akt pan c67e7 rabbit monoclonal antibody rabbit monoclonal antibody mab  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc akt pan c67e7 rabbit monoclonal antibody rabbit monoclonal antibody mab
    Akt Pan C67e7 Rabbit Monoclonal Antibody Rabbit Monoclonal Antibody Mab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    akt 4691  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc akt 4691
    Akt 4691, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    akt pan c67e7 rabbit monoclonal antibody rabbit monoclonal antibody mab  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc akt pan c67e7 rabbit monoclonal antibody rabbit monoclonal antibody mab
    Akt Pan C67e7 Rabbit Monoclonal Antibody Rabbit Monoclonal Antibody Mab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    akt  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc akt
    Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    akt ab  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc akt ab
    The expression <t>of</t> <t>Caveolin-1,</t> <t>p-AKT/AKT,</t> and PI3K in adipose tissue of NC, type 2 diabetic mice, and insulin-treated T2DM mice (a). The band intensity of Caveolin-1, p-AKT/AKT, and PI3K was quantified as shown in (b–d), respectively (data presented as mean ± SEM. ∗ P < 0.05 vs. NC mice. # P < 0.05 compared with T2DM mice, n = 5).
    Akt Ab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Caveolin-1 Is Essential for the Improvement of Insulin Sensitivity through AKT Activation during Glargine Treatment on Diabetic Mice"

    Article Title: Caveolin-1 Is Essential for the Improvement of Insulin Sensitivity through AKT Activation during Glargine Treatment on Diabetic Mice

    Journal: Journal of Diabetes Research

    doi: 10.1155/2021/9943344

    The expression of Caveolin-1, p-AKT/AKT, and PI3K in adipose tissue of NC, type 2 diabetic mice, and insulin-treated T2DM mice (a). The band intensity of Caveolin-1, p-AKT/AKT, and PI3K was quantified as shown in (b–d), respectively (data presented as mean ± SEM. ∗ P < 0.05 vs. NC mice. # P < 0.05 compared with T2DM mice, n = 5).
    Figure Legend Snippet: The expression of Caveolin-1, p-AKT/AKT, and PI3K in adipose tissue of NC, type 2 diabetic mice, and insulin-treated T2DM mice (a). The band intensity of Caveolin-1, p-AKT/AKT, and PI3K was quantified as shown in (b–d), respectively (data presented as mean ± SEM. ∗ P < 0.05 vs. NC mice. # P < 0.05 compared with T2DM mice, n = 5).

    Techniques Used: Expressing

    The expression of Caveolin-1, p-AKT/AKT, and PI3K among five different groups (a). The band intensity of Caveolin-1, p-AKT/AKT, and PI3K was quantified as shown in (b–d), respectively (data are expressed as mean ± SEM. ∗ P < 0.05 compared with the insulin group. # P < 0.05 compared with the Ctrl-shRNA group; a represents P < 0.05 compared with the NC group, and b represents P < 0.05 compared with the T2DM group, n = 5).
    Figure Legend Snippet: The expression of Caveolin-1, p-AKT/AKT, and PI3K among five different groups (a). The band intensity of Caveolin-1, p-AKT/AKT, and PI3K was quantified as shown in (b–d), respectively (data are expressed as mean ± SEM. ∗ P < 0.05 compared with the insulin group. # P < 0.05 compared with the Ctrl-shRNA group; a represents P < 0.05 compared with the NC group, and b represents P < 0.05 compared with the T2DM group, n = 5).

    Techniques Used: Expressing, shRNA

    akt  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc akt
    Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti akt  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti akt
    <t>AGK</t> inhibits BCL-2 expression by phosphorylation PTEN and subsequent <t>AKT-FOXO1</t> signaling. A. The levels of AGK and BCL-2 were determined in SU-DHL2, OCI-LY1, TMD8, SU-DHL4, SU-DHL6, SU-DHL10, and SU-DHL16 DLBCL cell lines. B. Spearman correlation analysis of AGK and BCL-2 expression in DLBCL cell lines. C. AGK and BCL-2 expression was measured with immunoblotting and BCL-2 expression was quantified in shRNA control and shRNA AGK SU-DHL4 cells from three independent experiments. D. AGK and BCL-2 expression was measured in control and AGK overexpression SU-DHL4 cells, and BCL-2 expression was quantified from three independent experiments. E. The amounts of p-PTEN and PTEN in SU-DHL2, OCI-LY1, TMD8, SU-DHL4, SU-DHL6, SU-DHL10, and SU-DHL16 DLBCL cell lines were determined by immunoblotting. F. Spearman correlation analysis of AGK and PTEN phosphorylation levels in DLBCL cell lines. G-H. Phosphorylation levels of PTEN, AKT and FOXO1 were measured and quantified in control and AGK knockdown SU-DHL4 cells from three independent experiments. I-J The levels of FOXO1 and p-FOXO1 were measured in cytoplasmic and nuclear fractions (I) and the band intensities were quantified (J). K. The binding of FOXO1 to BCL-2 promoter in SU-DHL4 was determined by chromatin immunoprecipitation analysis. Data were expressed as mean ± SEM from three independent experiments (A-J) or two independent experiments with triplicates (K), and analyzed for statistical significance by t -test. (* P < 0.05; ** P < 0.01; *** P < 0.001).
    Anti Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Inhibition of acylglycerol kinase sensitizes DLBCL to venetoclax via upregulation of FOXO1-mediated BCL-2 expression"

    Article Title: Inhibition of acylglycerol kinase sensitizes DLBCL to venetoclax via upregulation of FOXO1-mediated BCL-2 expression

    Journal: Theranostics

    doi: 10.7150/thno.72786

    AGK inhibits BCL-2 expression by phosphorylation PTEN and subsequent AKT-FOXO1 signaling. A. The levels of AGK and BCL-2 were determined in SU-DHL2, OCI-LY1, TMD8, SU-DHL4, SU-DHL6, SU-DHL10, and SU-DHL16 DLBCL cell lines. B. Spearman correlation analysis of AGK and BCL-2 expression in DLBCL cell lines. C. AGK and BCL-2 expression was measured with immunoblotting and BCL-2 expression was quantified in shRNA control and shRNA AGK SU-DHL4 cells from three independent experiments. D. AGK and BCL-2 expression was measured in control and AGK overexpression SU-DHL4 cells, and BCL-2 expression was quantified from three independent experiments. E. The amounts of p-PTEN and PTEN in SU-DHL2, OCI-LY1, TMD8, SU-DHL4, SU-DHL6, SU-DHL10, and SU-DHL16 DLBCL cell lines were determined by immunoblotting. F. Spearman correlation analysis of AGK and PTEN phosphorylation levels in DLBCL cell lines. G-H. Phosphorylation levels of PTEN, AKT and FOXO1 were measured and quantified in control and AGK knockdown SU-DHL4 cells from three independent experiments. I-J The levels of FOXO1 and p-FOXO1 were measured in cytoplasmic and nuclear fractions (I) and the band intensities were quantified (J). K. The binding of FOXO1 to BCL-2 promoter in SU-DHL4 was determined by chromatin immunoprecipitation analysis. Data were expressed as mean ± SEM from three independent experiments (A-J) or two independent experiments with triplicates (K), and analyzed for statistical significance by t -test. (* P < 0.05; ** P < 0.01; *** P < 0.001).
    Figure Legend Snippet: AGK inhibits BCL-2 expression by phosphorylation PTEN and subsequent AKT-FOXO1 signaling. A. The levels of AGK and BCL-2 were determined in SU-DHL2, OCI-LY1, TMD8, SU-DHL4, SU-DHL6, SU-DHL10, and SU-DHL16 DLBCL cell lines. B. Spearman correlation analysis of AGK and BCL-2 expression in DLBCL cell lines. C. AGK and BCL-2 expression was measured with immunoblotting and BCL-2 expression was quantified in shRNA control and shRNA AGK SU-DHL4 cells from three independent experiments. D. AGK and BCL-2 expression was measured in control and AGK overexpression SU-DHL4 cells, and BCL-2 expression was quantified from three independent experiments. E. The amounts of p-PTEN and PTEN in SU-DHL2, OCI-LY1, TMD8, SU-DHL4, SU-DHL6, SU-DHL10, and SU-DHL16 DLBCL cell lines were determined by immunoblotting. F. Spearman correlation analysis of AGK and PTEN phosphorylation levels in DLBCL cell lines. G-H. Phosphorylation levels of PTEN, AKT and FOXO1 were measured and quantified in control and AGK knockdown SU-DHL4 cells from three independent experiments. I-J The levels of FOXO1 and p-FOXO1 were measured in cytoplasmic and nuclear fractions (I) and the band intensities were quantified (J). K. The binding of FOXO1 to BCL-2 promoter in SU-DHL4 was determined by chromatin immunoprecipitation analysis. Data were expressed as mean ± SEM from three independent experiments (A-J) or two independent experiments with triplicates (K), and analyzed for statistical significance by t -test. (* P < 0.05; ** P < 0.01; *** P < 0.001).

    Techniques Used: Expressing, Western Blot, shRNA, Over Expression, Binding Assay, Chromatin Immunoprecipitation

    Knockdown of AGK augments venetoclax efficacy in vivo . A. Schematic diagram of xenograft tumor model and venetoclax treatment strategy. B-E. Tumor growth curves of mice receiving shRNA control, shRNA AGK#1 cells with or without venetoclax treatment (n = 6, each group). F. Tumor weights of shRNA control and shRNA AGK#1 groups with or without venetoclax treatment (n = 6, each group). G-H. H&E staining, cleaved-caspase3 and TUNEL staining of shRNA control and shRNA AGK groups with or without venetoclax treatment, and the percentages of positive area of cleaved-caspase3 and TUNEL were quantified. I-J. The levels of AGK, BCL-2, p-FOXO1, FOXO1, p-AKT and AKT were measured (I) and quantified (J) in the tumor tissues isolated from shRNA control and shRNA AGK groups (n = 6, each group). K-L. FOXO1 staining of shRNA control and shRNA AGK group tumor tissues (K) and the percentages of FOXO1 expression in cytoplasmic and nuclear were quantified (L). Scale bar, 100 μm or 25 μm. Data were expressed as mean ± SEM and analyzed for statistical significance by One-way ANOVA (F, H, L) or t -test (J) (* P < 0.05; ** P < 0.01; *** P < 0.001).
    Figure Legend Snippet: Knockdown of AGK augments venetoclax efficacy in vivo . A. Schematic diagram of xenograft tumor model and venetoclax treatment strategy. B-E. Tumor growth curves of mice receiving shRNA control, shRNA AGK#1 cells with or without venetoclax treatment (n = 6, each group). F. Tumor weights of shRNA control and shRNA AGK#1 groups with or without venetoclax treatment (n = 6, each group). G-H. H&E staining, cleaved-caspase3 and TUNEL staining of shRNA control and shRNA AGK groups with or without venetoclax treatment, and the percentages of positive area of cleaved-caspase3 and TUNEL were quantified. I-J. The levels of AGK, BCL-2, p-FOXO1, FOXO1, p-AKT and AKT were measured (I) and quantified (J) in the tumor tissues isolated from shRNA control and shRNA AGK groups (n = 6, each group). K-L. FOXO1 staining of shRNA control and shRNA AGK group tumor tissues (K) and the percentages of FOXO1 expression in cytoplasmic and nuclear were quantified (L). Scale bar, 100 μm or 25 μm. Data were expressed as mean ± SEM and analyzed for statistical significance by One-way ANOVA (F, H, L) or t -test (J) (* P < 0.05; ** P < 0.01; *** P < 0.001).

    Techniques Used: In Vivo, shRNA, Staining, TUNEL Assay, Isolation, Expressing

    The expression of AGK is inversely associated with BCL-2 expression in DLBCL patients. A. H&E staining, BCL-2, AGK and FOXO1 staining of BCL-2 low and BCL-2 high DLBCL tissue samples. n = 33, scale bar, 100 μm or 25 μm. Black arrow: cytoplasmic FOXO1; Red arrow: nuclear FOXO1. B. Quantitation of the percentages of AGK positive cell in BCL-2 low (n = 17) and BCL-2 high (n = 16) DLBCL paraffin sections. C. Quantitation of the ratios of nuclear and cytoplasmic FOXO1 in BCL-2 low (n = 15) and BCL-2 high (n = 14) DLBCL paraffin sections. D. Spearman correlation analysis of the ratios of nuclear versus cytoplasmic FOXO1 with the expression of AGK. E. Schematic figure of the regulation of AGK on venetoclax sensitivity. In DLBCL cells, AGK phosphorylates and inactivates PTEN, leading to enhanced phosphorylation of AKT and FOXO1 and reduced FOXO1 nuclear translocation and its target gene BCL-2 expression. AGK knockdown could reverse the effect of AGK-PTEN-FOXO1-BCL-2 axis, upregulate the expression of BCL-2 and increase the sensibility to venetoclax-induced apoptosis. Ibrutinib inhibits the expression of AGK in DLBCL cells. Data were expressed as mean ± SEM and analyzed for statistical significance by t test (B, D). (** P < 0.01; *** P < 0.001; ns, not significant).
    Figure Legend Snippet: The expression of AGK is inversely associated with BCL-2 expression in DLBCL patients. A. H&E staining, BCL-2, AGK and FOXO1 staining of BCL-2 low and BCL-2 high DLBCL tissue samples. n = 33, scale bar, 100 μm or 25 μm. Black arrow: cytoplasmic FOXO1; Red arrow: nuclear FOXO1. B. Quantitation of the percentages of AGK positive cell in BCL-2 low (n = 17) and BCL-2 high (n = 16) DLBCL paraffin sections. C. Quantitation of the ratios of nuclear and cytoplasmic FOXO1 in BCL-2 low (n = 15) and BCL-2 high (n = 14) DLBCL paraffin sections. D. Spearman correlation analysis of the ratios of nuclear versus cytoplasmic FOXO1 with the expression of AGK. E. Schematic figure of the regulation of AGK on venetoclax sensitivity. In DLBCL cells, AGK phosphorylates and inactivates PTEN, leading to enhanced phosphorylation of AKT and FOXO1 and reduced FOXO1 nuclear translocation and its target gene BCL-2 expression. AGK knockdown could reverse the effect of AGK-PTEN-FOXO1-BCL-2 axis, upregulate the expression of BCL-2 and increase the sensibility to venetoclax-induced apoptosis. Ibrutinib inhibits the expression of AGK in DLBCL cells. Data were expressed as mean ± SEM and analyzed for statistical significance by t test (B, D). (** P < 0.01; *** P < 0.001; ns, not significant).

    Techniques Used: Expressing, Staining, Quantitation Assay, Translocation Assay

    antibodies against akt  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc antibodies against akt
    Antibodies Against Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    protein kinase b  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc protein kinase b
    ACG-RGI/KLT regulated Schwann cells in vitro . (A) Images of cultured Schwann cells in the ACG, ACG-RGI/KLT, and control groups. Schwann cells were stained with anti-S100 (red) and DAPI (blue). (B) The expression levels of several markers reflecting the proliferation, adhesion, and secretory function of cells were examined by Western blotting (WB). (C-I) Statistical analysis of brain-derived neurotrophic factor (BNGF), nerve growth factor (NGF), glial cell-derived neurotrophic factor (GDNF), vascular endothelial growth factor (VEGF), neural cell adhesion molecule 1 (NCAM1), proliferating cell nuclear antigen (PCNA), and phosphorylated protein <t>kinase</t> <t>B</t> (p-AKT) protein levels, respectively. (K-N) qRT-PCR results indicated the relative expression levels of BNGF, NGF, GDNF, VEGF, and NCAM1. Data are presented as means ± standard error of the mean, n = 3 for each group. ** p <0.01, * p <0.05.
    Protein Kinase B, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Aligned chitosan nanofiber hydrogel grafted with peptides mimicking bioactive brain-derived neurotrophic factor and vascular endothelial growth factor repair long-distance sciatic nerve defects in rats"

    Article Title: Aligned chitosan nanofiber hydrogel grafted with peptides mimicking bioactive brain-derived neurotrophic factor and vascular endothelial growth factor repair long-distance sciatic nerve defects in rats

    Journal: Theranostics

    doi: 10.7150/thno.36272

    ACG-RGI/KLT regulated Schwann cells in vitro . (A) Images of cultured Schwann cells in the ACG, ACG-RGI/KLT, and control groups. Schwann cells were stained with anti-S100 (red) and DAPI (blue). (B) The expression levels of several markers reflecting the proliferation, adhesion, and secretory function of cells were examined by Western blotting (WB). (C-I) Statistical analysis of brain-derived neurotrophic factor (BNGF), nerve growth factor (NGF), glial cell-derived neurotrophic factor (GDNF), vascular endothelial growth factor (VEGF), neural cell adhesion molecule 1 (NCAM1), proliferating cell nuclear antigen (PCNA), and phosphorylated protein kinase B (p-AKT) protein levels, respectively. (K-N) qRT-PCR results indicated the relative expression levels of BNGF, NGF, GDNF, VEGF, and NCAM1. Data are presented as means ± standard error of the mean, n = 3 for each group. ** p <0.01, * p <0.05.
    Figure Legend Snippet: ACG-RGI/KLT regulated Schwann cells in vitro . (A) Images of cultured Schwann cells in the ACG, ACG-RGI/KLT, and control groups. Schwann cells were stained with anti-S100 (red) and DAPI (blue). (B) The expression levels of several markers reflecting the proliferation, adhesion, and secretory function of cells were examined by Western blotting (WB). (C-I) Statistical analysis of brain-derived neurotrophic factor (BNGF), nerve growth factor (NGF), glial cell-derived neurotrophic factor (GDNF), vascular endothelial growth factor (VEGF), neural cell adhesion molecule 1 (NCAM1), proliferating cell nuclear antigen (PCNA), and phosphorylated protein kinase B (p-AKT) protein levels, respectively. (K-N) qRT-PCR results indicated the relative expression levels of BNGF, NGF, GDNF, VEGF, and NCAM1. Data are presented as means ± standard error of the mean, n = 3 for each group. ** p <0.01, * p <0.05.

    Techniques Used: In Vitro, Cell Culture, Staining, Expressing, Western Blot, Derivative Assay, Quantitative RT-PCR

    anti akt  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti akt
    Anti Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    t akt  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc t akt
    T Akt, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc akt pan c67e7 rabbit monoclonal antibody rabbit monoclonal antibody mab
    Akt Pan C67e7 Rabbit Monoclonal Antibody Rabbit Monoclonal Antibody Mab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc akt ab
    The expression <t>of</t> <t>Caveolin-1,</t> <t>p-AKT/AKT,</t> and PI3K in adipose tissue of NC, type 2 diabetic mice, and insulin-treated T2DM mice (a). The band intensity of Caveolin-1, p-AKT/AKT, and PI3K was quantified as shown in (b–d), respectively (data presented as mean ± SEM. ∗ P < 0.05 vs. NC mice. # P < 0.05 compared with T2DM mice, n = 5).
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    <t>AGK</t> inhibits BCL-2 expression by phosphorylation PTEN and subsequent <t>AKT-FOXO1</t> signaling. A. The levels of AGK and BCL-2 were determined in SU-DHL2, OCI-LY1, TMD8, SU-DHL4, SU-DHL6, SU-DHL10, and SU-DHL16 DLBCL cell lines. B. Spearman correlation analysis of AGK and BCL-2 expression in DLBCL cell lines. C. AGK and BCL-2 expression was measured with immunoblotting and BCL-2 expression was quantified in shRNA control and shRNA AGK SU-DHL4 cells from three independent experiments. D. AGK and BCL-2 expression was measured in control and AGK overexpression SU-DHL4 cells, and BCL-2 expression was quantified from three independent experiments. E. The amounts of p-PTEN and PTEN in SU-DHL2, OCI-LY1, TMD8, SU-DHL4, SU-DHL6, SU-DHL10, and SU-DHL16 DLBCL cell lines were determined by immunoblotting. F. Spearman correlation analysis of AGK and PTEN phosphorylation levels in DLBCL cell lines. G-H. Phosphorylation levels of PTEN, AKT and FOXO1 were measured and quantified in control and AGK knockdown SU-DHL4 cells from three independent experiments. I-J The levels of FOXO1 and p-FOXO1 were measured in cytoplasmic and nuclear fractions (I) and the band intensities were quantified (J). K. The binding of FOXO1 to BCL-2 promoter in SU-DHL4 was determined by chromatin immunoprecipitation analysis. Data were expressed as mean ± SEM from three independent experiments (A-J) or two independent experiments with triplicates (K), and analyzed for statistical significance by t -test. (* P < 0.05; ** P < 0.01; *** P < 0.001).
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    <t>AGK</t> inhibits BCL-2 expression by phosphorylation PTEN and subsequent <t>AKT-FOXO1</t> signaling. A. The levels of AGK and BCL-2 were determined in SU-DHL2, OCI-LY1, TMD8, SU-DHL4, SU-DHL6, SU-DHL10, and SU-DHL16 DLBCL cell lines. B. Spearman correlation analysis of AGK and BCL-2 expression in DLBCL cell lines. C. AGK and BCL-2 expression was measured with immunoblotting and BCL-2 expression was quantified in shRNA control and shRNA AGK SU-DHL4 cells from three independent experiments. D. AGK and BCL-2 expression was measured in control and AGK overexpression SU-DHL4 cells, and BCL-2 expression was quantified from three independent experiments. E. The amounts of p-PTEN and PTEN in SU-DHL2, OCI-LY1, TMD8, SU-DHL4, SU-DHL6, SU-DHL10, and SU-DHL16 DLBCL cell lines were determined by immunoblotting. F. Spearman correlation analysis of AGK and PTEN phosphorylation levels in DLBCL cell lines. G-H. Phosphorylation levels of PTEN, AKT and FOXO1 were measured and quantified in control and AGK knockdown SU-DHL4 cells from three independent experiments. I-J The levels of FOXO1 and p-FOXO1 were measured in cytoplasmic and nuclear fractions (I) and the band intensities were quantified (J). K. The binding of FOXO1 to BCL-2 promoter in SU-DHL4 was determined by chromatin immunoprecipitation analysis. Data were expressed as mean ± SEM from three independent experiments (A-J) or two independent experiments with triplicates (K), and analyzed for statistical significance by t -test. (* P < 0.05; ** P < 0.01; *** P < 0.001).
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    ACG-RGI/KLT regulated Schwann cells in vitro . (A) Images of cultured Schwann cells in the ACG, ACG-RGI/KLT, and control groups. Schwann cells were stained with anti-S100 (red) and DAPI (blue). (B) The expression levels of several markers reflecting the proliferation, adhesion, and secretory function of cells were examined by Western blotting (WB). (C-I) Statistical analysis of brain-derived neurotrophic factor (BNGF), nerve growth factor (NGF), glial cell-derived neurotrophic factor (GDNF), vascular endothelial growth factor (VEGF), neural cell adhesion molecule 1 (NCAM1), proliferating cell nuclear antigen (PCNA), and phosphorylated protein <t>kinase</t> <t>B</t> (p-AKT) protein levels, respectively. (K-N) qRT-PCR results indicated the relative expression levels of BNGF, NGF, GDNF, VEGF, and NCAM1. Data are presented as means ± standard error of the mean, n = 3 for each group. ** p <0.01, * p <0.05.
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    ACG-RGI/KLT regulated Schwann cells in vitro . (A) Images of cultured Schwann cells in the ACG, ACG-RGI/KLT, and control groups. Schwann cells were stained with anti-S100 (red) and DAPI (blue). (B) The expression levels of several markers reflecting the proliferation, adhesion, and secretory function of cells were examined by Western blotting (WB). (C-I) Statistical analysis of brain-derived neurotrophic factor (BNGF), nerve growth factor (NGF), glial cell-derived neurotrophic factor (GDNF), vascular endothelial growth factor (VEGF), neural cell adhesion molecule 1 (NCAM1), proliferating cell nuclear antigen (PCNA), and phosphorylated protein <t>kinase</t> <t>B</t> (p-AKT) protein levels, respectively. (K-N) qRT-PCR results indicated the relative expression levels of BNGF, NGF, GDNF, VEGF, and NCAM1. Data are presented as means ± standard error of the mean, n = 3 for each group. ** p <0.01, * p <0.05.
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    Image Search Results


    The expression of Caveolin-1, p-AKT/AKT, and PI3K in adipose tissue of NC, type 2 diabetic mice, and insulin-treated T2DM mice (a). The band intensity of Caveolin-1, p-AKT/AKT, and PI3K was quantified as shown in (b–d), respectively (data presented as mean ± SEM. ∗ P < 0.05 vs. NC mice. # P < 0.05 compared with T2DM mice, n = 5).

    Journal: Journal of Diabetes Research

    Article Title: Caveolin-1 Is Essential for the Improvement of Insulin Sensitivity through AKT Activation during Glargine Treatment on Diabetic Mice

    doi: 10.1155/2021/9943344

    Figure Lengend Snippet: The expression of Caveolin-1, p-AKT/AKT, and PI3K in adipose tissue of NC, type 2 diabetic mice, and insulin-treated T2DM mice (a). The band intensity of Caveolin-1, p-AKT/AKT, and PI3K was quantified as shown in (b–d), respectively (data presented as mean ± SEM. ∗ P < 0.05 vs. NC mice. # P < 0.05 compared with T2DM mice, n = 5).

    Article Snippet: The primary antibodies were purchased from Cell Signaling Technology (Danvers, MA, USA), which included Caveolin-1-Ab (Cat. #3267), phosphorylated (p)-Akt (Ser473)-Ab (Cat. #4060, 1 : 2000), Akt-Ab (Cat. #4691), PI3K-Ab (Cat. #4255), and β -actin (Cat. #8457).

    Techniques: Expressing

    The expression of Caveolin-1, p-AKT/AKT, and PI3K among five different groups (a). The band intensity of Caveolin-1, p-AKT/AKT, and PI3K was quantified as shown in (b–d), respectively (data are expressed as mean ± SEM. ∗ P < 0.05 compared with the insulin group. # P < 0.05 compared with the Ctrl-shRNA group; a represents P < 0.05 compared with the NC group, and b represents P < 0.05 compared with the T2DM group, n = 5).

    Journal: Journal of Diabetes Research

    Article Title: Caveolin-1 Is Essential for the Improvement of Insulin Sensitivity through AKT Activation during Glargine Treatment on Diabetic Mice

    doi: 10.1155/2021/9943344

    Figure Lengend Snippet: The expression of Caveolin-1, p-AKT/AKT, and PI3K among five different groups (a). The band intensity of Caveolin-1, p-AKT/AKT, and PI3K was quantified as shown in (b–d), respectively (data are expressed as mean ± SEM. ∗ P < 0.05 compared with the insulin group. # P < 0.05 compared with the Ctrl-shRNA group; a represents P < 0.05 compared with the NC group, and b represents P < 0.05 compared with the T2DM group, n = 5).

    Article Snippet: The primary antibodies were purchased from Cell Signaling Technology (Danvers, MA, USA), which included Caveolin-1-Ab (Cat. #3267), phosphorylated (p)-Akt (Ser473)-Ab (Cat. #4060, 1 : 2000), Akt-Ab (Cat. #4691), PI3K-Ab (Cat. #4255), and β -actin (Cat. #8457).

    Techniques: Expressing, shRNA

    AGK inhibits BCL-2 expression by phosphorylation PTEN and subsequent AKT-FOXO1 signaling. A. The levels of AGK and BCL-2 were determined in SU-DHL2, OCI-LY1, TMD8, SU-DHL4, SU-DHL6, SU-DHL10, and SU-DHL16 DLBCL cell lines. B. Spearman correlation analysis of AGK and BCL-2 expression in DLBCL cell lines. C. AGK and BCL-2 expression was measured with immunoblotting and BCL-2 expression was quantified in shRNA control and shRNA AGK SU-DHL4 cells from three independent experiments. D. AGK and BCL-2 expression was measured in control and AGK overexpression SU-DHL4 cells, and BCL-2 expression was quantified from three independent experiments. E. The amounts of p-PTEN and PTEN in SU-DHL2, OCI-LY1, TMD8, SU-DHL4, SU-DHL6, SU-DHL10, and SU-DHL16 DLBCL cell lines were determined by immunoblotting. F. Spearman correlation analysis of AGK and PTEN phosphorylation levels in DLBCL cell lines. G-H. Phosphorylation levels of PTEN, AKT and FOXO1 were measured and quantified in control and AGK knockdown SU-DHL4 cells from three independent experiments. I-J The levels of FOXO1 and p-FOXO1 were measured in cytoplasmic and nuclear fractions (I) and the band intensities were quantified (J). K. The binding of FOXO1 to BCL-2 promoter in SU-DHL4 was determined by chromatin immunoprecipitation analysis. Data were expressed as mean ± SEM from three independent experiments (A-J) or two independent experiments with triplicates (K), and analyzed for statistical significance by t -test. (* P < 0.05; ** P < 0.01; *** P < 0.001).

    Journal: Theranostics

    Article Title: Inhibition of acylglycerol kinase sensitizes DLBCL to venetoclax via upregulation of FOXO1-mediated BCL-2 expression

    doi: 10.7150/thno.72786

    Figure Lengend Snippet: AGK inhibits BCL-2 expression by phosphorylation PTEN and subsequent AKT-FOXO1 signaling. A. The levels of AGK and BCL-2 were determined in SU-DHL2, OCI-LY1, TMD8, SU-DHL4, SU-DHL6, SU-DHL10, and SU-DHL16 DLBCL cell lines. B. Spearman correlation analysis of AGK and BCL-2 expression in DLBCL cell lines. C. AGK and BCL-2 expression was measured with immunoblotting and BCL-2 expression was quantified in shRNA control and shRNA AGK SU-DHL4 cells from three independent experiments. D. AGK and BCL-2 expression was measured in control and AGK overexpression SU-DHL4 cells, and BCL-2 expression was quantified from three independent experiments. E. The amounts of p-PTEN and PTEN in SU-DHL2, OCI-LY1, TMD8, SU-DHL4, SU-DHL6, SU-DHL10, and SU-DHL16 DLBCL cell lines were determined by immunoblotting. F. Spearman correlation analysis of AGK and PTEN phosphorylation levels in DLBCL cell lines. G-H. Phosphorylation levels of PTEN, AKT and FOXO1 were measured and quantified in control and AGK knockdown SU-DHL4 cells from three independent experiments. I-J The levels of FOXO1 and p-FOXO1 were measured in cytoplasmic and nuclear fractions (I) and the band intensities were quantified (J). K. The binding of FOXO1 to BCL-2 promoter in SU-DHL4 was determined by chromatin immunoprecipitation analysis. Data were expressed as mean ± SEM from three independent experiments (A-J) or two independent experiments with triplicates (K), and analyzed for statistical significance by t -test. (* P < 0.05; ** P < 0.01; *** P < 0.001).

    Article Snippet: After blocking with 5% milk for 2 h, the blots were probed with the anti-AGK (Abcam, ab137616), anti-BCL-2 (Abclonal, A19693), anti-PTEN (CST, #9188), anti-pPTEN (CST, #9551), anti-AKT (CST, #4691), anti-pAKT(T308) (CST, #2965), anti-pAKT (S473) (CST, #4060), anti-FOXO1 (CST, #2880), anti-pFOXO1 (CST, #9464), anti-β-Actin (CST, #4970) and anti-GAPDH (Servicebio, GB11002) antibodies overnight at 4 °C.

    Techniques: Expressing, Western Blot, shRNA, Over Expression, Binding Assay, Chromatin Immunoprecipitation

    Knockdown of AGK augments venetoclax efficacy in vivo . A. Schematic diagram of xenograft tumor model and venetoclax treatment strategy. B-E. Tumor growth curves of mice receiving shRNA control, shRNA AGK#1 cells with or without venetoclax treatment (n = 6, each group). F. Tumor weights of shRNA control and shRNA AGK#1 groups with or without venetoclax treatment (n = 6, each group). G-H. H&E staining, cleaved-caspase3 and TUNEL staining of shRNA control and shRNA AGK groups with or without venetoclax treatment, and the percentages of positive area of cleaved-caspase3 and TUNEL were quantified. I-J. The levels of AGK, BCL-2, p-FOXO1, FOXO1, p-AKT and AKT were measured (I) and quantified (J) in the tumor tissues isolated from shRNA control and shRNA AGK groups (n = 6, each group). K-L. FOXO1 staining of shRNA control and shRNA AGK group tumor tissues (K) and the percentages of FOXO1 expression in cytoplasmic and nuclear were quantified (L). Scale bar, 100 μm or 25 μm. Data were expressed as mean ± SEM and analyzed for statistical significance by One-way ANOVA (F, H, L) or t -test (J) (* P < 0.05; ** P < 0.01; *** P < 0.001).

    Journal: Theranostics

    Article Title: Inhibition of acylglycerol kinase sensitizes DLBCL to venetoclax via upregulation of FOXO1-mediated BCL-2 expression

    doi: 10.7150/thno.72786

    Figure Lengend Snippet: Knockdown of AGK augments venetoclax efficacy in vivo . A. Schematic diagram of xenograft tumor model and venetoclax treatment strategy. B-E. Tumor growth curves of mice receiving shRNA control, shRNA AGK#1 cells with or without venetoclax treatment (n = 6, each group). F. Tumor weights of shRNA control and shRNA AGK#1 groups with or without venetoclax treatment (n = 6, each group). G-H. H&E staining, cleaved-caspase3 and TUNEL staining of shRNA control and shRNA AGK groups with or without venetoclax treatment, and the percentages of positive area of cleaved-caspase3 and TUNEL were quantified. I-J. The levels of AGK, BCL-2, p-FOXO1, FOXO1, p-AKT and AKT were measured (I) and quantified (J) in the tumor tissues isolated from shRNA control and shRNA AGK groups (n = 6, each group). K-L. FOXO1 staining of shRNA control and shRNA AGK group tumor tissues (K) and the percentages of FOXO1 expression in cytoplasmic and nuclear were quantified (L). Scale bar, 100 μm or 25 μm. Data were expressed as mean ± SEM and analyzed for statistical significance by One-way ANOVA (F, H, L) or t -test (J) (* P < 0.05; ** P < 0.01; *** P < 0.001).

    Article Snippet: After blocking with 5% milk for 2 h, the blots were probed with the anti-AGK (Abcam, ab137616), anti-BCL-2 (Abclonal, A19693), anti-PTEN (CST, #9188), anti-pPTEN (CST, #9551), anti-AKT (CST, #4691), anti-pAKT(T308) (CST, #2965), anti-pAKT (S473) (CST, #4060), anti-FOXO1 (CST, #2880), anti-pFOXO1 (CST, #9464), anti-β-Actin (CST, #4970) and anti-GAPDH (Servicebio, GB11002) antibodies overnight at 4 °C.

    Techniques: In Vivo, shRNA, Staining, TUNEL Assay, Isolation, Expressing

    The expression of AGK is inversely associated with BCL-2 expression in DLBCL patients. A. H&E staining, BCL-2, AGK and FOXO1 staining of BCL-2 low and BCL-2 high DLBCL tissue samples. n = 33, scale bar, 100 μm or 25 μm. Black arrow: cytoplasmic FOXO1; Red arrow: nuclear FOXO1. B. Quantitation of the percentages of AGK positive cell in BCL-2 low (n = 17) and BCL-2 high (n = 16) DLBCL paraffin sections. C. Quantitation of the ratios of nuclear and cytoplasmic FOXO1 in BCL-2 low (n = 15) and BCL-2 high (n = 14) DLBCL paraffin sections. D. Spearman correlation analysis of the ratios of nuclear versus cytoplasmic FOXO1 with the expression of AGK. E. Schematic figure of the regulation of AGK on venetoclax sensitivity. In DLBCL cells, AGK phosphorylates and inactivates PTEN, leading to enhanced phosphorylation of AKT and FOXO1 and reduced FOXO1 nuclear translocation and its target gene BCL-2 expression. AGK knockdown could reverse the effect of AGK-PTEN-FOXO1-BCL-2 axis, upregulate the expression of BCL-2 and increase the sensibility to venetoclax-induced apoptosis. Ibrutinib inhibits the expression of AGK in DLBCL cells. Data were expressed as mean ± SEM and analyzed for statistical significance by t test (B, D). (** P < 0.01; *** P < 0.001; ns, not significant).

    Journal: Theranostics

    Article Title: Inhibition of acylglycerol kinase sensitizes DLBCL to venetoclax via upregulation of FOXO1-mediated BCL-2 expression

    doi: 10.7150/thno.72786

    Figure Lengend Snippet: The expression of AGK is inversely associated with BCL-2 expression in DLBCL patients. A. H&E staining, BCL-2, AGK and FOXO1 staining of BCL-2 low and BCL-2 high DLBCL tissue samples. n = 33, scale bar, 100 μm or 25 μm. Black arrow: cytoplasmic FOXO1; Red arrow: nuclear FOXO1. B. Quantitation of the percentages of AGK positive cell in BCL-2 low (n = 17) and BCL-2 high (n = 16) DLBCL paraffin sections. C. Quantitation of the ratios of nuclear and cytoplasmic FOXO1 in BCL-2 low (n = 15) and BCL-2 high (n = 14) DLBCL paraffin sections. D. Spearman correlation analysis of the ratios of nuclear versus cytoplasmic FOXO1 with the expression of AGK. E. Schematic figure of the regulation of AGK on venetoclax sensitivity. In DLBCL cells, AGK phosphorylates and inactivates PTEN, leading to enhanced phosphorylation of AKT and FOXO1 and reduced FOXO1 nuclear translocation and its target gene BCL-2 expression. AGK knockdown could reverse the effect of AGK-PTEN-FOXO1-BCL-2 axis, upregulate the expression of BCL-2 and increase the sensibility to venetoclax-induced apoptosis. Ibrutinib inhibits the expression of AGK in DLBCL cells. Data were expressed as mean ± SEM and analyzed for statistical significance by t test (B, D). (** P < 0.01; *** P < 0.001; ns, not significant).

    Article Snippet: After blocking with 5% milk for 2 h, the blots were probed with the anti-AGK (Abcam, ab137616), anti-BCL-2 (Abclonal, A19693), anti-PTEN (CST, #9188), anti-pPTEN (CST, #9551), anti-AKT (CST, #4691), anti-pAKT(T308) (CST, #2965), anti-pAKT (S473) (CST, #4060), anti-FOXO1 (CST, #2880), anti-pFOXO1 (CST, #9464), anti-β-Actin (CST, #4970) and anti-GAPDH (Servicebio, GB11002) antibodies overnight at 4 °C.

    Techniques: Expressing, Staining, Quantitation Assay, Translocation Assay

    ACG-RGI/KLT regulated Schwann cells in vitro . (A) Images of cultured Schwann cells in the ACG, ACG-RGI/KLT, and control groups. Schwann cells were stained with anti-S100 (red) and DAPI (blue). (B) The expression levels of several markers reflecting the proliferation, adhesion, and secretory function of cells were examined by Western blotting (WB). (C-I) Statistical analysis of brain-derived neurotrophic factor (BNGF), nerve growth factor (NGF), glial cell-derived neurotrophic factor (GDNF), vascular endothelial growth factor (VEGF), neural cell adhesion molecule 1 (NCAM1), proliferating cell nuclear antigen (PCNA), and phosphorylated protein kinase B (p-AKT) protein levels, respectively. (K-N) qRT-PCR results indicated the relative expression levels of BNGF, NGF, GDNF, VEGF, and NCAM1. Data are presented as means ± standard error of the mean, n = 3 for each group. ** p <0.01, * p <0.05.

    Journal: Theranostics

    Article Title: Aligned chitosan nanofiber hydrogel grafted with peptides mimicking bioactive brain-derived neurotrophic factor and vascular endothelial growth factor repair long-distance sciatic nerve defects in rats

    doi: 10.7150/thno.36272

    Figure Lengend Snippet: ACG-RGI/KLT regulated Schwann cells in vitro . (A) Images of cultured Schwann cells in the ACG, ACG-RGI/KLT, and control groups. Schwann cells were stained with anti-S100 (red) and DAPI (blue). (B) The expression levels of several markers reflecting the proliferation, adhesion, and secretory function of cells were examined by Western blotting (WB). (C-I) Statistical analysis of brain-derived neurotrophic factor (BNGF), nerve growth factor (NGF), glial cell-derived neurotrophic factor (GDNF), vascular endothelial growth factor (VEGF), neural cell adhesion molecule 1 (NCAM1), proliferating cell nuclear antigen (PCNA), and phosphorylated protein kinase B (p-AKT) protein levels, respectively. (K-N) qRT-PCR results indicated the relative expression levels of BNGF, NGF, GDNF, VEGF, and NCAM1. Data are presented as means ± standard error of the mean, n = 3 for each group. ** p <0.01, * p <0.05.

    Article Snippet: WB was performed using antibodies to VEGF (ab32152), nerve growth factor (NGF; ab6199), BDNF (ab108319), glial cell-derived neurotrophic factor (GDNF; ab18956), neural cell adhesion molecule 1 (NCAM1; ab9018), and growth associated protein 43 (GAP43; ab12274) purchased from Abcam, and to proliferating cell nuclear antigen (PCNA; #13110), protein kinase B (AKT; #4691), phosphorylated protein kinase B (p-AKT; #4060), CD31 (#77699), and GAPDH (#51332) purchased from Cell Signaling Technology.

    Techniques: In Vitro, Cell Culture, Staining, Expressing, Western Blot, Derivative Assay, Quantitative RT-PCR