p gsk 3 β  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p gsk 3 β
    ZSD induced the apoptosis of H1299 cells partially by regulating <t>AKT/GSK-3</t> β / β -catenin signaling. (a) ZSD induced the apoptosis of H1299 cells after treatment with ZSD (4 mg/mL) for 12 h, 24 h, and 48 h. (b) ZSD induced apoptosis of H1299 cells in a dose-dependent manner. (c) Pathway enrichment analysis of the genes in Human Signal Transduction Pathway Finder PCR Array. (d) The mRNA expression of AKT/GSK-3 β / β -catenin signal cascades in H1299 cells after treatment with ZSD (4 mg/mL). ∗ p < 0.05 and ∗∗ p < 0.01 vs. the control group.
    P Gsk 3 β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    p gsk 3 β - by Bioz Stars, 2023-02
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    Images

    1) Product Images from "Zi Shen Decoction Inhibits Growth and Metastasis of Lung Cancer via Regulating the AKT/GSK-3 β / β -Catenin Pathway"

    Article Title: Zi Shen Decoction Inhibits Growth and Metastasis of Lung Cancer via Regulating the AKT/GSK-3 β / β -Catenin Pathway

    Journal: Oxidative Medicine and Cellular Longevity

    doi: 10.1155/2021/6685282

    ZSD induced the apoptosis of H1299 cells partially by regulating AKT/GSK-3 β / β -catenin signaling. (a) ZSD induced the apoptosis of H1299 cells after treatment with ZSD (4 mg/mL) for 12 h, 24 h, and 48 h. (b) ZSD induced apoptosis of H1299 cells in a dose-dependent manner. (c) Pathway enrichment analysis of the genes in Human Signal Transduction Pathway Finder PCR Array. (d) The mRNA expression of AKT/GSK-3 β / β -catenin signal cascades in H1299 cells after treatment with ZSD (4 mg/mL). ∗ p < 0.05 and ∗∗ p < 0.01 vs. the control group.
    Figure Legend Snippet: ZSD induced the apoptosis of H1299 cells partially by regulating AKT/GSK-3 β / β -catenin signaling. (a) ZSD induced the apoptosis of H1299 cells after treatment with ZSD (4 mg/mL) for 12 h, 24 h, and 48 h. (b) ZSD induced apoptosis of H1299 cells in a dose-dependent manner. (c) Pathway enrichment analysis of the genes in Human Signal Transduction Pathway Finder PCR Array. (d) The mRNA expression of AKT/GSK-3 β / β -catenin signal cascades in H1299 cells after treatment with ZSD (4 mg/mL). ∗ p < 0.05 and ∗∗ p < 0.01 vs. the control group.

    Techniques Used: Transduction, Expressing

    ZSD inhibited the AKT/GSK-3 β / β -catenin pathway in lung cancer cells and tumor tissues. (a) Western blot analysis was used to assess the expression of multiple proteins involved in the AKT/GSK-3 β / β -catenin pathway in lung cancer cells after ZSD treatment for 12 h, 24 h, and 48 h. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the control group. (b) Western blots showing the protein expression of AKT, p-AKT, GSK-3 β , p-GSK-3 β , β -catenin, cleaved caspase-3, and Bax and Bcl-2 in isolated tumor tissues. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the model group.
    Figure Legend Snippet: ZSD inhibited the AKT/GSK-3 β / β -catenin pathway in lung cancer cells and tumor tissues. (a) Western blot analysis was used to assess the expression of multiple proteins involved in the AKT/GSK-3 β / β -catenin pathway in lung cancer cells after ZSD treatment for 12 h, 24 h, and 48 h. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the control group. (b) Western blots showing the protein expression of AKT, p-AKT, GSK-3 β , p-GSK-3 β , β -catenin, cleaved caspase-3, and Bax and Bcl-2 in isolated tumor tissues. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the model group.

    Techniques Used: Western Blot, Expressing, Isolation

    The AKT/GSK-3 β / β -catenin pathway medicated anticancer effect of ZSD in lung cancer cells. H1299 cells were treated with ZSD and/or SC-79 for 24 h. (a) Representative western blots and quantitative analysis of the AKT/GSK-3 β / β -catenin pathway related proteins. (b) The mobility of H1299 cells was detected by wound-healing assay. (c) The migration and invasion abilities of H1299 cells were detected by transwell assays. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the control group.
    Figure Legend Snippet: The AKT/GSK-3 β / β -catenin pathway medicated anticancer effect of ZSD in lung cancer cells. H1299 cells were treated with ZSD and/or SC-79 for 24 h. (a) Representative western blots and quantitative analysis of the AKT/GSK-3 β / β -catenin pathway related proteins. (b) The mobility of H1299 cells was detected by wound-healing assay. (c) The migration and invasion abilities of H1299 cells were detected by transwell assays. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the control group.

    Techniques Used: Western Blot, Wound Healing Assay, Migration

    p gsk 3 β  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p gsk 3 β
    ZSD induced the apoptosis of H1299 cells partially by regulating <t>AKT/GSK-3</t> β / β -catenin signaling. (a) ZSD induced the apoptosis of H1299 cells after treatment with ZSD (4 mg/mL) for 12 h, 24 h, and 48 h. (b) ZSD induced apoptosis of H1299 cells in a dose-dependent manner. (c) Pathway enrichment analysis of the genes in Human Signal Transduction Pathway Finder PCR Array. (d) The mRNA expression of AKT/GSK-3 β / β -catenin signal cascades in H1299 cells after treatment with ZSD (4 mg/mL). ∗ p < 0.05 and ∗∗ p < 0.01 vs. the control group.
    P Gsk 3 β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p gsk 3 β - by Bioz Stars, 2023-02
    97/100 stars

    Images

    1) Product Images from "Zi Shen Decoction Inhibits Growth and Metastasis of Lung Cancer via Regulating the AKT/GSK-3 β / β -Catenin Pathway"

    Article Title: Zi Shen Decoction Inhibits Growth and Metastasis of Lung Cancer via Regulating the AKT/GSK-3 β / β -Catenin Pathway

    Journal: Oxidative Medicine and Cellular Longevity

    doi: 10.1155/2021/6685282

    ZSD induced the apoptosis of H1299 cells partially by regulating AKT/GSK-3 β / β -catenin signaling. (a) ZSD induced the apoptosis of H1299 cells after treatment with ZSD (4 mg/mL) for 12 h, 24 h, and 48 h. (b) ZSD induced apoptosis of H1299 cells in a dose-dependent manner. (c) Pathway enrichment analysis of the genes in Human Signal Transduction Pathway Finder PCR Array. (d) The mRNA expression of AKT/GSK-3 β / β -catenin signal cascades in H1299 cells after treatment with ZSD (4 mg/mL). ∗ p < 0.05 and ∗∗ p < 0.01 vs. the control group.
    Figure Legend Snippet: ZSD induced the apoptosis of H1299 cells partially by regulating AKT/GSK-3 β / β -catenin signaling. (a) ZSD induced the apoptosis of H1299 cells after treatment with ZSD (4 mg/mL) for 12 h, 24 h, and 48 h. (b) ZSD induced apoptosis of H1299 cells in a dose-dependent manner. (c) Pathway enrichment analysis of the genes in Human Signal Transduction Pathway Finder PCR Array. (d) The mRNA expression of AKT/GSK-3 β / β -catenin signal cascades in H1299 cells after treatment with ZSD (4 mg/mL). ∗ p < 0.05 and ∗∗ p < 0.01 vs. the control group.

    Techniques Used: Transduction, Expressing

    ZSD inhibited the AKT/GSK-3 β / β -catenin pathway in lung cancer cells and tumor tissues. (a) Western blot analysis was used to assess the expression of multiple proteins involved in the AKT/GSK-3 β / β -catenin pathway in lung cancer cells after ZSD treatment for 12 h, 24 h, and 48 h. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the control group. (b) Western blots showing the protein expression of AKT, p-AKT, GSK-3 β , p-GSK-3 β , β -catenin, cleaved caspase-3, and Bax and Bcl-2 in isolated tumor tissues. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the model group.
    Figure Legend Snippet: ZSD inhibited the AKT/GSK-3 β / β -catenin pathway in lung cancer cells and tumor tissues. (a) Western blot analysis was used to assess the expression of multiple proteins involved in the AKT/GSK-3 β / β -catenin pathway in lung cancer cells after ZSD treatment for 12 h, 24 h, and 48 h. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the control group. (b) Western blots showing the protein expression of AKT, p-AKT, GSK-3 β , p-GSK-3 β , β -catenin, cleaved caspase-3, and Bax and Bcl-2 in isolated tumor tissues. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the model group.

    Techniques Used: Western Blot, Expressing, Isolation

    The AKT/GSK-3 β / β -catenin pathway medicated anticancer effect of ZSD in lung cancer cells. H1299 cells were treated with ZSD and/or SC-79 for 24 h. (a) Representative western blots and quantitative analysis of the AKT/GSK-3 β / β -catenin pathway related proteins. (b) The mobility of H1299 cells was detected by wound-healing assay. (c) The migration and invasion abilities of H1299 cells were detected by transwell assays. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the control group.
    Figure Legend Snippet: The AKT/GSK-3 β / β -catenin pathway medicated anticancer effect of ZSD in lung cancer cells. H1299 cells were treated with ZSD and/or SC-79 for 24 h. (a) Representative western blots and quantitative analysis of the AKT/GSK-3 β / β -catenin pathway related proteins. (b) The mobility of H1299 cells was detected by wound-healing assay. (c) The migration and invasion abilities of H1299 cells were detected by transwell assays. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the control group.

    Techniques Used: Western Blot, Wound Healing Assay, Migration

    phosphor gsk3 β  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phosphor gsk3 β
    HRT inhibited cancer cell proliferation via suppressing Akt signaling. (a) The expression of phosphor-ERK or -Akt was examined in HCT116 cells treated with HRT in a time-dependent manner. HRT induced dephosphorylation of Akt not ERK at 24 h. (b) The effect of HRT on PI3K/Akt signaling pathway. Phosphorylation levels of Akt, mTOR, and <t>GSK3</t> <t>β</t> were examined in HCT116 cells treated with LY294002 (10 μ M), HRT (300 μ g/mL) or cotreated with LY294002 and HRT for 24 h.
    Phosphor Gsk3 β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "HRT, Herbal Formula, Induces G 2 /M Cell Cycle Arrest and Apoptosis via Suppressing Akt Signaling Pathway in Human Colon Cancer Cells"

    Article Title: HRT, Herbal Formula, Induces G 2 /M Cell Cycle Arrest and Apoptosis via Suppressing Akt Signaling Pathway in Human Colon Cancer Cells

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    doi: 10.1155/2012/871893

    HRT inhibited cancer cell proliferation via suppressing Akt signaling. (a) The expression of phosphor-ERK or -Akt was examined in HCT116 cells treated with HRT in a time-dependent manner. HRT induced dephosphorylation of Akt not ERK at 24 h. (b) The effect of HRT on PI3K/Akt signaling pathway. Phosphorylation levels of Akt, mTOR, and GSK3 β were examined in HCT116 cells treated with LY294002 (10 μ M), HRT (300 μ g/mL) or cotreated with LY294002 and HRT for 24 h.
    Figure Legend Snippet: HRT inhibited cancer cell proliferation via suppressing Akt signaling. (a) The expression of phosphor-ERK or -Akt was examined in HCT116 cells treated with HRT in a time-dependent manner. HRT induced dephosphorylation of Akt not ERK at 24 h. (b) The effect of HRT on PI3K/Akt signaling pathway. Phosphorylation levels of Akt, mTOR, and GSK3 β were examined in HCT116 cells treated with LY294002 (10 μ M), HRT (300 μ g/mL) or cotreated with LY294002 and HRT for 24 h.

    Techniques Used: Expressing, De-Phosphorylation Assay

    gsk 3 β  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc gsk 3 β
    The relationship between CRIP1 and EMT indicates that CRIP1 may function in ovarian cancer development via the Wnt/ β -catenin pathway. (a) KEGG pathway enrichment analysis was performed to identify which pathway was significantly enriched in CRIP1-related ovarian cancer progression. (b) The effect of CRIP1 silencing on EMT-related signaling pathways. EMT markers, such as E-cadherin, N-cadherin, and vimentin proteins, were detected by western blot. (c) The effect of CRIP1 silencing on Wnt/ β -catenin signaling pathway. The important molecules of this pathway, including β -catenin, <t>GSK-3</t> β , p-GSK-3 β , MMP2, and MMP9, were assessed by western blot.
    Gsk 3 β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Cysteine-Rich Intestinal Protein 1 Served as an Epithelial Ovarian Cancer Marker via Promoting Wnt/ β -Catenin-Mediated EMT and Tumour Metastasis"

    Article Title: Cysteine-Rich Intestinal Protein 1 Served as an Epithelial Ovarian Cancer Marker via Promoting Wnt/ β -Catenin-Mediated EMT and Tumour Metastasis

    Journal: Disease Markers

    doi: 10.1155/2021/3566749

    The relationship between CRIP1 and EMT indicates that CRIP1 may function in ovarian cancer development via the Wnt/ β -catenin pathway. (a) KEGG pathway enrichment analysis was performed to identify which pathway was significantly enriched in CRIP1-related ovarian cancer progression. (b) The effect of CRIP1 silencing on EMT-related signaling pathways. EMT markers, such as E-cadherin, N-cadherin, and vimentin proteins, were detected by western blot. (c) The effect of CRIP1 silencing on Wnt/ β -catenin signaling pathway. The important molecules of this pathway, including β -catenin, GSK-3 β , p-GSK-3 β , MMP2, and MMP9, were assessed by western blot.
    Figure Legend Snippet: The relationship between CRIP1 and EMT indicates that CRIP1 may function in ovarian cancer development via the Wnt/ β -catenin pathway. (a) KEGG pathway enrichment analysis was performed to identify which pathway was significantly enriched in CRIP1-related ovarian cancer progression. (b) The effect of CRIP1 silencing on EMT-related signaling pathways. EMT markers, such as E-cadherin, N-cadherin, and vimentin proteins, were detected by western blot. (c) The effect of CRIP1 silencing on Wnt/ β -catenin signaling pathway. The important molecules of this pathway, including β -catenin, GSK-3 β , p-GSK-3 β , MMP2, and MMP9, were assessed by western blot.

    Techniques Used: Western Blot

    gsk3 β  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc gsk3 β
    Gsk3 β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, 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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    Cell Signaling Technology Inc p gsk3 β
    P Gsk3 β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    gsk3 β 9332 antibodies  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc gsk3 β 9332 antibodies
    Gsk3 β 9332 Antibodies, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti gsk3 β  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti gsk3 β
    Artemether increased phosphorylation of <t>AMPK/GSK3</t> β (ser9)in PC12 cell cultures exposed to A β 1-42. (a, c) PC12 cells pretreated for 2 h with different concentrations of Artemether were incubated with 1 μ M A β 1-42 for 24 h .The lysates were submitted for measurements of phosphorylations by western blotting using specific antibodies for AMPK (P-AMPK), total AMPK (T-AMPK), <t>GSK3</t> <t>β</t> (ser9) (P-GSK3 β ), and total GSK3 β (T-GSK3 β ). GAPDH was used for normalization. Three independent experiments were included. (b, d) Quantitation of phosphorylated kinases. ∗ p < 0.05 and ∗∗ p < 0.01 were considered significantly different.
    Anti Gsk3 β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Artemether Activation of AMPK/GSK3 β (ser9)/Nrf2 Signaling Confers Neuroprotection towards β- Amyloid-Induced Neurotoxicity in 3xTg Alzheimer's Mouse Model"

    Article Title: Artemether Activation of AMPK/GSK3 β (ser9)/Nrf2 Signaling Confers Neuroprotection towards β- Amyloid-Induced Neurotoxicity in 3xTg Alzheimer's Mouse Model

    Journal: Oxidative Medicine and Cellular Longevity

    doi: 10.1155/2019/1862437

    Artemether increased phosphorylation of AMPK/GSK3 β (ser9)in PC12 cell cultures exposed to A β 1-42. (a, c) PC12 cells pretreated for 2 h with different concentrations of Artemether were incubated with 1 μ M A β 1-42 for 24 h .The lysates were submitted for measurements of phosphorylations by western blotting using specific antibodies for AMPK (P-AMPK), total AMPK (T-AMPK), GSK3 β (ser9) (P-GSK3 β ), and total GSK3 β (T-GSK3 β ). GAPDH was used for normalization. Three independent experiments were included. (b, d) Quantitation of phosphorylated kinases. ∗ p < 0.05 and ∗∗ p < 0.01 were considered significantly different.
    Figure Legend Snippet: Artemether increased phosphorylation of AMPK/GSK3 β (ser9)in PC12 cell cultures exposed to A β 1-42. (a, c) PC12 cells pretreated for 2 h with different concentrations of Artemether were incubated with 1 μ M A β 1-42 for 24 h .The lysates were submitted for measurements of phosphorylations by western blotting using specific antibodies for AMPK (P-AMPK), total AMPK (T-AMPK), GSK3 β (ser9) (P-GSK3 β ), and total GSK3 β (T-GSK3 β ). GAPDH was used for normalization. Three independent experiments were included. (b, d) Quantitation of phosphorylated kinases. ∗ p < 0.05 and ∗∗ p < 0.01 were considered significantly different.

    Techniques Used: Incubation, Western Blot, Quantitation Assay

    Direct relationship between Artemether effects on AMPK/GSK3 β (ser9) phosphorylation and neuroprotection towards A β 1-42 -induced apoptotic cell death in PC12 cells. PC12 cells pretreated with 5 μ M compound C (AMPK inhibitor) for 30 min, followed by incubation with 1 μ M A β 1-42 in the presence or absence of different concentrations of Artemether. (a) Cell viability was measured by MTT assay. ∗ p < 0.05 and ∗∗∗ p < 0.001 were considered significantly different. (b) Apoptosis was determined by flow cytometry. (c) Quantitation of the percentage of cell apoptosis. ∗∗∗ p < 0.001 was considered significantly different. (d) Phosphorylation activities of AMPK/GSK3 β (ser9). GAPDH was used for normalization. (e, f) Quantitation of phosphorylation activities of AMPK/GSK3 β . All results are presented as mean ± SEM ( n = 3); ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 were considered significantly different.
    Figure Legend Snippet: Direct relationship between Artemether effects on AMPK/GSK3 β (ser9) phosphorylation and neuroprotection towards A β 1-42 -induced apoptotic cell death in PC12 cells. PC12 cells pretreated with 5 μ M compound C (AMPK inhibitor) for 30 min, followed by incubation with 1 μ M A β 1-42 in the presence or absence of different concentrations of Artemether. (a) Cell viability was measured by MTT assay. ∗ p < 0.05 and ∗∗∗ p < 0.001 were considered significantly different. (b) Apoptosis was determined by flow cytometry. (c) Quantitation of the percentage of cell apoptosis. ∗∗∗ p < 0.001 was considered significantly different. (d) Phosphorylation activities of AMPK/GSK3 β (ser9). GAPDH was used for normalization. (e, f) Quantitation of phosphorylation activities of AMPK/GSK3 β . All results are presented as mean ± SEM ( n = 3); ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 were considered significantly different.

    Techniques Used: Incubation, MTT Assay, Flow Cytometry, Quantitation Assay

    Artemether stimulated the phosphorylation of AMPK/GSK3 β (ser9) and increased the expression levels of Nrf2 and heme oxygenase-1 (HO-1) in the brain cortex of 3xTg-AD mice. Artemether was administered to mice by intraperitoneal injection, once a day, at low doses of 5 mg/kg and high doses of 20 mg/kg for 4 weeks. Thereafter, the brain cortex extracts of wild-type (WT) compared to 3xTg-AD mice treated with either a low (Arte low) or high dose (Arte high) of Artemether or untreated (3xTg) were submitted for analyses. (a) Phosphorylations of AMPK/GSK3 β (ser9) and protein expression levels of Nrf2 and heme oxygenase-1 (HO-1); three mice per treatment group were used for western blot. (b–e) Quantitation of western blotting results of the different experimental groups. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 were considered significantly different.
    Figure Legend Snippet: Artemether stimulated the phosphorylation of AMPK/GSK3 β (ser9) and increased the expression levels of Nrf2 and heme oxygenase-1 (HO-1) in the brain cortex of 3xTg-AD mice. Artemether was administered to mice by intraperitoneal injection, once a day, at low doses of 5 mg/kg and high doses of 20 mg/kg for 4 weeks. Thereafter, the brain cortex extracts of wild-type (WT) compared to 3xTg-AD mice treated with either a low (Arte low) or high dose (Arte high) of Artemether or untreated (3xTg) were submitted for analyses. (a) Phosphorylations of AMPK/GSK3 β (ser9) and protein expression levels of Nrf2 and heme oxygenase-1 (HO-1); three mice per treatment group were used for western blot. (b–e) Quantitation of western blotting results of the different experimental groups. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 were considered significantly different.

    Techniques Used: Expressing, Injection, Western Blot, Quantitation Assay

    A schematic diagram of Artemether-induced AMPK/GSK3 β (ser9)/Nrf2 activation towards reduction of amyloid- β -evoked oxidative stress to confer neuroprotection. Artemether stimulated AMPK/GSK3 β (ser9) phosphorylation output in neuronal cells and animal brain cortex to increase the nuclear expression of Nrf2 with induction of the phase II antioxidant enzymes and anti-inflammatory genes containing ARE. This process (dotted line) caused attenuation of APP-derived and A β -induced ROS production, reduction of oxidative stress, correction of mitochondrial dysfunction, reduction of inflammation, and conferring neuroprotection.
    Figure Legend Snippet: A schematic diagram of Artemether-induced AMPK/GSK3 β (ser9)/Nrf2 activation towards reduction of amyloid- β -evoked oxidative stress to confer neuroprotection. Artemether stimulated AMPK/GSK3 β (ser9) phosphorylation output in neuronal cells and animal brain cortex to increase the nuclear expression of Nrf2 with induction of the phase II antioxidant enzymes and anti-inflammatory genes containing ARE. This process (dotted line) caused attenuation of APP-derived and A β -induced ROS production, reduction of oxidative stress, correction of mitochondrial dysfunction, reduction of inflammation, and conferring neuroprotection.

    Techniques Used: Activation Assay, Expressing, Derivative Assay

    p gsk 3 β  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p gsk 3 β
    Expression levels of <t>p-GSK-3</t> β (Ser9) in heart tissue (mean ± SD, n = 4). ∗ P < 0.05 compared with DM-I/R; # P < 0.05 compared with DM-D.
    P Gsk 3 β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Effects of Dexmedetomidine Postconditioning on Myocardial Ischemia/Reperfusion Injury in Diabetic Rats: Role of the PI3K/Akt-Dependent Signaling Pathway"

    Article Title: Effects of Dexmedetomidine Postconditioning on Myocardial Ischemia/Reperfusion Injury in Diabetic Rats: Role of the PI3K/Akt-Dependent Signaling Pathway

    Journal: Journal of Diabetes Research

    doi: 10.1155/2018/3071959

    Expression levels of p-GSK-3 β (Ser9) in heart tissue (mean ± SD, n = 4). ∗ P < 0.05 compared with DM-I/R; # P < 0.05 compared with DM-D.
    Figure Legend Snippet: Expression levels of p-GSK-3 β (Ser9) in heart tissue (mean ± SD, n = 4). ∗ P < 0.05 compared with DM-I/R; # P < 0.05 compared with DM-D.

    Techniques Used: Expressing

    gsk3 β  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc gsk3 β
    CWP inhibits <t>PI3K/AKT/GSK3</t> β / β -catenin signaling pathway. (a) Extracts from transplanted tumor of different groups were analyzed for the expression of PI3K, p-AKT, AKT, p-GSK3 β , <t>GSK3</t> <t>β</t> , β -catenin, and nuclear β -catenin. (b) Extracts from SGC-7901 cells of different groups were analyzed for the expression of PI3K, p-AKT, AKT, p-GSK3 β , GSK3 β , β -catenin, and nuclear β -catenin. (c) The histogram shows the relative expression of each protein in (a). (d) The histogram shows the relative expression of each protein in (b). (e) Histogram indicates the ratio of p-AKT/AKT and p-GSK3 β /GSK3 β of (a). (f) The histogram indicates the ratio of p-AKT/AKT and p-GSK3 β /GSK3 β of (b). Data are expressed as the mean ± SD of three experiments ( ∗ P < 0.05 compared with control group; ∗∗ P < 0.01 compared with control group).
    Gsk3 β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/gsk3 β/product/Cell Signaling Technology Inc
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    1) Product Images from "Compound Wumei Powder Inhibits the Invasion and Metastasis of Gastric Cancer via Cox-2/PGE2-PI3K/AKT/GSK3 β / β -Catenin Signaling Pathway"

    Article Title: Compound Wumei Powder Inhibits the Invasion and Metastasis of Gastric Cancer via Cox-2/PGE2-PI3K/AKT/GSK3 β / β -Catenin Signaling Pathway

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    doi: 10.1155/2017/3039450

    CWP inhibits PI3K/AKT/GSK3 β / β -catenin signaling pathway. (a) Extracts from transplanted tumor of different groups were analyzed for the expression of PI3K, p-AKT, AKT, p-GSK3 β , GSK3 β , β -catenin, and nuclear β -catenin. (b) Extracts from SGC-7901 cells of different groups were analyzed for the expression of PI3K, p-AKT, AKT, p-GSK3 β , GSK3 β , β -catenin, and nuclear β -catenin. (c) The histogram shows the relative expression of each protein in (a). (d) The histogram shows the relative expression of each protein in (b). (e) Histogram indicates the ratio of p-AKT/AKT and p-GSK3 β /GSK3 β of (a). (f) The histogram indicates the ratio of p-AKT/AKT and p-GSK3 β /GSK3 β of (b). Data are expressed as the mean ± SD of three experiments ( ∗ P < 0.05 compared with control group; ∗∗ P < 0.01 compared with control group).
    Figure Legend Snippet: CWP inhibits PI3K/AKT/GSK3 β / β -catenin signaling pathway. (a) Extracts from transplanted tumor of different groups were analyzed for the expression of PI3K, p-AKT, AKT, p-GSK3 β , GSK3 β , β -catenin, and nuclear β -catenin. (b) Extracts from SGC-7901 cells of different groups were analyzed for the expression of PI3K, p-AKT, AKT, p-GSK3 β , GSK3 β , β -catenin, and nuclear β -catenin. (c) The histogram shows the relative expression of each protein in (a). (d) The histogram shows the relative expression of each protein in (b). (e) Histogram indicates the ratio of p-AKT/AKT and p-GSK3 β /GSK3 β of (a). (f) The histogram indicates the ratio of p-AKT/AKT and p-GSK3 β /GSK3 β of (b). Data are expressed as the mean ± SD of three experiments ( ∗ P < 0.05 compared with control group; ∗∗ P < 0.01 compared with control group).

    Techniques Used: Expressing

    CWP inhibits PI3K/AKT/GSK3 β / β -catenin signaling pathway. (a) The expressions of p-AKT, AKT, p-GSK3 β , GSK3 β , and β -catenin were detected after treatment with IGF for 2 h and LY294002 for 24 hours. (b) The histogram shows the relative expression of protein in (a). (c) Observation of cell migration after the cells were treated with PI3K/AKT agonist IGF-1 and inhibitor LY294002. (d) The histogram shows the percentage of wound healing in SGC-7901 cells after administration. (e) Observation of cell invasion after the SGC-7901 cells were treated with IGF-1 and LY294002. (f) The histogram shows the number of SGC-7901 cells passing through the 8 μ m pore size into the lower chamber. Data are expressed as the mean ± SD of three experiments ( ∗ P < 0.05 compared with control group; ∗∗ P < 0.01 compared with control group; NS means no significance).
    Figure Legend Snippet: CWP inhibits PI3K/AKT/GSK3 β / β -catenin signaling pathway. (a) The expressions of p-AKT, AKT, p-GSK3 β , GSK3 β , and β -catenin were detected after treatment with IGF for 2 h and LY294002 for 24 hours. (b) The histogram shows the relative expression of protein in (a). (c) Observation of cell migration after the cells were treated with PI3K/AKT agonist IGF-1 and inhibitor LY294002. (d) The histogram shows the percentage of wound healing in SGC-7901 cells after administration. (e) Observation of cell invasion after the SGC-7901 cells were treated with IGF-1 and LY294002. (f) The histogram shows the number of SGC-7901 cells passing through the 8 μ m pore size into the lower chamber. Data are expressed as the mean ± SD of three experiments ( ∗ P < 0.05 compared with control group; ∗∗ P < 0.01 compared with control group; NS means no significance).

    Techniques Used: Expressing, Migration

    Cox-2/PGE2 promotes the invasion and migration and regulates PI3K/AKT/GSK3 β / β -catenin signaling pathway. (a) Observation of cell invasion after the SGC-7901 cells were treated with PGE2 and Celecoxib. (b) The histogram shows the number of SGC-7901 cells passing through the 8 μ m pore size into the lower chamber. (c) Observation of cell migration after the cells were treated with PGE2 and Celecoxib. (d) The histogram shows the percentage of wound healing in SGC-7901 cells after administration. (e) Extracts from SGC-7901 cells treated with PGE2 and Celecoxib were analyzed for the expression of p-AKT, AKT, p-GSK3 β , GSK3 β , β -catenin, and nuclear β -catenin. (f) The histogram shows the relative expression of each protein in (e). (g) The histogram shows the relative ratios of p-AKT/AKT and p-GSK3 β /GSK3 β in each group. Data are expressed as the mean ± SD of three experiments ( ∗ P < 0.05 compared with control group; ∗∗ P < 0.01 compared with control group).
    Figure Legend Snippet: Cox-2/PGE2 promotes the invasion and migration and regulates PI3K/AKT/GSK3 β / β -catenin signaling pathway. (a) Observation of cell invasion after the SGC-7901 cells were treated with PGE2 and Celecoxib. (b) The histogram shows the number of SGC-7901 cells passing through the 8 μ m pore size into the lower chamber. (c) Observation of cell migration after the cells were treated with PGE2 and Celecoxib. (d) The histogram shows the percentage of wound healing in SGC-7901 cells after administration. (e) Extracts from SGC-7901 cells treated with PGE2 and Celecoxib were analyzed for the expression of p-AKT, AKT, p-GSK3 β , GSK3 β , β -catenin, and nuclear β -catenin. (f) The histogram shows the relative expression of each protein in (e). (g) The histogram shows the relative ratios of p-AKT/AKT and p-GSK3 β /GSK3 β in each group. Data are expressed as the mean ± SD of three experiments ( ∗ P < 0.05 compared with control group; ∗∗ P < 0.01 compared with control group).

    Techniques Used: Migration, Expressing

    CWP can inhibit the invasion and metastasis of SGC-7901 via Cox-2/PGE2-PI3K/AKT/GSK3 β / β -catenin signal axis. (a) Extracts from SGC-7901 cells of different groups treated with LY294002 and CWP were analyzed for the expressions of p-AKT/AKT, p-GSK3 β /GSK3 β , β -catenin, and nuclear β -catenin. (b) Extracts from SGC-7901 cells of different groups treated with PGE2 and LY294002 were analyzed for the expressions of p-AKT/AKT, p-GSK3 β /GSK3 β , β -catenin, and nuclear β -catenin. (c) The histogram shows the relative expression of each protein in (a). (d) The histogram shows the relative expression of each protein in (b). Data are expressed as the mean ± SD of three experiments ( ∗∗ P < 0.01 compared with control group; NS means no significance).
    Figure Legend Snippet: CWP can inhibit the invasion and metastasis of SGC-7901 via Cox-2/PGE2-PI3K/AKT/GSK3 β / β -catenin signal axis. (a) Extracts from SGC-7901 cells of different groups treated with LY294002 and CWP were analyzed for the expressions of p-AKT/AKT, p-GSK3 β /GSK3 β , β -catenin, and nuclear β -catenin. (b) Extracts from SGC-7901 cells of different groups treated with PGE2 and LY294002 were analyzed for the expressions of p-AKT/AKT, p-GSK3 β /GSK3 β , β -catenin, and nuclear β -catenin. (c) The histogram shows the relative expression of each protein in (a). (d) The histogram shows the relative expression of each protein in (b). Data are expressed as the mean ± SD of three experiments ( ∗∗ P < 0.01 compared with control group; NS means no significance).

    Techniques Used: Expressing

    A hypothetical illustration for the role of CWP. PGE2, the main catalyzed product of Cox-2 from arachidonic acid, could bind to the EP receptor on the cell membrane, thereby activating the PI3K. Next, phosphorylation of AKT on Ser473 sites generated by PI3K and p-AKT can inhibit the activity of GSK3 β by phosphorylating it. β -Catenin was accumulated in the cytoplasm and translocated into the nucleus, thereby activating downstream target genes MMPs.
    Figure Legend Snippet: A hypothetical illustration for the role of CWP. PGE2, the main catalyzed product of Cox-2 from arachidonic acid, could bind to the EP receptor on the cell membrane, thereby activating the PI3K. Next, phosphorylation of AKT on Ser473 sites generated by PI3K and p-AKT can inhibit the activity of GSK3 β by phosphorylating it. β -Catenin was accumulated in the cytoplasm and translocated into the nucleus, thereby activating downstream target genes MMPs.

    Techniques Used: Generated, Activity Assay

    p gsk3 β  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p gsk3 β
    CWP inhibits <t>PI3K/AKT/GSK3</t> β / β -catenin signaling pathway. (a) Extracts from transplanted tumor of different groups were analyzed for the expression of PI3K, p-AKT, AKT, p-GSK3 β , <t>GSK3</t> <t>β</t> , β -catenin, and nuclear β -catenin. (b) Extracts from SGC-7901 cells of different groups were analyzed for the expression of PI3K, p-AKT, AKT, p-GSK3 β , GSK3 β , β -catenin, and nuclear β -catenin. (c) The histogram shows the relative expression of each protein in (a). (d) The histogram shows the relative expression of each protein in (b). (e) Histogram indicates the ratio of p-AKT/AKT and p-GSK3 β /GSK3 β of (a). (f) The histogram indicates the ratio of p-AKT/AKT and p-GSK3 β /GSK3 β of (b). Data are expressed as the mean ± SD of three experiments ( ∗ P < 0.05 compared with control group; ∗∗ P < 0.01 compared with control group).
    P Gsk3 β, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p gsk3 β/product/Cell Signaling Technology Inc
    Average 97 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p gsk3 β - by Bioz Stars, 2023-02
    97/100 stars

    Images

    1) Product Images from "Compound Wumei Powder Inhibits the Invasion and Metastasis of Gastric Cancer via Cox-2/PGE2-PI3K/AKT/GSK3 β / β -Catenin Signaling Pathway"

    Article Title: Compound Wumei Powder Inhibits the Invasion and Metastasis of Gastric Cancer via Cox-2/PGE2-PI3K/AKT/GSK3 β / β -Catenin Signaling Pathway

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    doi: 10.1155/2017/3039450

    CWP inhibits PI3K/AKT/GSK3 β / β -catenin signaling pathway. (a) Extracts from transplanted tumor of different groups were analyzed for the expression of PI3K, p-AKT, AKT, p-GSK3 β , GSK3 β , β -catenin, and nuclear β -catenin. (b) Extracts from SGC-7901 cells of different groups were analyzed for the expression of PI3K, p-AKT, AKT, p-GSK3 β , GSK3 β , β -catenin, and nuclear β -catenin. (c) The histogram shows the relative expression of each protein in (a). (d) The histogram shows the relative expression of each protein in (b). (e) Histogram indicates the ratio of p-AKT/AKT and p-GSK3 β /GSK3 β of (a). (f) The histogram indicates the ratio of p-AKT/AKT and p-GSK3 β /GSK3 β of (b). Data are expressed as the mean ± SD of three experiments ( ∗ P < 0.05 compared with control group; ∗∗ P < 0.01 compared with control group).
    Figure Legend Snippet: CWP inhibits PI3K/AKT/GSK3 β / β -catenin signaling pathway. (a) Extracts from transplanted tumor of different groups were analyzed for the expression of PI3K, p-AKT, AKT, p-GSK3 β , GSK3 β , β -catenin, and nuclear β -catenin. (b) Extracts from SGC-7901 cells of different groups were analyzed for the expression of PI3K, p-AKT, AKT, p-GSK3 β , GSK3 β , β -catenin, and nuclear β -catenin. (c) The histogram shows the relative expression of each protein in (a). (d) The histogram shows the relative expression of each protein in (b). (e) Histogram indicates the ratio of p-AKT/AKT and p-GSK3 β /GSK3 β of (a). (f) The histogram indicates the ratio of p-AKT/AKT and p-GSK3 β /GSK3 β of (b). Data are expressed as the mean ± SD of three experiments ( ∗ P < 0.05 compared with control group; ∗∗ P < 0.01 compared with control group).

    Techniques Used: Expressing

    CWP inhibits PI3K/AKT/GSK3 β / β -catenin signaling pathway. (a) The expressions of p-AKT, AKT, p-GSK3 β , GSK3 β , and β -catenin were detected after treatment with IGF for 2 h and LY294002 for 24 hours. (b) The histogram shows the relative expression of protein in (a). (c) Observation of cell migration after the cells were treated with PI3K/AKT agonist IGF-1 and inhibitor LY294002. (d) The histogram shows the percentage of wound healing in SGC-7901 cells after administration. (e) Observation of cell invasion after the SGC-7901 cells were treated with IGF-1 and LY294002. (f) The histogram shows the number of SGC-7901 cells passing through the 8 μ m pore size into the lower chamber. Data are expressed as the mean ± SD of three experiments ( ∗ P < 0.05 compared with control group; ∗∗ P < 0.01 compared with control group; NS means no significance).
    Figure Legend Snippet: CWP inhibits PI3K/AKT/GSK3 β / β -catenin signaling pathway. (a) The expressions of p-AKT, AKT, p-GSK3 β , GSK3 β , and β -catenin were detected after treatment with IGF for 2 h and LY294002 for 24 hours. (b) The histogram shows the relative expression of protein in (a). (c) Observation of cell migration after the cells were treated with PI3K/AKT agonist IGF-1 and inhibitor LY294002. (d) The histogram shows the percentage of wound healing in SGC-7901 cells after administration. (e) Observation of cell invasion after the SGC-7901 cells were treated with IGF-1 and LY294002. (f) The histogram shows the number of SGC-7901 cells passing through the 8 μ m pore size into the lower chamber. Data are expressed as the mean ± SD of three experiments ( ∗ P < 0.05 compared with control group; ∗∗ P < 0.01 compared with control group; NS means no significance).

    Techniques Used: Expressing, Migration

    Cox-2/PGE2 promotes the invasion and migration and regulates PI3K/AKT/GSK3 β / β -catenin signaling pathway. (a) Observation of cell invasion after the SGC-7901 cells were treated with PGE2 and Celecoxib. (b) The histogram shows the number of SGC-7901 cells passing through the 8 μ m pore size into the lower chamber. (c) Observation of cell migration after the cells were treated with PGE2 and Celecoxib. (d) The histogram shows the percentage of wound healing in SGC-7901 cells after administration. (e) Extracts from SGC-7901 cells treated with PGE2 and Celecoxib were analyzed for the expression of p-AKT, AKT, p-GSK3 β , GSK3 β , β -catenin, and nuclear β -catenin. (f) The histogram shows the relative expression of each protein in (e). (g) The histogram shows the relative ratios of p-AKT/AKT and p-GSK3 β /GSK3 β in each group. Data are expressed as the mean ± SD of three experiments ( ∗ P < 0.05 compared with control group; ∗∗ P < 0.01 compared with control group).
    Figure Legend Snippet: Cox-2/PGE2 promotes the invasion and migration and regulates PI3K/AKT/GSK3 β / β -catenin signaling pathway. (a) Observation of cell invasion after the SGC-7901 cells were treated with PGE2 and Celecoxib. (b) The histogram shows the number of SGC-7901 cells passing through the 8 μ m pore size into the lower chamber. (c) Observation of cell migration after the cells were treated with PGE2 and Celecoxib. (d) The histogram shows the percentage of wound healing in SGC-7901 cells after administration. (e) Extracts from SGC-7901 cells treated with PGE2 and Celecoxib were analyzed for the expression of p-AKT, AKT, p-GSK3 β , GSK3 β , β -catenin, and nuclear β -catenin. (f) The histogram shows the relative expression of each protein in (e). (g) The histogram shows the relative ratios of p-AKT/AKT and p-GSK3 β /GSK3 β in each group. Data are expressed as the mean ± SD of three experiments ( ∗ P < 0.05 compared with control group; ∗∗ P < 0.01 compared with control group).

    Techniques Used: Migration, Expressing

    CWP can inhibit the invasion and metastasis of SGC-7901 via Cox-2/PGE2-PI3K/AKT/GSK3 β / β -catenin signal axis. (a) Extracts from SGC-7901 cells of different groups treated with LY294002 and CWP were analyzed for the expressions of p-AKT/AKT, p-GSK3 β /GSK3 β , β -catenin, and nuclear β -catenin. (b) Extracts from SGC-7901 cells of different groups treated with PGE2 and LY294002 were analyzed for the expressions of p-AKT/AKT, p-GSK3 β /GSK3 β , β -catenin, and nuclear β -catenin. (c) The histogram shows the relative expression of each protein in (a). (d) The histogram shows the relative expression of each protein in (b). Data are expressed as the mean ± SD of three experiments ( ∗∗ P < 0.01 compared with control group; NS means no significance).
    Figure Legend Snippet: CWP can inhibit the invasion and metastasis of SGC-7901 via Cox-2/PGE2-PI3K/AKT/GSK3 β / β -catenin signal axis. (a) Extracts from SGC-7901 cells of different groups treated with LY294002 and CWP were analyzed for the expressions of p-AKT/AKT, p-GSK3 β /GSK3 β , β -catenin, and nuclear β -catenin. (b) Extracts from SGC-7901 cells of different groups treated with PGE2 and LY294002 were analyzed for the expressions of p-AKT/AKT, p-GSK3 β /GSK3 β , β -catenin, and nuclear β -catenin. (c) The histogram shows the relative expression of each protein in (a). (d) The histogram shows the relative expression of each protein in (b). Data are expressed as the mean ± SD of three experiments ( ∗∗ P < 0.01 compared with control group; NS means no significance).

    Techniques Used: Expressing

    A hypothetical illustration for the role of CWP. PGE2, the main catalyzed product of Cox-2 from arachidonic acid, could bind to the EP receptor on the cell membrane, thereby activating the PI3K. Next, phosphorylation of AKT on Ser473 sites generated by PI3K and p-AKT can inhibit the activity of GSK3 β by phosphorylating it. β -Catenin was accumulated in the cytoplasm and translocated into the nucleus, thereby activating downstream target genes MMPs.
    Figure Legend Snippet: A hypothetical illustration for the role of CWP. PGE2, the main catalyzed product of Cox-2 from arachidonic acid, could bind to the EP receptor on the cell membrane, thereby activating the PI3K. Next, phosphorylation of AKT on Ser473 sites generated by PI3K and p-AKT can inhibit the activity of GSK3 β by phosphorylating it. β -Catenin was accumulated in the cytoplasm and translocated into the nucleus, thereby activating downstream target genes MMPs.

    Techniques Used: Generated, Activity Assay

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    Cell Signaling Technology Inc anti gsk3 β
    Artemether increased phosphorylation of <t>AMPK/GSK3</t> β (ser9)in PC12 cell cultures exposed to A β 1-42. (a, c) PC12 cells pretreated for 2 h with different concentrations of Artemether were incubated with 1 μ M A β 1-42 for 24 h .The lysates were submitted for measurements of phosphorylations by western blotting using specific antibodies for AMPK (P-AMPK), total AMPK (T-AMPK), <t>GSK3</t> <t>β</t> (ser9) (P-GSK3 β ), and total GSK3 β (T-GSK3 β ). GAPDH was used for normalization. Three independent experiments were included. (b, d) Quantitation of phosphorylated kinases. ∗ p < 0.05 and ∗∗ p < 0.01 were considered significantly different.
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    ZSD induced the apoptosis of H1299 cells partially by regulating AKT/GSK-3 β / β -catenin signaling. (a) ZSD induced the apoptosis of H1299 cells after treatment with ZSD (4 mg/mL) for 12 h, 24 h, and 48 h. (b) ZSD induced apoptosis of H1299 cells in a dose-dependent manner. (c) Pathway enrichment analysis of the genes in Human Signal Transduction Pathway Finder PCR Array. (d) The mRNA expression of AKT/GSK-3 β / β -catenin signal cascades in H1299 cells after treatment with ZSD (4 mg/mL). ∗ p < 0.05 and ∗∗ p < 0.01 vs. the control group.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Zi Shen Decoction Inhibits Growth and Metastasis of Lung Cancer via Regulating the AKT/GSK-3 β / β -Catenin Pathway

    doi: 10.1155/2021/6685282

    Figure Lengend Snippet: ZSD induced the apoptosis of H1299 cells partially by regulating AKT/GSK-3 β / β -catenin signaling. (a) ZSD induced the apoptosis of H1299 cells after treatment with ZSD (4 mg/mL) for 12 h, 24 h, and 48 h. (b) ZSD induced apoptosis of H1299 cells in a dose-dependent manner. (c) Pathway enrichment analysis of the genes in Human Signal Transduction Pathway Finder PCR Array. (d) The mRNA expression of AKT/GSK-3 β / β -catenin signal cascades in H1299 cells after treatment with ZSD (4 mg/mL). ∗ p < 0.05 and ∗∗ p < 0.01 vs. the control group.

    Article Snippet: Antibodies against total AKT and p-AKT, total GSK-3 β and p-GSK-3 β , β -catenin, cleaved caspase-3, and GAPDH were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Transduction, Expressing

    ZSD inhibited the AKT/GSK-3 β / β -catenin pathway in lung cancer cells and tumor tissues. (a) Western blot analysis was used to assess the expression of multiple proteins involved in the AKT/GSK-3 β / β -catenin pathway in lung cancer cells after ZSD treatment for 12 h, 24 h, and 48 h. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the control group. (b) Western blots showing the protein expression of AKT, p-AKT, GSK-3 β , p-GSK-3 β , β -catenin, cleaved caspase-3, and Bax and Bcl-2 in isolated tumor tissues. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the model group.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Zi Shen Decoction Inhibits Growth and Metastasis of Lung Cancer via Regulating the AKT/GSK-3 β / β -Catenin Pathway

    doi: 10.1155/2021/6685282

    Figure Lengend Snippet: ZSD inhibited the AKT/GSK-3 β / β -catenin pathway in lung cancer cells and tumor tissues. (a) Western blot analysis was used to assess the expression of multiple proteins involved in the AKT/GSK-3 β / β -catenin pathway in lung cancer cells after ZSD treatment for 12 h, 24 h, and 48 h. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the control group. (b) Western blots showing the protein expression of AKT, p-AKT, GSK-3 β , p-GSK-3 β , β -catenin, cleaved caspase-3, and Bax and Bcl-2 in isolated tumor tissues. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the model group.

    Article Snippet: Antibodies against total AKT and p-AKT, total GSK-3 β and p-GSK-3 β , β -catenin, cleaved caspase-3, and GAPDH were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Western Blot, Expressing, Isolation

    The AKT/GSK-3 β / β -catenin pathway medicated anticancer effect of ZSD in lung cancer cells. H1299 cells were treated with ZSD and/or SC-79 for 24 h. (a) Representative western blots and quantitative analysis of the AKT/GSK-3 β / β -catenin pathway related proteins. (b) The mobility of H1299 cells was detected by wound-healing assay. (c) The migration and invasion abilities of H1299 cells were detected by transwell assays. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the control group.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Zi Shen Decoction Inhibits Growth and Metastasis of Lung Cancer via Regulating the AKT/GSK-3 β / β -Catenin Pathway

    doi: 10.1155/2021/6685282

    Figure Lengend Snippet: The AKT/GSK-3 β / β -catenin pathway medicated anticancer effect of ZSD in lung cancer cells. H1299 cells were treated with ZSD and/or SC-79 for 24 h. (a) Representative western blots and quantitative analysis of the AKT/GSK-3 β / β -catenin pathway related proteins. (b) The mobility of H1299 cells was detected by wound-healing assay. (c) The migration and invasion abilities of H1299 cells were detected by transwell assays. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 vs. the control group.

    Article Snippet: Antibodies against total AKT and p-AKT, total GSK-3 β and p-GSK-3 β , β -catenin, cleaved caspase-3, and GAPDH were purchased from Cell Signaling Technology (Danvers, MA, USA).

    Techniques: Western Blot, Wound Healing Assay, Migration

    HRT inhibited cancer cell proliferation via suppressing Akt signaling. (a) The expression of phosphor-ERK or -Akt was examined in HCT116 cells treated with HRT in a time-dependent manner. HRT induced dephosphorylation of Akt not ERK at 24 h. (b) The effect of HRT on PI3K/Akt signaling pathway. Phosphorylation levels of Akt, mTOR, and GSK3 β were examined in HCT116 cells treated with LY294002 (10 μ M), HRT (300 μ g/mL) or cotreated with LY294002 and HRT for 24 h.

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: HRT, Herbal Formula, Induces G 2 /M Cell Cycle Arrest and Apoptosis via Suppressing Akt Signaling Pathway in Human Colon Cancer Cells

    doi: 10.1155/2012/871893

    Figure Lengend Snippet: HRT inhibited cancer cell proliferation via suppressing Akt signaling. (a) The expression of phosphor-ERK or -Akt was examined in HCT116 cells treated with HRT in a time-dependent manner. HRT induced dephosphorylation of Akt not ERK at 24 h. (b) The effect of HRT on PI3K/Akt signaling pathway. Phosphorylation levels of Akt, mTOR, and GSK3 β were examined in HCT116 cells treated with LY294002 (10 μ M), HRT (300 μ g/mL) or cotreated with LY294002 and HRT for 24 h.

    Article Snippet: Primary antibodies against caspase-3, -8, -9, PARP, BID, Akt, phosphor-Akt, ERK, phosphor-ERK, phosphor-GSK3 β , GAPDH, and secondary antibodies were purchased from Cell Signaling (Danver, MA, USA) and cyclin D1, cyclin B1, CDK7, Bcl-2, and β -actin were purchased from Santa Cruz Biotechnology (CA, USA).

    Techniques: Expressing, De-Phosphorylation Assay

    The relationship between CRIP1 and EMT indicates that CRIP1 may function in ovarian cancer development via the Wnt/ β -catenin pathway. (a) KEGG pathway enrichment analysis was performed to identify which pathway was significantly enriched in CRIP1-related ovarian cancer progression. (b) The effect of CRIP1 silencing on EMT-related signaling pathways. EMT markers, such as E-cadherin, N-cadherin, and vimentin proteins, were detected by western blot. (c) The effect of CRIP1 silencing on Wnt/ β -catenin signaling pathway. The important molecules of this pathway, including β -catenin, GSK-3 β , p-GSK-3 β , MMP2, and MMP9, were assessed by western blot.

    Journal: Disease Markers

    Article Title: Cysteine-Rich Intestinal Protein 1 Served as an Epithelial Ovarian Cancer Marker via Promoting Wnt/ β -Catenin-Mediated EMT and Tumour Metastasis

    doi: 10.1155/2021/3566749

    Figure Lengend Snippet: The relationship between CRIP1 and EMT indicates that CRIP1 may function in ovarian cancer development via the Wnt/ β -catenin pathway. (a) KEGG pathway enrichment analysis was performed to identify which pathway was significantly enriched in CRIP1-related ovarian cancer progression. (b) The effect of CRIP1 silencing on EMT-related signaling pathways. EMT markers, such as E-cadherin, N-cadherin, and vimentin proteins, were detected by western blot. (c) The effect of CRIP1 silencing on Wnt/ β -catenin signaling pathway. The important molecules of this pathway, including β -catenin, GSK-3 β , p-GSK-3 β , MMP2, and MMP9, were assessed by western blot.

    Article Snippet: The antibodies used in this experiment were as follows: β -actin (Cat No. 4970S), β -catenin (Cat No. 8084S), MMP-2 (Cat No. 87809S), and MMP-9 (Cat No. 13667S) were bought from Cell Signaling Technology (Danvers, MA, USA); CRIP1 (Cat No. 15349-1-AP), E-cadherin (Cat No. 20874-1-AP), N-cadherin (Cat No. 22018-1-AP), GSK-3 β (Cat No. 22104-1-AP), and p-GSK-3 β (Cat No. 14850-1-AP) were purchased from Proteintech (Wuhan, China); vimentin (Cat No. bs-8533R) was obtained from Bioss (Beijing, China).

    Techniques: Western Blot

    Artemether increased phosphorylation of AMPK/GSK3 β (ser9)in PC12 cell cultures exposed to A β 1-42. (a, c) PC12 cells pretreated for 2 h with different concentrations of Artemether were incubated with 1 μ M A β 1-42 for 24 h .The lysates were submitted for measurements of phosphorylations by western blotting using specific antibodies for AMPK (P-AMPK), total AMPK (T-AMPK), GSK3 β (ser9) (P-GSK3 β ), and total GSK3 β (T-GSK3 β ). GAPDH was used for normalization. Three independent experiments were included. (b, d) Quantitation of phosphorylated kinases. ∗ p < 0.05 and ∗∗ p < 0.01 were considered significantly different.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Artemether Activation of AMPK/GSK3 β (ser9)/Nrf2 Signaling Confers Neuroprotection towards β- Amyloid-Induced Neurotoxicity in 3xTg Alzheimer's Mouse Model

    doi: 10.1155/2019/1862437

    Figure Lengend Snippet: Artemether increased phosphorylation of AMPK/GSK3 β (ser9)in PC12 cell cultures exposed to A β 1-42. (a, c) PC12 cells pretreated for 2 h with different concentrations of Artemether were incubated with 1 μ M A β 1-42 for 24 h .The lysates were submitted for measurements of phosphorylations by western blotting using specific antibodies for AMPK (P-AMPK), total AMPK (T-AMPK), GSK3 β (ser9) (P-GSK3 β ), and total GSK3 β (T-GSK3 β ). GAPDH was used for normalization. Three independent experiments were included. (b, d) Quantitation of phosphorylated kinases. ∗ p < 0.05 and ∗∗ p < 0.01 were considered significantly different.

    Article Snippet: Anti-phospho-AMPK, anti-AMPK, anti-phospho-GSK3 β (ser9), anti-GSK3 β , anti-Nrf2, anti-HO-1, anti-phospho-tau, anti-tau, cleaved caspase 3, β -amyloid, anti-GFAP, and anti- β -actin antibodies were purchased from Cell Signaling Technology (Woburn, MA, USA).

    Techniques: Incubation, Western Blot, Quantitation Assay

    Direct relationship between Artemether effects on AMPK/GSK3 β (ser9) phosphorylation and neuroprotection towards A β 1-42 -induced apoptotic cell death in PC12 cells. PC12 cells pretreated with 5 μ M compound C (AMPK inhibitor) for 30 min, followed by incubation with 1 μ M A β 1-42 in the presence or absence of different concentrations of Artemether. (a) Cell viability was measured by MTT assay. ∗ p < 0.05 and ∗∗∗ p < 0.001 were considered significantly different. (b) Apoptosis was determined by flow cytometry. (c) Quantitation of the percentage of cell apoptosis. ∗∗∗ p < 0.001 was considered significantly different. (d) Phosphorylation activities of AMPK/GSK3 β (ser9). GAPDH was used for normalization. (e, f) Quantitation of phosphorylation activities of AMPK/GSK3 β . All results are presented as mean ± SEM ( n = 3); ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 were considered significantly different.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Artemether Activation of AMPK/GSK3 β (ser9)/Nrf2 Signaling Confers Neuroprotection towards β- Amyloid-Induced Neurotoxicity in 3xTg Alzheimer's Mouse Model

    doi: 10.1155/2019/1862437

    Figure Lengend Snippet: Direct relationship between Artemether effects on AMPK/GSK3 β (ser9) phosphorylation and neuroprotection towards A β 1-42 -induced apoptotic cell death in PC12 cells. PC12 cells pretreated with 5 μ M compound C (AMPK inhibitor) for 30 min, followed by incubation with 1 μ M A β 1-42 in the presence or absence of different concentrations of Artemether. (a) Cell viability was measured by MTT assay. ∗ p < 0.05 and ∗∗∗ p < 0.001 were considered significantly different. (b) Apoptosis was determined by flow cytometry. (c) Quantitation of the percentage of cell apoptosis. ∗∗∗ p < 0.001 was considered significantly different. (d) Phosphorylation activities of AMPK/GSK3 β (ser9). GAPDH was used for normalization. (e, f) Quantitation of phosphorylation activities of AMPK/GSK3 β . All results are presented as mean ± SEM ( n = 3); ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 were considered significantly different.

    Article Snippet: Anti-phospho-AMPK, anti-AMPK, anti-phospho-GSK3 β (ser9), anti-GSK3 β , anti-Nrf2, anti-HO-1, anti-phospho-tau, anti-tau, cleaved caspase 3, β -amyloid, anti-GFAP, and anti- β -actin antibodies were purchased from Cell Signaling Technology (Woburn, MA, USA).

    Techniques: Incubation, MTT Assay, Flow Cytometry, Quantitation Assay

    Artemether stimulated the phosphorylation of AMPK/GSK3 β (ser9) and increased the expression levels of Nrf2 and heme oxygenase-1 (HO-1) in the brain cortex of 3xTg-AD mice. Artemether was administered to mice by intraperitoneal injection, once a day, at low doses of 5 mg/kg and high doses of 20 mg/kg for 4 weeks. Thereafter, the brain cortex extracts of wild-type (WT) compared to 3xTg-AD mice treated with either a low (Arte low) or high dose (Arte high) of Artemether or untreated (3xTg) were submitted for analyses. (a) Phosphorylations of AMPK/GSK3 β (ser9) and protein expression levels of Nrf2 and heme oxygenase-1 (HO-1); three mice per treatment group were used for western blot. (b–e) Quantitation of western blotting results of the different experimental groups. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 were considered significantly different.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Artemether Activation of AMPK/GSK3 β (ser9)/Nrf2 Signaling Confers Neuroprotection towards β- Amyloid-Induced Neurotoxicity in 3xTg Alzheimer's Mouse Model

    doi: 10.1155/2019/1862437

    Figure Lengend Snippet: Artemether stimulated the phosphorylation of AMPK/GSK3 β (ser9) and increased the expression levels of Nrf2 and heme oxygenase-1 (HO-1) in the brain cortex of 3xTg-AD mice. Artemether was administered to mice by intraperitoneal injection, once a day, at low doses of 5 mg/kg and high doses of 20 mg/kg for 4 weeks. Thereafter, the brain cortex extracts of wild-type (WT) compared to 3xTg-AD mice treated with either a low (Arte low) or high dose (Arte high) of Artemether or untreated (3xTg) were submitted for analyses. (a) Phosphorylations of AMPK/GSK3 β (ser9) and protein expression levels of Nrf2 and heme oxygenase-1 (HO-1); three mice per treatment group were used for western blot. (b–e) Quantitation of western blotting results of the different experimental groups. ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 were considered significantly different.

    Article Snippet: Anti-phospho-AMPK, anti-AMPK, anti-phospho-GSK3 β (ser9), anti-GSK3 β , anti-Nrf2, anti-HO-1, anti-phospho-tau, anti-tau, cleaved caspase 3, β -amyloid, anti-GFAP, and anti- β -actin antibodies were purchased from Cell Signaling Technology (Woburn, MA, USA).

    Techniques: Expressing, Injection, Western Blot, Quantitation Assay

    A schematic diagram of Artemether-induced AMPK/GSK3 β (ser9)/Nrf2 activation towards reduction of amyloid- β -evoked oxidative stress to confer neuroprotection. Artemether stimulated AMPK/GSK3 β (ser9) phosphorylation output in neuronal cells and animal brain cortex to increase the nuclear expression of Nrf2 with induction of the phase II antioxidant enzymes and anti-inflammatory genes containing ARE. This process (dotted line) caused attenuation of APP-derived and A β -induced ROS production, reduction of oxidative stress, correction of mitochondrial dysfunction, reduction of inflammation, and conferring neuroprotection.

    Journal: Oxidative Medicine and Cellular Longevity

    Article Title: Artemether Activation of AMPK/GSK3 β (ser9)/Nrf2 Signaling Confers Neuroprotection towards β- Amyloid-Induced Neurotoxicity in 3xTg Alzheimer's Mouse Model

    doi: 10.1155/2019/1862437

    Figure Lengend Snippet: A schematic diagram of Artemether-induced AMPK/GSK3 β (ser9)/Nrf2 activation towards reduction of amyloid- β -evoked oxidative stress to confer neuroprotection. Artemether stimulated AMPK/GSK3 β (ser9) phosphorylation output in neuronal cells and animal brain cortex to increase the nuclear expression of Nrf2 with induction of the phase II antioxidant enzymes and anti-inflammatory genes containing ARE. This process (dotted line) caused attenuation of APP-derived and A β -induced ROS production, reduction of oxidative stress, correction of mitochondrial dysfunction, reduction of inflammation, and conferring neuroprotection.

    Article Snippet: Anti-phospho-AMPK, anti-AMPK, anti-phospho-GSK3 β (ser9), anti-GSK3 β , anti-Nrf2, anti-HO-1, anti-phospho-tau, anti-tau, cleaved caspase 3, β -amyloid, anti-GFAP, and anti- β -actin antibodies were purchased from Cell Signaling Technology (Woburn, MA, USA).

    Techniques: Activation Assay, Expressing, Derivative Assay