathway which was detected by TOP/FOP flash assay in MDA-MB-231 cells. E, The expression of PAK7 was positively correlated with β-catenin (CTNNB1), c-myc (MYC) expression which was analyzed in GEPIA database by bioinformatics methods. Values represent the mean ± SD from three independent measurements. *P

    Journal: Journal of Cancer

    Article Title: P21-activated kinase 7 (PAK7) interacts with and activates Wnt/β-catenin signaling pathway in breast cancer

    doi: 10.7150/jca.24934

    Figure Lengend Snippet: PAK7 activates Wnt/β-catenin signaling pathway in breast cancer cells. A, The effect of transfecting with flag-PAK7 overexpression plasmid or flag-NC negative control vector on the protein levels of flag-PAK7, β-catenin, p-β-catenin (S33/S37/T41), GSK3β, p-GSK3β(S9), c-myc, cyclin D1 and β-catenin (nucleus), c-myc (nucleus) in MCF-7 cells. B, The effect of transfecting with small interfering RNA of PAK7 (siR-PAK7) or negative control (siR-NC) vector on the protein levels of flag-PAK7, β-catenin, p-β-catenin (S33/S37/T41), GSK3β, p-GSK3β(S9), c-myc, cyclin D1 and β-catenin (nucleus), c-myc (nucleus) in MDA-MB-231 cells. C, PAK7 overexpression increases the activity of Wnt/β-catenin signaling pathway which was detected by TOP/FOP flash assay in MCF-7 cells. D, PAK7 knockdown inhibits the activity of Wnt/β-catenin signaling pathway which was detected by TOP/FOP flash assay in MDA-MB-231 cells. E, The expression of PAK7 was positively correlated with β-catenin (CTNNB1), c-myc (MYC) expression which was analyzed in GEPIA database by bioinformatics methods. Values represent the mean ± SD from three independent measurements. *P

    Article Snippet: The membranes were blocked with Tris-buffered saline containing 5% nonfat milk for 2 h, then probed with primary antibodies of target protein, including PAK7, flag, GSK3β, p-GSK3β, β-catenin, p-β-catenin, c-myc, cyclin D1 and GAPDH at 4℃ overnight, followed by incubation with horseradish peroxidase (HRP)-linked secondary antibodies (1:5000, Santa Cruz Biotechnology, Santa Cruz, CA) for 1 h at room temperature, and detected by ECL reagents (Pierce).

    Techniques: Over Expression, Plasmid Preparation, Negative Control, Small Interfering RNA, Multiple Displacement Amplification, Activity Assay, Expressing

    PAK7 interacts with β-catenin and GSK3β. A, PAK7 was binding to β-catenin and GSK3β by immunoprecipitation. β-catenin (GFP tagged) was cotransfected with PAK7 (flag tagged) or empty vector into HEK293T cells. Immunoprecipitation was performed with flag antibody and GFP antibody, respectively. β-catenin, GSK3β and PAK7 were analyzed with a GFP antibody, GSK3β antibody, and flag antibody, respectively. B, PAK7 and β-catenin were co-localized in the cell cytoplasm and nucleus. PAK7 (GFP tagged) and pCherry-β-catenin (Cherry tagged) were cotransfected into HEK293T cells. Co-localization (yellow fluorescence) of PAK7 (green fluorescence) and β-catenin (red fluorescence) was detected in the cytoplasm and nucleus. C, Working model for the regulation of β-catenin degradation by PAK7 via phosphorylating GSK3β in Wnt/β-catenin signaling pathway.

    Journal: Journal of Cancer

    Article Title: P21-activated kinase 7 (PAK7) interacts with and activates Wnt/β-catenin signaling pathway in breast cancer

    doi: 10.7150/jca.24934

    Figure Lengend Snippet: PAK7 interacts with β-catenin and GSK3β. A, PAK7 was binding to β-catenin and GSK3β by immunoprecipitation. β-catenin (GFP tagged) was cotransfected with PAK7 (flag tagged) or empty vector into HEK293T cells. Immunoprecipitation was performed with flag antibody and GFP antibody, respectively. β-catenin, GSK3β and PAK7 were analyzed with a GFP antibody, GSK3β antibody, and flag antibody, respectively. B, PAK7 and β-catenin were co-localized in the cell cytoplasm and nucleus. PAK7 (GFP tagged) and pCherry-β-catenin (Cherry tagged) were cotransfected into HEK293T cells. Co-localization (yellow fluorescence) of PAK7 (green fluorescence) and β-catenin (red fluorescence) was detected in the cytoplasm and nucleus. C, Working model for the regulation of β-catenin degradation by PAK7 via phosphorylating GSK3β in Wnt/β-catenin signaling pathway.

    Article Snippet: The membranes were blocked with Tris-buffered saline containing 5% nonfat milk for 2 h, then probed with primary antibodies of target protein, including PAK7, flag, GSK3β, p-GSK3β, β-catenin, p-β-catenin, c-myc, cyclin D1 and GAPDH at 4℃ overnight, followed by incubation with horseradish peroxidase (HRP)-linked secondary antibodies (1:5000, Santa Cruz Biotechnology, Santa Cruz, CA) for 1 h at room temperature, and detected by ECL reagents (Pierce).

    Techniques: Binding Assay, Immunoprecipitation, Plasmid Preparation, Fluorescence

    Effect of CBL on neuropathological alterations in Tau/GSK3β bigenic mice. (A) Immunohistochemical analysis of dendritic pathology as evidenced by MAP2 immunoreactivity in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. Boxes in upper panels are represented at higher magnification in the lower panels. (B) Quantitative analysis of MAP2 immunoreactivity in the CA1 region of the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (C) Quantitative analysis of MAP2 immunoreactivity in the molecular layer (ML) of the dentate gyrus of the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (D) Immunohistochemical analysis neuronal density as evidenced by NeuN immunoreactivity in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. Boxes in upper panels are represented at higher magnification in the lower panels. (E) Quantitative analysis of NeuN immunoreactivity in the CA1 region of the hippocampus the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (F) Quantitative analysis of NeuN immunoreactivity in the molecular layer of the dentate gyrus of the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (A, D) Scale bar in upper panels = 250 μm, in lower panels = 50 μm. (B, C, E, F) Error bars represent mean ± SEM (n = 6 per group, 6 m/o). *Indicates a significant difference (p

    Journal: BMC Neuroscience

    Article Title: Cerebrolysin™ efficacy in a transgenic model of tauopathy: role in regulation of mitochondrial structure

    doi: 10.1186/1471-2202-15-90

    Figure Lengend Snippet: Effect of CBL on neuropathological alterations in Tau/GSK3β bigenic mice. (A) Immunohistochemical analysis of dendritic pathology as evidenced by MAP2 immunoreactivity in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. Boxes in upper panels are represented at higher magnification in the lower panels. (B) Quantitative analysis of MAP2 immunoreactivity in the CA1 region of the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (C) Quantitative analysis of MAP2 immunoreactivity in the molecular layer (ML) of the dentate gyrus of the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (D) Immunohistochemical analysis neuronal density as evidenced by NeuN immunoreactivity in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. Boxes in upper panels are represented at higher magnification in the lower panels. (E) Quantitative analysis of NeuN immunoreactivity in the CA1 region of the hippocampus the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (F) Quantitative analysis of NeuN immunoreactivity in the molecular layer of the dentate gyrus of the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (A, D) Scale bar in upper panels = 250 μm, in lower panels = 50 μm. (B, C, E, F) Error bars represent mean ± SEM (n = 6 per group, 6 m/o). *Indicates a significant difference (p

    Article Snippet: Immunohistochemical analysis For this purpose as previously described [ , ], blind-coded 40 μm thick vibratome sections were immunolabeled with the mouse monoclonal antibodies against Drp-1 (1:500, Santa Cruz), Tom40 (1:1000, Santa Cruz), synaptophysin (presynaptic terminal marker, 1:40, Chemicon), GFAP (astroglial marker, 1:1000, Chemicon), p-Tau (AT8, 1:500, Pierce; AT270 1:500, Pierce), t-Tau (1:500, Dako), t-GSK3β (1:500, Cell Signaling) and p-GSK3β (GSK3βY216, 1:500, Life Technologies), as previously described [ , ].

    Techniques: Mouse Assay, Immunohistochemistry

    Comparison of effects of aging on p-Tau in non-tg single tg and Tau/GSK3β bigenic mice. (A) Representative images of immunohistochemical analysis with the p-Tau (AT8) in the neocortex and hippocampus in the non-tg, single tg and Tau/GSK3β bigenic mice at 3, 6 and 12 months of age. (B) Image analysis of optical density in the hippocampus represented as a line graph in the non-tg, single tg and Tau/GSK3β bigenic mice at 3, 6 and 12 months of age. Scale bar = 250 μm, in lower panels = 250 μm. Error bars represent mean ± SEM (n = 6 per age and genotype).

    Journal: BMC Neuroscience

    Article Title: Cerebrolysin™ efficacy in a transgenic model of tauopathy: role in regulation of mitochondrial structure

    doi: 10.1186/1471-2202-15-90

    Figure Lengend Snippet: Comparison of effects of aging on p-Tau in non-tg single tg and Tau/GSK3β bigenic mice. (A) Representative images of immunohistochemical analysis with the p-Tau (AT8) in the neocortex and hippocampus in the non-tg, single tg and Tau/GSK3β bigenic mice at 3, 6 and 12 months of age. (B) Image analysis of optical density in the hippocampus represented as a line graph in the non-tg, single tg and Tau/GSK3β bigenic mice at 3, 6 and 12 months of age. Scale bar = 250 μm, in lower panels = 250 μm. Error bars represent mean ± SEM (n = 6 per age and genotype).

    Article Snippet: Immunohistochemical analysis For this purpose as previously described [ , ], blind-coded 40 μm thick vibratome sections were immunolabeled with the mouse monoclonal antibodies against Drp-1 (1:500, Santa Cruz), Tom40 (1:1000, Santa Cruz), synaptophysin (presynaptic terminal marker, 1:40, Chemicon), GFAP (astroglial marker, 1:1000, Chemicon), p-Tau (AT8, 1:500, Pierce; AT270 1:500, Pierce), t-Tau (1:500, Dako), t-GSK3β (1:500, Cell Signaling) and p-GSK3β (GSK3βY216, 1:500, Life Technologies), as previously described [ , ].

    Techniques: Mouse Assay, Immunohistochemistry

    Immunoblot and immunocytochemical analysis of effect of CBL on Tau in Tau/GSK3β bigenic mice. (A) Representative Immunoblot image of total-tau (t-Tau), phospho-Tau (p-Tau) at epitopes recognized by the AT8 (Ser202/Thr205) and AT270 (Thr181) antibodies and actin levels in vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (B- D) Image analysis of levels of t-Tau, p-Tau (AT8) and p-Tau (AT270) respectively in vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (E) Immunohistochemical analysis of p-Tau (AT8) immunoreactivity in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. Boxes in upper panels are represented at higher magnification in the lower panels. (F) Image analysis of p-GSK3β immunoreactivity in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (A, C) Scale bar in upper panels = 250 μm, in lower panels = 50 μm. (B, D) Error bars represent mean ± SEM (n = 6 per group, 6 m/o). *Indicates a significant difference (p

    Journal: BMC Neuroscience

    Article Title: Cerebrolysin™ efficacy in a transgenic model of tauopathy: role in regulation of mitochondrial structure

    doi: 10.1186/1471-2202-15-90

    Figure Lengend Snippet: Immunoblot and immunocytochemical analysis of effect of CBL on Tau in Tau/GSK3β bigenic mice. (A) Representative Immunoblot image of total-tau (t-Tau), phospho-Tau (p-Tau) at epitopes recognized by the AT8 (Ser202/Thr205) and AT270 (Thr181) antibodies and actin levels in vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (B- D) Image analysis of levels of t-Tau, p-Tau (AT8) and p-Tau (AT270) respectively in vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (E) Immunohistochemical analysis of p-Tau (AT8) immunoreactivity in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. Boxes in upper panels are represented at higher magnification in the lower panels. (F) Image analysis of p-GSK3β immunoreactivity in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (A, C) Scale bar in upper panels = 250 μm, in lower panels = 50 μm. (B, D) Error bars represent mean ± SEM (n = 6 per group, 6 m/o). *Indicates a significant difference (p

    Article Snippet: Immunohistochemical analysis For this purpose as previously described [ , ], blind-coded 40 μm thick vibratome sections were immunolabeled with the mouse monoclonal antibodies against Drp-1 (1:500, Santa Cruz), Tom40 (1:1000, Santa Cruz), synaptophysin (presynaptic terminal marker, 1:40, Chemicon), GFAP (astroglial marker, 1:1000, Chemicon), p-Tau (AT8, 1:500, Pierce; AT270 1:500, Pierce), t-Tau (1:500, Dako), t-GSK3β (1:500, Cell Signaling) and p-GSK3β (GSK3βY216, 1:500, Life Technologies), as previously described [ , ].

    Techniques: Mouse Assay, Immunohistochemistry

    Effect of CBL on mitochondrial proteins in Tau/GSK3β bigenic mice. (A) Immunoblot analysis of Drp-1 levels in hippocampal homogenates from vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. Actin was used as a loading control. (B) Quantitative analysis of Drp-1 levels in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (C) Quantitative analysis of p-Drp-1 levels in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (D) Immunohistochemical analysis of Drp-1 and Tom40 levels in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. Arrows indicate immunoreactive mitochondria. (E) Quantitative analysis of Drp-1 levels in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (F) Quantitative analysis of Tom40 levels in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. Scale Bars = 5 μm, Error bars represent mean ± SEM (n = 6 per group, 6 m/o). *Indicates a significant difference (p

    Journal: BMC Neuroscience

    Article Title: Cerebrolysin™ efficacy in a transgenic model of tauopathy: role in regulation of mitochondrial structure

    doi: 10.1186/1471-2202-15-90

    Figure Lengend Snippet: Effect of CBL on mitochondrial proteins in Tau/GSK3β bigenic mice. (A) Immunoblot analysis of Drp-1 levels in hippocampal homogenates from vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. Actin was used as a loading control. (B) Quantitative analysis of Drp-1 levels in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (C) Quantitative analysis of p-Drp-1 levels in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (D) Immunohistochemical analysis of Drp-1 and Tom40 levels in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. Arrows indicate immunoreactive mitochondria. (E) Quantitative analysis of Drp-1 levels in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (F) Quantitative analysis of Tom40 levels in the hippocampus of vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. Scale Bars = 5 μm, Error bars represent mean ± SEM (n = 6 per group, 6 m/o). *Indicates a significant difference (p

    Article Snippet: Immunohistochemical analysis For this purpose as previously described [ , ], blind-coded 40 μm thick vibratome sections were immunolabeled with the mouse monoclonal antibodies against Drp-1 (1:500, Santa Cruz), Tom40 (1:1000, Santa Cruz), synaptophysin (presynaptic terminal marker, 1:40, Chemicon), GFAP (astroglial marker, 1:1000, Chemicon), p-Tau (AT8, 1:500, Pierce; AT270 1:500, Pierce), t-Tau (1:500, Dako), t-GSK3β (1:500, Cell Signaling) and p-GSK3β (GSK3βY216, 1:500, Life Technologies), as previously described [ , ].

    Techniques: Mouse Assay, Immunohistochemistry

    Characterization of Tau/GSK3β bigenic mice. (A) Representative immunoblot image for total GSK3β (t-GSK3β), phospho-GSK3β (p-GSK3β)(Y216), total Tau (t-Tau) and phospho-Tau (p-Tau) levels in the hippocampus of the Tau/GSK3β bigenic mice compared to Tau tg, GSK3β tg and non-tg mice. Actin was used as a loading control. (B) Analysis of levels of t-GSK3β and p-GSK3β showing 3 fold higher levels in GSK3β bigenic mice. (C) Analysis of levels of t-Tau and p-Tau (AT8) showing higher levels of p-Tau in bigenic mice compared to Tau tg mice. (D, E) Immunohistochemical and image analysis of pGSK3β immunoreactivity in the dentate gyrus of the hippocampus (inset) in the non-tg, single tg and Tau/GSK3β bigenic mice. (F, G) Immunohistochemical and image analysis of p-Tau (AT8) immunoreactivity in the dentate gyrus of the hippocampus (inset) in the non-tg, single tg and Tau/GSK3β bigenic mice The boxes indicate regions shown at higher magnification in the lower panels. Scale bar in upper panel = 250 μm, in lower panels = 30 μm. Error bars represent mean ± SEM (n = 6 per group, 6 m/o). *Indicates a significant difference (p

    Journal: BMC Neuroscience

    Article Title: Cerebrolysin™ efficacy in a transgenic model of tauopathy: role in regulation of mitochondrial structure

    doi: 10.1186/1471-2202-15-90

    Figure Lengend Snippet: Characterization of Tau/GSK3β bigenic mice. (A) Representative immunoblot image for total GSK3β (t-GSK3β), phospho-GSK3β (p-GSK3β)(Y216), total Tau (t-Tau) and phospho-Tau (p-Tau) levels in the hippocampus of the Tau/GSK3β bigenic mice compared to Tau tg, GSK3β tg and non-tg mice. Actin was used as a loading control. (B) Analysis of levels of t-GSK3β and p-GSK3β showing 3 fold higher levels in GSK3β bigenic mice. (C) Analysis of levels of t-Tau and p-Tau (AT8) showing higher levels of p-Tau in bigenic mice compared to Tau tg mice. (D, E) Immunohistochemical and image analysis of pGSK3β immunoreactivity in the dentate gyrus of the hippocampus (inset) in the non-tg, single tg and Tau/GSK3β bigenic mice. (F, G) Immunohistochemical and image analysis of p-Tau (AT8) immunoreactivity in the dentate gyrus of the hippocampus (inset) in the non-tg, single tg and Tau/GSK3β bigenic mice The boxes indicate regions shown at higher magnification in the lower panels. Scale bar in upper panel = 250 μm, in lower panels = 30 μm. Error bars represent mean ± SEM (n = 6 per group, 6 m/o). *Indicates a significant difference (p

    Article Snippet: Immunohistochemical analysis For this purpose as previously described [ , ], blind-coded 40 μm thick vibratome sections were immunolabeled with the mouse monoclonal antibodies against Drp-1 (1:500, Santa Cruz), Tom40 (1:1000, Santa Cruz), synaptophysin (presynaptic terminal marker, 1:40, Chemicon), GFAP (astroglial marker, 1:1000, Chemicon), p-Tau (AT8, 1:500, Pierce; AT270 1:500, Pierce), t-Tau (1:500, Dako), t-GSK3β (1:500, Cell Signaling) and p-GSK3β (GSK3βY216, 1:500, Life Technologies), as previously described [ , ].

    Techniques: Mouse Assay, Immunohistochemistry

    Ultrastructural analysis of mitochondrial structure in Tau/GSK3β bigenic mice. (A) Ultrastructural analysis of mitochondrial structure in vehicle-treated and CBL treated non-tg mice. (B) Ultrastructural analysis of mitochondrial structure in vehicle-treated Tau/GSK3β bigenic mice, boxes in upper panel are shown at a higher magnification in the lower panels. (C) Ultrastructural analysis of mitochondrial structure in CBL-treated Tau/GSK3β bigenic mice. (D) Quantitative analysis of number of small mitochondria (less than 5 μm) in vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (E) Quantitative analysis of number of dividing mitochondria in vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (F) Quantitative analysis of number of mitochondrial inclusions in vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. Scale Bar = 0.5 μm, error bars represent mean ± SEM (n = 6 per group, 6 m/o). *Indicates a significant difference (p

    Journal: BMC Neuroscience

    Article Title: Cerebrolysin™ efficacy in a transgenic model of tauopathy: role in regulation of mitochondrial structure

    doi: 10.1186/1471-2202-15-90

    Figure Lengend Snippet: Ultrastructural analysis of mitochondrial structure in Tau/GSK3β bigenic mice. (A) Ultrastructural analysis of mitochondrial structure in vehicle-treated and CBL treated non-tg mice. (B) Ultrastructural analysis of mitochondrial structure in vehicle-treated Tau/GSK3β bigenic mice, boxes in upper panel are shown at a higher magnification in the lower panels. (C) Ultrastructural analysis of mitochondrial structure in CBL-treated Tau/GSK3β bigenic mice. (D) Quantitative analysis of number of small mitochondria (less than 5 μm) in vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (E) Quantitative analysis of number of dividing mitochondria in vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. (F) Quantitative analysis of number of mitochondrial inclusions in vehicle and CBL treated Tau/GSK3β bigenic mice in comparison to non-tg mice. Scale Bar = 0.5 μm, error bars represent mean ± SEM (n = 6 per group, 6 m/o). *Indicates a significant difference (p

    Article Snippet: Immunohistochemical analysis For this purpose as previously described [ , ], blind-coded 40 μm thick vibratome sections were immunolabeled with the mouse monoclonal antibodies against Drp-1 (1:500, Santa Cruz), Tom40 (1:1000, Santa Cruz), synaptophysin (presynaptic terminal marker, 1:40, Chemicon), GFAP (astroglial marker, 1:1000, Chemicon), p-Tau (AT8, 1:500, Pierce; AT270 1:500, Pierce), t-Tau (1:500, Dako), t-GSK3β (1:500, Cell Signaling) and p-GSK3β (GSK3βY216, 1:500, Life Technologies), as previously described [ , ].

    Techniques: Mouse Assay

    (A) By western blot analysis, ILK silencing combined with hyperthermia could inhibit the proteins level of p-Akt, p-GSK3β and p-HSF1, and promote the expression of Bax protein (P

    Journal: Oncology Letters

    Article Title: Association between integrin-linked kinase and hyperthermia in oral squamous cell carcinoma

    doi: 10.3892/ol.2017.7222

    Figure Lengend Snippet: (A) By western blot analysis, ILK silencing combined with hyperthermia could inhibit the proteins level of p-Akt, p-GSK3β and p-HSF1, and promote the expression of Bax protein (P

    Article Snippet: The primary antibodies used were: ILK (cat. no. 3862; 1:100; Cell Signaling Technology, Inc.), p-Akt (cat. no. 9271; 1:300; Cell Signaling Technology, Inc.), total Akt (cat. no. 9272; 1:300; Cell Signaling Technology, Inc.), p-GSK3β (cat. no. BS6365; 1:100; BioWorld Technology, Inc.), total GSK3β (cat. no. BS4084; 1:100; BioWorld Technology, Inc.), Bax (cat. no. bs2538; 1:100, BioWorld Technology, Inc.), p-HSF1 (cat. no. pS303/307; 2108-1, 1:100; Epitomics; Abcam) and total HSF1 (2043–1; 1:100, Epitomics; Abcam).

    Techniques: Western Blot, Expressing

    In vivo experiments of ILK silencing combined with hyperthermia (×400). (A) A total of 7 days after inoculation, the xenograft tumor formed. (B) There was no significant organic damage in heart, liver, brain, spleen, lung and kidney of nude mice following ILK silencing combined with hyperthermiaby H E staining (×100). (C) Results of H E staining and immunohistochemical analysis in the control group. Polygonal cells were in dense flocks, nuclei were large and deeply stained, the expression of ILK, p-Akt, p-GSK3β and p-HSF1 was high, and the expression of Bax was low. (D) The figures of the NC group were same as the control group. (E) Results of H E staining and IHC analysis in the KD group. (F) Results of H E staining and IHC analysis in the HT group. (G) Results of the NC + HT group were same as the HT group. (H) Results of the KD + HT group were similar to the HT group. (I) TUNEL analysis was used to detect cell apoptosis. Cell apoptosis was significantly increased in the KD group and KD + HT group. Fewer apoptotic cells were found in the HT group and the NC + HT group, and the smallest number of apoptotic cells were found in the control and NC groups. (J) IgG negative control. ILK, integrin-linked kinase; HT, hyperthermia; p-, phosphorylated; GSK3β, glycogen synthase kinase 3β; HSF1, heat shock factor 1; Bax, B cell-2-associated X protein; H E, hematoxylin and eosin; NC, negative control; Con, control; HT, hyperthermia; KD, ILK silencing.

    Journal: Oncology Letters

    Article Title: Association between integrin-linked kinase and hyperthermia in oral squamous cell carcinoma

    doi: 10.3892/ol.2017.7222

    Figure Lengend Snippet: In vivo experiments of ILK silencing combined with hyperthermia (×400). (A) A total of 7 days after inoculation, the xenograft tumor formed. (B) There was no significant organic damage in heart, liver, brain, spleen, lung and kidney of nude mice following ILK silencing combined with hyperthermiaby H E staining (×100). (C) Results of H E staining and immunohistochemical analysis in the control group. Polygonal cells were in dense flocks, nuclei were large and deeply stained, the expression of ILK, p-Akt, p-GSK3β and p-HSF1 was high, and the expression of Bax was low. (D) The figures of the NC group were same as the control group. (E) Results of H E staining and IHC analysis in the KD group. (F) Results of H E staining and IHC analysis in the HT group. (G) Results of the NC + HT group were same as the HT group. (H) Results of the KD + HT group were similar to the HT group. (I) TUNEL analysis was used to detect cell apoptosis. Cell apoptosis was significantly increased in the KD group and KD + HT group. Fewer apoptotic cells were found in the HT group and the NC + HT group, and the smallest number of apoptotic cells were found in the control and NC groups. (J) IgG negative control. ILK, integrin-linked kinase; HT, hyperthermia; p-, phosphorylated; GSK3β, glycogen synthase kinase 3β; HSF1, heat shock factor 1; Bax, B cell-2-associated X protein; H E, hematoxylin and eosin; NC, negative control; Con, control; HT, hyperthermia; KD, ILK silencing.

    Article Snippet: The primary antibodies used were: ILK (cat. no. 3862; 1:100; Cell Signaling Technology, Inc.), p-Akt (cat. no. 9271; 1:300; Cell Signaling Technology, Inc.), total Akt (cat. no. 9272; 1:300; Cell Signaling Technology, Inc.), p-GSK3β (cat. no. BS6365; 1:100; BioWorld Technology, Inc.), total GSK3β (cat. no. BS4084; 1:100; BioWorld Technology, Inc.), Bax (cat. no. bs2538; 1:100, BioWorld Technology, Inc.), p-HSF1 (cat. no. pS303/307; 2108-1, 1:100; Epitomics; Abcam) and total HSF1 (2043–1; 1:100, Epitomics; Abcam).

    Techniques: In Vivo, Mouse Assay, Staining, Immunohistochemistry, Expressing, TUNEL Assay, Negative Control