rapamycin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rapamycin
    Rapamycin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    rapamycin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rapamycin
    Rapamycin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    mtor inhibitor rapamycin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc mtor inhibitor rapamycin
    NGF treatment reverses impairment of angiogenesis in aging GECs through PI3 kinase/Akt and <t>mTOR</t> pathways. ( A ) NGF treatment dose-dependently increases in vitro angiogenesis in aging GECs. Aging GECs were treated with either PBS (control) or exogenous NGF (10, 50, 100, or 1000 ng/mL) and in vitro angiogenesis on Matrigel was examined. Data are means ± SD (N = 6). Treatment of aging GECs with NGF dose-dependently increased angiogenesis with the maximal threshold stimulating dose of 100 ng/mL at 6 hours ( P < .001). There was no significant difference in angiogenesis between cells treated with NGF 100 ng/mL and 1000 ng/mL. † P > .05 (NS). ( B ) In vitro angiogenesis on Matrigel at 6 hours in aging GECs treated with PBS or recombinant rat NGF (100 ng/mL) with or without pretreatment with specific PI3 kinase inhibitor (LY294002; 50 μmol/L for 30 minutes), or mTOR inhibitor <t>(rapamycin;</t> 10 nmol/L for 60 minutes). Short-term (6 hours) treatment with exogenous NGF significantly increased in vitro angiogenesis and in aging GECs by 1.5-fold and pretreatment with LY294002, and rapamycin abolished the NGF-induced increase in angiogenesis. Data are means ± SD (N = 6). ( C ) Representative Western blots for phosphorylated Akt (pAkt) and Akt expression in aging GECs treated with exogenous NGF (0.1 μg/mL) for 4 and 24 hours. Treatment of aging GECs with exogenous NGF significantly increased Akt phosphorylation at 4 and 24 hours. Data are means ± SD (N = 3). The Student t test and 1-way analysis of variance with the Tukey multiple comparison test were used to determine statistical significance between 2 or multiple groups, respectively.
    Mtor Inhibitor Rapamycin, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Reduced NGF in Gastric Endothelial Cells Is One of the Main Causes of Impaired Angiogenesis in Aging Gastric Mucosa"

    Article Title: Reduced NGF in Gastric Endothelial Cells Is One of the Main Causes of Impaired Angiogenesis in Aging Gastric Mucosa

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    doi: 10.1016/j.jcmgh.2018.05.003

    NGF treatment reverses impairment of angiogenesis in aging GECs through PI3 kinase/Akt and mTOR pathways. ( A ) NGF treatment dose-dependently increases in vitro angiogenesis in aging GECs. Aging GECs were treated with either PBS (control) or exogenous NGF (10, 50, 100, or 1000 ng/mL) and in vitro angiogenesis on Matrigel was examined. Data are means ± SD (N = 6). Treatment of aging GECs with NGF dose-dependently increased angiogenesis with the maximal threshold stimulating dose of 100 ng/mL at 6 hours ( P < .001). There was no significant difference in angiogenesis between cells treated with NGF 100 ng/mL and 1000 ng/mL. † P > .05 (NS). ( B ) In vitro angiogenesis on Matrigel at 6 hours in aging GECs treated with PBS or recombinant rat NGF (100 ng/mL) with or without pretreatment with specific PI3 kinase inhibitor (LY294002; 50 μmol/L for 30 minutes), or mTOR inhibitor (rapamycin; 10 nmol/L for 60 minutes). Short-term (6 hours) treatment with exogenous NGF significantly increased in vitro angiogenesis and in aging GECs by 1.5-fold and pretreatment with LY294002, and rapamycin abolished the NGF-induced increase in angiogenesis. Data are means ± SD (N = 6). ( C ) Representative Western blots for phosphorylated Akt (pAkt) and Akt expression in aging GECs treated with exogenous NGF (0.1 μg/mL) for 4 and 24 hours. Treatment of aging GECs with exogenous NGF significantly increased Akt phosphorylation at 4 and 24 hours. Data are means ± SD (N = 3). The Student t test and 1-way analysis of variance with the Tukey multiple comparison test were used to determine statistical significance between 2 or multiple groups, respectively.
    Figure Legend Snippet: NGF treatment reverses impairment of angiogenesis in aging GECs through PI3 kinase/Akt and mTOR pathways. ( A ) NGF treatment dose-dependently increases in vitro angiogenesis in aging GECs. Aging GECs were treated with either PBS (control) or exogenous NGF (10, 50, 100, or 1000 ng/mL) and in vitro angiogenesis on Matrigel was examined. Data are means ± SD (N = 6). Treatment of aging GECs with NGF dose-dependently increased angiogenesis with the maximal threshold stimulating dose of 100 ng/mL at 6 hours ( P < .001). There was no significant difference in angiogenesis between cells treated with NGF 100 ng/mL and 1000 ng/mL. † P > .05 (NS). ( B ) In vitro angiogenesis on Matrigel at 6 hours in aging GECs treated with PBS or recombinant rat NGF (100 ng/mL) with or without pretreatment with specific PI3 kinase inhibitor (LY294002; 50 μmol/L for 30 minutes), or mTOR inhibitor (rapamycin; 10 nmol/L for 60 minutes). Short-term (6 hours) treatment with exogenous NGF significantly increased in vitro angiogenesis and in aging GECs by 1.5-fold and pretreatment with LY294002, and rapamycin abolished the NGF-induced increase in angiogenesis. Data are means ± SD (N = 6). ( C ) Representative Western blots for phosphorylated Akt (pAkt) and Akt expression in aging GECs treated with exogenous NGF (0.1 μg/mL) for 4 and 24 hours. Treatment of aging GECs with exogenous NGF significantly increased Akt phosphorylation at 4 and 24 hours. Data are means ± SD (N = 3). The Student t test and 1-way analysis of variance with the Tukey multiple comparison test were used to determine statistical significance between 2 or multiple groups, respectively.

    Techniques Used: In Vitro, Recombinant, Western Blot, Expressing

    phospho mtor  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phospho mtor
    Curcumin enhanced <t>the</t> <t>SIRT1-AMPK/mTOR</t> signal pathway. (a) Representative western blot for SIRT1 p-AMPK and p-mTOR levels in cardiomyocyte lysates ( n = 5). (b) Quantitation results of p-mTOR. (c) Quantitation results of SIRT1. (d). Quantitation results of p-AMPK. ∗∗ P < 0.01 vs. control. # P < 0.05, # # P < 0.01, vs. D-gal. The data are expressed as the mean ± SEM.
    Phospho Mtor, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    1) Product Images from "Curcumin Alleviates D-Galactose-Induced Cardiomyocyte Senescence by Promoting Autophagy via the SIRT1/AMPK/mTOR Pathway"

    Article Title: Curcumin Alleviates D-Galactose-Induced Cardiomyocyte Senescence by Promoting Autophagy via the SIRT1/AMPK/mTOR Pathway

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    doi: 10.1155/2022/2990843

    Curcumin enhanced the SIRT1-AMPK/mTOR signal pathway. (a) Representative western blot for SIRT1 p-AMPK and p-mTOR levels in cardiomyocyte lysates ( n = 5). (b) Quantitation results of p-mTOR. (c) Quantitation results of SIRT1. (d). Quantitation results of p-AMPK. ∗∗ P < 0.01 vs. control. # P < 0.05, # # P < 0.01, vs. D-gal. The data are expressed as the mean ± SEM.
    Figure Legend Snippet: Curcumin enhanced the SIRT1-AMPK/mTOR signal pathway. (a) Representative western blot for SIRT1 p-AMPK and p-mTOR levels in cardiomyocyte lysates ( n = 5). (b) Quantitation results of p-mTOR. (c) Quantitation results of SIRT1. (d). Quantitation results of p-AMPK. ∗∗ P < 0.01 vs. control. # P < 0.05, # # P < 0.01, vs. D-gal. The data are expressed as the mean ± SEM.

    Techniques Used: Western Blot, Quantitation Assay

    (a) Representative western blot of the levels of SIRT1 p-AMPK and p-mTOR. siSIRT1-mediated knockdown blocked the inducing effect of curcumin on the SIRT1/AMPK/mTOR pathway in cardiac aging ( n = 5). (b) The quantitation results of SIRT1. (c) The quantitation results of p-AMPK. (d) The quantitation results of p-mTOR. # P < 0.05, # # P < 0.01, vs. control. The data are expressed as the mean ± SEM.
    Figure Legend Snippet: (a) Representative western blot of the levels of SIRT1 p-AMPK and p-mTOR. siSIRT1-mediated knockdown blocked the inducing effect of curcumin on the SIRT1/AMPK/mTOR pathway in cardiac aging ( n = 5). (b) The quantitation results of SIRT1. (c) The quantitation results of p-AMPK. (d) The quantitation results of p-mTOR. # P < 0.05, # # P < 0.01, vs. control. The data are expressed as the mean ± SEM.

    Techniques Used: Western Blot, Quantitation Assay

    rapamycin mtor  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rapamycin mtor
    Rapamycin Mtor, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 98 stars, based on 1 article reviews
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    t mtor  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc t mtor
    List of antibodies used for western blot analyses.
    T Mtor, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/t mtor/product/Cell Signaling Technology Inc
    Average 98 stars, based on 1 article reviews
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    t mtor - by Bioz Stars, 2023-02
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    1) Product Images from "Growth Hormone Increases BDNF and mTOR Expression in Specific Brain Regions after Photothrombotic Stroke in Mice"

    Article Title: Growth Hormone Increases BDNF and mTOR Expression in Specific Brain Regions after Photothrombotic Stroke in Mice

    Journal: Neural Plasticity

    doi: 10.1155/2022/9983042

    List of antibodies used for western blot analyses.
    Figure Legend Snippet: List of antibodies used for western blot analyses.

    Techniques Used: Western Blot

    t -test and Pearson's results summary table.
    Figure Legend Snippet: t -test and Pearson's results summary table.

    Techniques Used:

    The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the peri-infarct region. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70S6-kinase P-p70S6K), and total-p70S6k (T-p70S6K). (b) T-mTOR and T-p70S6K levels were normalized to β -actin. P-mTOR and P-p70S6K levels were normalized to T-mTOR and T-p70S6K, respectively. Levels were expressed as a fold change (FC) of mean ± SD for each group relative to the mean of the Sham+Saline group (dotted line). We found a significant increase in T-mTOR protein expression within the peri-infarct region in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗ p < 0.05, 2-tailed t -test.
    Figure Legend Snippet: The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the peri-infarct region. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70S6-kinase P-p70S6K), and total-p70S6k (T-p70S6K). (b) T-mTOR and T-p70S6K levels were normalized to β -actin. P-mTOR and P-p70S6K levels were normalized to T-mTOR and T-p70S6K, respectively. Levels were expressed as a fold change (FC) of mean ± SD for each group relative to the mean of the Sham+Saline group (dotted line). We found a significant increase in T-mTOR protein expression within the peri-infarct region in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗ p < 0.05, 2-tailed t -test.

    Techniques Used: Recombinant, Expressing

    The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the hippocampus. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70s6-kinase (P-p70S6K), and total-p70s6k (T-p70S6K). (b) Data are presented as in . We found a significant increase in T-p70S6K protein expression within the hippocampus in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗ p < 0.05, 2-tailed t -test.
    Figure Legend Snippet: The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the hippocampus. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70s6-kinase (P-p70S6K), and total-p70s6k (T-p70S6K). (b) Data are presented as in . We found a significant increase in T-p70S6K protein expression within the hippocampus in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗ p < 0.05, 2-tailed t -test.

    Techniques Used: Recombinant, Expressing

    The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the thalamus. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70S6-kinase (P-p70S6K), and total-p70S6K (T-p70S6K). (b) Data are presented as in . We found a significant increase in T-mTOR protein expression within the thalamus in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗∗ p < 0.01, 2-tailed t -test.
    Figure Legend Snippet: The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the thalamus. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70S6-kinase (P-p70S6K), and total-p70S6K (T-p70S6K). (b) Data are presented as in . We found a significant increase in T-mTOR protein expression within the thalamus in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗∗ p < 0.01, 2-tailed t -test.

    Techniques Used: Recombinant, Expressing

    Correlation of uncleaved immature form of BDNF (pro-BDNF) with mammalian target of rapamycin (mTOR) and markers of neuroplasticity. Correlation of pro-BDNF, with T-mTOR (top panel), α -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-receptor subunit GluR1 (marker of synaptic plasticity, second from top panel), NeuN (neuronal marker, third from top panel), and doublecortin (DCX, neuronal migration marker, bottom panel) in the peri-infarct region (a), hippocampus (b), and thalamus (c). Dataset GluR1, NeuN, and DCX was an excerpt from previous study [ , ]. Correlations contain all three experimental groups, Sham+Saline (black crosses), Stroke+Saline (red circles), and Stroke+r-hGH (blue squares) and analyzed using Pearson's correlation. Pearson's r and associated p values for each correlation are reported on the corresponding graph.
    Figure Legend Snippet: Correlation of uncleaved immature form of BDNF (pro-BDNF) with mammalian target of rapamycin (mTOR) and markers of neuroplasticity. Correlation of pro-BDNF, with T-mTOR (top panel), α -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-receptor subunit GluR1 (marker of synaptic plasticity, second from top panel), NeuN (neuronal marker, third from top panel), and doublecortin (DCX, neuronal migration marker, bottom panel) in the peri-infarct region (a), hippocampus (b), and thalamus (c). Dataset GluR1, NeuN, and DCX was an excerpt from previous study [ , ]. Correlations contain all three experimental groups, Sham+Saline (black crosses), Stroke+Saline (red circles), and Stroke+r-hGH (blue squares) and analyzed using Pearson's correlation. Pearson's r and associated p values for each correlation are reported on the corresponding graph.

    Techniques Used: Marker, Migration

    p mtor  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p mtor
    List of antibodies used for western blot analyses.
    P Mtor, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p mtor/product/Cell Signaling Technology Inc
    Average 98 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    p mtor - by Bioz Stars, 2023-02
    98/100 stars

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    1) Product Images from "Growth Hormone Increases BDNF and mTOR Expression in Specific Brain Regions after Photothrombotic Stroke in Mice"

    Article Title: Growth Hormone Increases BDNF and mTOR Expression in Specific Brain Regions after Photothrombotic Stroke in Mice

    Journal: Neural Plasticity

    doi: 10.1155/2022/9983042

    List of antibodies used for western blot analyses.
    Figure Legend Snippet: List of antibodies used for western blot analyses.

    Techniques Used: Western Blot

    t -test and Pearson's results summary table.
    Figure Legend Snippet: t -test and Pearson's results summary table.

    Techniques Used:

    The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the peri-infarct region. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70S6-kinase P-p70S6K), and total-p70S6k (T-p70S6K). (b) T-mTOR and T-p70S6K levels were normalized to β -actin. P-mTOR and P-p70S6K levels were normalized to T-mTOR and T-p70S6K, respectively. Levels were expressed as a fold change (FC) of mean ± SD for each group relative to the mean of the Sham+Saline group (dotted line). We found a significant increase in T-mTOR protein expression within the peri-infarct region in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗ p < 0.05, 2-tailed t -test.
    Figure Legend Snippet: The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the peri-infarct region. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70S6-kinase P-p70S6K), and total-p70S6k (T-p70S6K). (b) T-mTOR and T-p70S6K levels were normalized to β -actin. P-mTOR and P-p70S6K levels were normalized to T-mTOR and T-p70S6K, respectively. Levels were expressed as a fold change (FC) of mean ± SD for each group relative to the mean of the Sham+Saline group (dotted line). We found a significant increase in T-mTOR protein expression within the peri-infarct region in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗ p < 0.05, 2-tailed t -test.

    Techniques Used: Recombinant, Expressing

    The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the hippocampus. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70s6-kinase (P-p70S6K), and total-p70s6k (T-p70S6K). (b) Data are presented as in . We found a significant increase in T-p70S6K protein expression within the hippocampus in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗ p < 0.05, 2-tailed t -test.
    Figure Legend Snippet: The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the hippocampus. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70s6-kinase (P-p70S6K), and total-p70s6k (T-p70S6K). (b) Data are presented as in . We found a significant increase in T-p70S6K protein expression within the hippocampus in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗ p < 0.05, 2-tailed t -test.

    Techniques Used: Recombinant, Expressing

    The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the thalamus. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70S6-kinase (P-p70S6K), and total-p70S6K (T-p70S6K). (b) Data are presented as in . We found a significant increase in T-mTOR protein expression within the thalamus in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗∗ p < 0.01, 2-tailed t -test.
    Figure Legend Snippet: The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the thalamus. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70S6-kinase (P-p70S6K), and total-p70S6K (T-p70S6K). (b) Data are presented as in . We found a significant increase in T-mTOR protein expression within the thalamus in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗∗ p < 0.01, 2-tailed t -test.

    Techniques Used: Recombinant, Expressing

    p mtor  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p mtor
    Astaxanthin induces active expression of several functional genes and stemness genes, and proliferation-related signal proteins in NPCs. ( A ) Astaxanthin induced upregulation of proliferation-related transcription factors (Rex1, CDK1, and CDK2), coupled with overexpression of stemness genes (OCT4, SOX2, Nanog, and KLF4); ( B ) Astaxanthin induced significant activation of PI3K and its downstream mediators, p-Rac, p-c-Raf, p-MEK, p-ERK, <t>p-Akt,</t> <t>p-mTOR,</t> and p-Stat3 in a time-dependent manner.
    P Mtor, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/p mtor/product/Cell Signaling Technology Inc
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    p mtor - by Bioz Stars, 2023-02
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    1) Product Images from "Astaxanthin Improves Stem Cell Potency via an Increase in the Proliferation of Neural Progenitor Cells"

    Article Title: Astaxanthin Improves Stem Cell Potency via an Increase in the Proliferation of Neural Progenitor Cells

    Journal: International Journal of Molecular Sciences

    doi: 10.3390/ijms11125109

    Astaxanthin induces active expression of several functional genes and stemness genes, and proliferation-related signal proteins in NPCs. ( A ) Astaxanthin induced upregulation of proliferation-related transcription factors (Rex1, CDK1, and CDK2), coupled with overexpression of stemness genes (OCT4, SOX2, Nanog, and KLF4); ( B ) Astaxanthin induced significant activation of PI3K and its downstream mediators, p-Rac, p-c-Raf, p-MEK, p-ERK, p-Akt, p-mTOR, and p-Stat3 in a time-dependent manner.
    Figure Legend Snippet: Astaxanthin induces active expression of several functional genes and stemness genes, and proliferation-related signal proteins in NPCs. ( A ) Astaxanthin induced upregulation of proliferation-related transcription factors (Rex1, CDK1, and CDK2), coupled with overexpression of stemness genes (OCT4, SOX2, Nanog, and KLF4); ( B ) Astaxanthin induced significant activation of PI3K and its downstream mediators, p-Rac, p-c-Raf, p-MEK, p-ERK, p-Akt, p-mTOR, and p-Stat3 in a time-dependent manner.

    Techniques Used: Expressing, Functional Assay, Over Expression, Activation Assay

    Astaxanthin induces proliferation of NPCs via the PI3K and MEK signaling pathways. To estimate the relevance of the PI3K and MEK signaling pathways in cell growth in astaxanthin-treated NPCs, inhibition assays were performed with LY294002 (10 μM) and PD98059 (10 μM). ( A ) Inhibition of PI3K and MEK has been shown to cause inhibition of cell growth in astaxanthin-treated NPCs in vitro ; ( B ) LY294002 induced downregulation of PI3K, p-Rac, p-c-Raf, p-MEK, p-ERK, p-Akt, p-mTOR, and p-Stat3 proteins; ( C ) PD98059 significantly induced reduction of p-MEK, p-ERK, and p-Stat3; ( D ) PD98059 caused downregulation of proliferation-related transcription factors and stemness genes.
    Figure Legend Snippet: Astaxanthin induces proliferation of NPCs via the PI3K and MEK signaling pathways. To estimate the relevance of the PI3K and MEK signaling pathways in cell growth in astaxanthin-treated NPCs, inhibition assays were performed with LY294002 (10 μM) and PD98059 (10 μM). ( A ) Inhibition of PI3K and MEK has been shown to cause inhibition of cell growth in astaxanthin-treated NPCs in vitro ; ( B ) LY294002 induced downregulation of PI3K, p-Rac, p-c-Raf, p-MEK, p-ERK, p-Akt, p-mTOR, and p-Stat3 proteins; ( C ) PD98059 significantly induced reduction of p-MEK, p-ERK, and p-Stat3; ( D ) PD98059 caused downregulation of proliferation-related transcription factors and stemness genes.

    Techniques Used: Inhibition, In Vitro

    p mtor  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p mtor
    Effect of ketamine on autophagy in the lungs from mice sensitized to OVA. (a, b) Electron micrographs and quantification of autophagic vacuoles. (c–j) With Western blot, <t>MTOR,</t> <t>p-MTOR,</t> LC-3I, LC-3II, and Beclin-1 were determined and quantified. (k, l) With immunohistochemistry (magnification, <t>×200),</t> <t>p-MTOR</t> were determined and quantified. Data are expressed as the mean ± SD of six mice per group. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001 versus the control group; && P < 0.01 and &&& P < 0.001 versus the OVA group.
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    1) Product Images from "MTOR-Mediated Autophagy Is Involved in the Protective Effect of Ketamine on Allergic Airway Inflammation"

    Article Title: MTOR-Mediated Autophagy Is Involved in the Protective Effect of Ketamine on Allergic Airway Inflammation

    Journal: Journal of Immunology Research

    doi: 10.1155/2019/5879714

    Effect of ketamine on autophagy in the lungs from mice sensitized to OVA. (a, b) Electron micrographs and quantification of autophagic vacuoles. (c–j) With Western blot, MTOR, p-MTOR, LC-3I, LC-3II, and Beclin-1 were determined and quantified. (k, l) With immunohistochemistry (magnification, ×200), p-MTOR were determined and quantified. Data are expressed as the mean ± SD of six mice per group. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001 versus the control group; && P < 0.01 and &&& P < 0.001 versus the OVA group.
    Figure Legend Snippet: Effect of ketamine on autophagy in the lungs from mice sensitized to OVA. (a, b) Electron micrographs and quantification of autophagic vacuoles. (c–j) With Western blot, MTOR, p-MTOR, LC-3I, LC-3II, and Beclin-1 were determined and quantified. (k, l) With immunohistochemistry (magnification, ×200), p-MTOR were determined and quantified. Data are expressed as the mean ± SD of six mice per group. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001 versus the control group; && P < 0.01 and &&& P < 0.001 versus the OVA group.

    Techniques Used: Western Blot, Immunohistochemistry

    Effect of rapamycin on autophagy in the lungs from asthmatic mice treated with 50 mg/kg ketamine. (a, b) Electron micrographs and quantification of autophagic vacuoles. (c–h) With Western blot, MTOR, p-MTOR, LC-3I, LC-3II, and Beclin-1 were determined and quantified. (i, j) With immunohistochemistry (magnification, ×200), p-MTOR were determined and quantified. Data are expressed as the mean ± SD of six mice per group. ∗ P < 0.05, ∗∗ P < 0.01 versus the OVA groups; & P < 0.05, && P < 0.01, and &&& P < 0.001 versus the OVA+Ket50 group.
    Figure Legend Snippet: Effect of rapamycin on autophagy in the lungs from asthmatic mice treated with 50 mg/kg ketamine. (a, b) Electron micrographs and quantification of autophagic vacuoles. (c–h) With Western blot, MTOR, p-MTOR, LC-3I, LC-3II, and Beclin-1 were determined and quantified. (i, j) With immunohistochemistry (magnification, ×200), p-MTOR were determined and quantified. Data are expressed as the mean ± SD of six mice per group. ∗ P < 0.05, ∗∗ P < 0.01 versus the OVA groups; & P < 0.05, && P < 0.01, and &&& P < 0.001 versus the OVA+Ket50 group.

    Techniques Used: Western Blot, Immunohistochemistry

    rapamycin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rapamycin
    A. Western blots showing poly-ubiquitinated proteins (Ub) with or without transfection with siRNAs for Mdm20 and Nat5. To evaluate the effects of each siRNA, blots for Mdm20 and Nat5 were performed with β-actin controls. In the panel for Mdm20, the arrow indicates the bands at 120 kD corresponding to the expected size of Mdm20, and the asterisk denotes possible cross-reacting materials. B. Proteasome activity is unaffected in both Mdm20 and Nat5 knockdown in HEK293 cells. The activity of the proteasome was measured using a fluorescent-tagged polypeptide (Suc-LLVY-AMC) as a model substrate. Proteasome activities were calculated relative to the control cell extracts with control siRNA-transfected cells. The data represent the mean +/- S.D. (n=3) *P<0.01. C. Immunohistochemistry against LC3, a marker for autophagy, in Mdm20- and Nat5-KD cells. Panels d, e, f are high-magnification images of the area indicated in a, b, c. Note that punctate staining is apparent in the Mdm20-KD cells (e; allow). (Scale bar: 20 μm). D. Western blots for LC3-I and LC3-II to evaluate the induction of macroautophagy. DMSO, <t>rapamycin</t> (100 nM) are treated at 6h in control, Mdm20-KD, Nat5-KD HEK293cells. Note that the LC3-II bands are abundant in cells treated with rapamycin, in particular in Mdm20-KD cells. Actin was used as a loading control. The amounts of LC3II per LC3I were calculated relative to the control cell extracts with control siRNA-transfected cells. The data represent the mean +/- S.D. (n=5) *P<0.0001, **P<0.001, and ***P<0.01.
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    1) Product Images from "Mdm20 Stimulates PolyQ Aggregation via Inhibiting Autophagy Through Akt-Ser473 Phosphorylation"

    Article Title: Mdm20 Stimulates PolyQ Aggregation via Inhibiting Autophagy Through Akt-Ser473 Phosphorylation

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0082523

    A. Western blots showing poly-ubiquitinated proteins (Ub) with or without transfection with siRNAs for Mdm20 and Nat5. To evaluate the effects of each siRNA, blots for Mdm20 and Nat5 were performed with β-actin controls. In the panel for Mdm20, the arrow indicates the bands at 120 kD corresponding to the expected size of Mdm20, and the asterisk denotes possible cross-reacting materials. B. Proteasome activity is unaffected in both Mdm20 and Nat5 knockdown in HEK293 cells. The activity of the proteasome was measured using a fluorescent-tagged polypeptide (Suc-LLVY-AMC) as a model substrate. Proteasome activities were calculated relative to the control cell extracts with control siRNA-transfected cells. The data represent the mean +/- S.D. (n=3) *P<0.01. C. Immunohistochemistry against LC3, a marker for autophagy, in Mdm20- and Nat5-KD cells. Panels d, e, f are high-magnification images of the area indicated in a, b, c. Note that punctate staining is apparent in the Mdm20-KD cells (e; allow). (Scale bar: 20 μm). D. Western blots for LC3-I and LC3-II to evaluate the induction of macroautophagy. DMSO, rapamycin (100 nM) are treated at 6h in control, Mdm20-KD, Nat5-KD HEK293cells. Note that the LC3-II bands are abundant in cells treated with rapamycin, in particular in Mdm20-KD cells. Actin was used as a loading control. The amounts of LC3II per LC3I were calculated relative to the control cell extracts with control siRNA-transfected cells. The data represent the mean +/- S.D. (n=5) *P<0.0001, **P<0.001, and ***P<0.01.
    Figure Legend Snippet: A. Western blots showing poly-ubiquitinated proteins (Ub) with or without transfection with siRNAs for Mdm20 and Nat5. To evaluate the effects of each siRNA, blots for Mdm20 and Nat5 were performed with β-actin controls. In the panel for Mdm20, the arrow indicates the bands at 120 kD corresponding to the expected size of Mdm20, and the asterisk denotes possible cross-reacting materials. B. Proteasome activity is unaffected in both Mdm20 and Nat5 knockdown in HEK293 cells. The activity of the proteasome was measured using a fluorescent-tagged polypeptide (Suc-LLVY-AMC) as a model substrate. Proteasome activities were calculated relative to the control cell extracts with control siRNA-transfected cells. The data represent the mean +/- S.D. (n=3) *P<0.01. C. Immunohistochemistry against LC3, a marker for autophagy, in Mdm20- and Nat5-KD cells. Panels d, e, f are high-magnification images of the area indicated in a, b, c. Note that punctate staining is apparent in the Mdm20-KD cells (e; allow). (Scale bar: 20 μm). D. Western blots for LC3-I and LC3-II to evaluate the induction of macroautophagy. DMSO, rapamycin (100 nM) are treated at 6h in control, Mdm20-KD, Nat5-KD HEK293cells. Note that the LC3-II bands are abundant in cells treated with rapamycin, in particular in Mdm20-KD cells. Actin was used as a loading control. The amounts of LC3II per LC3I were calculated relative to the control cell extracts with control siRNA-transfected cells. The data represent the mean +/- S.D. (n=5) *P<0.0001, **P<0.001, and ***P<0.01.

    Techniques Used: Western Blot, Transfection, Activity Assay, Immunohistochemistry, Marker, Staining

    A. A phospho-mimic mutant of Akt (Akt-S473D) increases polyQ aggregate formation. Left: Shown are western blots for Akt and phospho-Akt (at Ser473 and Thr308). HEK293 cells were co-transfected with GFP-polyQ81 and Flag-tagged wild type Akt (F-Akt) or various phospho- and none-phospho-mimic Akt mutants as indicated. Right: The relative levels of polyQ aggregate formation were evaluated in each of the transfectants and compared with the mock-transfected control. Experiments were performed in naïve HEK293 cells (green bars) and Mdm20-KD cells (red bars). The numbers of polyQ-bearing cells among the GFP-positive cells were calculated and normalized to the level of mock transfection. The data represent the mean +/- S.D. (n=3) ***P<0.01. B. Mdm20-KD cells also reduce the phosphorylation level of Akt and polyQ aggregate formation. Left: The effects of Mdm20-KD on the phosphorylation level of Akt in the presense of various chemical treatment (DMSO, rapamycin (100 nM), Akt-inhibitor-VIII (5 μM) or 3MA (1 mM)). Right: The relative levels of polyQ aggregate formation were evaluated in each of the transfectants and compared with the mock-transfected control. The numbers of polyQ-bearing cells among the GFP-positive cells were calculated and normalized to the level of control transfection. The data represent the mean +/- S.D. (n=3) **P<0.001. ***P<0.01. C. Mdm20-OE cells also increase the phosphorylation level of Akt and polyQ aggregate formation. Left: The effects of Mdm20-OE on the phosphorylation level of Akt in the presense of various chemical treatment same as B. The arrow indicates a correct mCherry-Nat5 band. An asterisk denotes a cross-reacting band. Right: The relative levels of polyQ aggregate formation were evaluated in each of the transfectants and compared with the mock-transfected control. The numbers of polyQ-bearing cells among the GFP-positive cells were calculated and normalized to the level of mock transfection. The data represent the mean +/- S.D. (n=3) **P<0.001. ***P<0.01.
    Figure Legend Snippet: A. A phospho-mimic mutant of Akt (Akt-S473D) increases polyQ aggregate formation. Left: Shown are western blots for Akt and phospho-Akt (at Ser473 and Thr308). HEK293 cells were co-transfected with GFP-polyQ81 and Flag-tagged wild type Akt (F-Akt) or various phospho- and none-phospho-mimic Akt mutants as indicated. Right: The relative levels of polyQ aggregate formation were evaluated in each of the transfectants and compared with the mock-transfected control. Experiments were performed in naïve HEK293 cells (green bars) and Mdm20-KD cells (red bars). The numbers of polyQ-bearing cells among the GFP-positive cells were calculated and normalized to the level of mock transfection. The data represent the mean +/- S.D. (n=3) ***P<0.01. B. Mdm20-KD cells also reduce the phosphorylation level of Akt and polyQ aggregate formation. Left: The effects of Mdm20-KD on the phosphorylation level of Akt in the presense of various chemical treatment (DMSO, rapamycin (100 nM), Akt-inhibitor-VIII (5 μM) or 3MA (1 mM)). Right: The relative levels of polyQ aggregate formation were evaluated in each of the transfectants and compared with the mock-transfected control. The numbers of polyQ-bearing cells among the GFP-positive cells were calculated and normalized to the level of control transfection. The data represent the mean +/- S.D. (n=3) **P<0.001. ***P<0.01. C. Mdm20-OE cells also increase the phosphorylation level of Akt and polyQ aggregate formation. Left: The effects of Mdm20-OE on the phosphorylation level of Akt in the presense of various chemical treatment same as B. The arrow indicates a correct mCherry-Nat5 band. An asterisk denotes a cross-reacting band. Right: The relative levels of polyQ aggregate formation were evaluated in each of the transfectants and compared with the mock-transfected control. The numbers of polyQ-bearing cells among the GFP-positive cells were calculated and normalized to the level of mock transfection. The data represent the mean +/- S.D. (n=3) **P<0.001. ***P<0.01.

    Techniques Used: Mutagenesis, Western Blot, Transfection

    rapamycin  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc rapamycin
    A mTOR signaling was highly activated in CD133- subpopulations when compared with CD133+ compartments. Immunoblotting was performed for CD133, phosphorylated p70 S6 (p-p70 S6), p70 S6, and α-tubulin as a loading control. B, C Enrichment of CD133+ cells in LPC-H and LPC-H12 cells after <t>rapamycin</t> (RAPA) treatment (10 nM) for 3 days. Representative FACS profiles (B); summary bar graphs illustrate percentage of CD133+ cells as means±S.E.M. of the results from three experiments (C). D Stem cell-associated gene expression measured via qPCR in LPC-H12 cells treated with or without rapamycin (10 nM for 24 h). Real-time PCR experiments were conducted in triplicate and with GAPDH for expression normalization. E Immunoblotting for mTOR, p-p70 S6, and p70 S6 confirmed mTOR knockdown by shRNAs. F, G Sustained increases of CD133 expression were observed in LPC-H cells stably expressing shRNAs targeting mTOR. The means±S.E.M. of the percentages of CD133+ cells in LPC-H cells infected with retrovirus expressing mTOR-shRNA (n = 3) are shown in F. The magnitude of the change in percentage of CD133+ cells in LPC-H on days 13, 17 and 20 after infection with mTOR-sh1 and mTOR-sh2 containing retrovirus (means±S.E.M., n = 3) (G).
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    1) Product Images from "Transient mTOR Inhibition Facilitates Continuous Growth of Liver Tumors by Modulating the Maintenance of CD133+ Cell Populations"

    Article Title: Transient mTOR Inhibition Facilitates Continuous Growth of Liver Tumors by Modulating the Maintenance of CD133+ Cell Populations

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0028405

    A mTOR signaling was highly activated in CD133- subpopulations when compared with CD133+ compartments. Immunoblotting was performed for CD133, phosphorylated p70 S6 (p-p70 S6), p70 S6, and α-tubulin as a loading control. B, C Enrichment of CD133+ cells in LPC-H and LPC-H12 cells after rapamycin (RAPA) treatment (10 nM) for 3 days. Representative FACS profiles (B); summary bar graphs illustrate percentage of CD133+ cells as means±S.E.M. of the results from three experiments (C). D Stem cell-associated gene expression measured via qPCR in LPC-H12 cells treated with or without rapamycin (10 nM for 24 h). Real-time PCR experiments were conducted in triplicate and with GAPDH for expression normalization. E Immunoblotting for mTOR, p-p70 S6, and p70 S6 confirmed mTOR knockdown by shRNAs. F, G Sustained increases of CD133 expression were observed in LPC-H cells stably expressing shRNAs targeting mTOR. The means±S.E.M. of the percentages of CD133+ cells in LPC-H cells infected with retrovirus expressing mTOR-shRNA (n = 3) are shown in F. The magnitude of the change in percentage of CD133+ cells in LPC-H on days 13, 17 and 20 after infection with mTOR-sh1 and mTOR-sh2 containing retrovirus (means±S.E.M., n = 3) (G).
    Figure Legend Snippet: A mTOR signaling was highly activated in CD133- subpopulations when compared with CD133+ compartments. Immunoblotting was performed for CD133, phosphorylated p70 S6 (p-p70 S6), p70 S6, and α-tubulin as a loading control. B, C Enrichment of CD133+ cells in LPC-H and LPC-H12 cells after rapamycin (RAPA) treatment (10 nM) for 3 days. Representative FACS profiles (B); summary bar graphs illustrate percentage of CD133+ cells as means±S.E.M. of the results from three experiments (C). D Stem cell-associated gene expression measured via qPCR in LPC-H12 cells treated with or without rapamycin (10 nM for 24 h). Real-time PCR experiments were conducted in triplicate and with GAPDH for expression normalization. E Immunoblotting for mTOR, p-p70 S6, and p70 S6 confirmed mTOR knockdown by shRNAs. F, G Sustained increases of CD133 expression were observed in LPC-H cells stably expressing shRNAs targeting mTOR. The means±S.E.M. of the percentages of CD133+ cells in LPC-H cells infected with retrovirus expressing mTOR-shRNA (n = 3) are shown in F. The magnitude of the change in percentage of CD133+ cells in LPC-H on days 13, 17 and 20 after infection with mTOR-sh1 and mTOR-sh2 containing retrovirus (means±S.E.M., n = 3) (G).

    Techniques Used: Western Blot, Expressing, Real-time Polymerase Chain Reaction, Stable Transfection, Infection, shRNA

    A, B Enhanced CD133+ subpopulations in Huh7 cells with treatment of rapamycin (100 nM) for 5 days. Representative FACS profiles (A); Percentages of CD133+ cells are presented as means±S.E.M. (n = 3) (B). C, D qPCR analysis shows enrichment of CD133 expression in human liver tumor cell lines after exposed to rapamycin (100 nM). Relative expression of CD133 in Hep3B, Huh7, and PLC/PRF/5 with or without treatment of rapamycin for 48 h is shown in C. Sustained increase of CD133 expression in Huh7 after treatment of rapamycin with 10 nM or 100 nM is illustrated in D. The sustained GAPDH was used as an internal control. E qPCR ananlysis was performed for stem cell-associated genes in multiple human liver tumor cell lines. Cells without treatment of rapamycin (100 nM) were defined as 1, and the relative expression of each gene in cells with treatment of rapamycin for 48 h was expressed as the fold difference over this baseline. GAPDH was used as an internal control.
    Figure Legend Snippet: A, B Enhanced CD133+ subpopulations in Huh7 cells with treatment of rapamycin (100 nM) for 5 days. Representative FACS profiles (A); Percentages of CD133+ cells are presented as means±S.E.M. (n = 3) (B). C, D qPCR analysis shows enrichment of CD133 expression in human liver tumor cell lines after exposed to rapamycin (100 nM). Relative expression of CD133 in Hep3B, Huh7, and PLC/PRF/5 with or without treatment of rapamycin for 48 h is shown in C. Sustained increase of CD133 expression in Huh7 after treatment of rapamycin with 10 nM or 100 nM is illustrated in D. The sustained GAPDH was used as an internal control. E qPCR ananlysis was performed for stem cell-associated genes in multiple human liver tumor cell lines. Cells without treatment of rapamycin (100 nM) were defined as 1, and the relative expression of each gene in cells with treatment of rapamycin for 48 h was expressed as the fold difference over this baseline. GAPDH was used as an internal control.

    Techniques Used: Expressing

    A – C De novo generation of CD133+ cells after long-term single-cell culture of CD133- LPC-H12 cells. Single CD133- LPC-H12 cells were deposited by FACS into each well of 96-well plates with or without rapamycin (10 nM). After expansion, the single-cell derived LPC-H12 cells were analyzed by FACS. Schematic diagram shows FACS isolation and robotic plating of single CD133- cells into 96-well plates (A). Phase image of a single cell in one well after sorting (bottom). Bar = 10 µm. The percentages of the colonies containing CD133+ cells are shown in B (n = 10 per group). The proportions of CD133+ cells in each colony are shown in C. D-G Knockdown of mTOR expression enhanced the rate of conversion of CD133- to CD133+ cells. The percentages of CD133+ colonies derived from single CD133- LPC-H12 cells infected with retrovirus containing mTOR-sh2 and control, respectively, are shown in D (n = 12 per group). The proportions of CD133+ cells in each colony are shown in E. The expression of CD133 mRNA in each clone examined by Real-time PCR experiments in triplicate, and all samples were normalized to GAPDH expression (F). The result of RT-PCR is shown in G.
    Figure Legend Snippet: A – C De novo generation of CD133+ cells after long-term single-cell culture of CD133- LPC-H12 cells. Single CD133- LPC-H12 cells were deposited by FACS into each well of 96-well plates with or without rapamycin (10 nM). After expansion, the single-cell derived LPC-H12 cells were analyzed by FACS. Schematic diagram shows FACS isolation and robotic plating of single CD133- cells into 96-well plates (A). Phase image of a single cell in one well after sorting (bottom). Bar = 10 µm. The percentages of the colonies containing CD133+ cells are shown in B (n = 10 per group). The proportions of CD133+ cells in each colony are shown in C. D-G Knockdown of mTOR expression enhanced the rate of conversion of CD133- to CD133+ cells. The percentages of CD133+ colonies derived from single CD133- LPC-H12 cells infected with retrovirus containing mTOR-sh2 and control, respectively, are shown in D (n = 12 per group). The proportions of CD133+ cells in each colony are shown in E. The expression of CD133 mRNA in each clone examined by Real-time PCR experiments in triplicate, and all samples were normalized to GAPDH expression (F). The result of RT-PCR is shown in G.

    Techniques Used: Cell Culture, Derivative Assay, Isolation, Expressing, Infection, Real-time Polymerase Chain Reaction, Reverse Transcription Polymerase Chain Reaction

    A, B Inhibition of mTOR signaling by rapamycin severely blocked the rapid decrease of the CD133+ subsets over time in sorted CD133+ LPC-H12 cells. Representative FACS profiles of LPC-H12 cells are shown in A. Changes of CD133 expression in LPC-H12 cells at days 3, 7, and 10 after cell sorting are shown in B. Data shown are the means±S.E.M. of the results of three experiments. C Single-cell culture for analysis of the effect of rapamycin on the maintenance of the CD133+ subpopulations. The single CD133+ cell-derived colonies cultured in the media with rapamycin had more CD133+ cells than those in rapamycin-free media. Single CD133+ LPC-H12 cells were sorted into 96-well plates and cultured with or without rapamycin (10 nM). Each symbol represents an individual single-cell-derived colony; small horizontal lines indicate the means (n = 8). D The percentage of CD133+ cells in each colony derived from single CD133+ LPC-H12 stably expressing mTOR-sh2 was higher than that from single CD133+ LPC-H12 infected with control retrovirus. Data are shown as the means±SD (n = 8).
    Figure Legend Snippet: A, B Inhibition of mTOR signaling by rapamycin severely blocked the rapid decrease of the CD133+ subsets over time in sorted CD133+ LPC-H12 cells. Representative FACS profiles of LPC-H12 cells are shown in A. Changes of CD133 expression in LPC-H12 cells at days 3, 7, and 10 after cell sorting are shown in B. Data shown are the means±S.E.M. of the results of three experiments. C Single-cell culture for analysis of the effect of rapamycin on the maintenance of the CD133+ subpopulations. The single CD133+ cell-derived colonies cultured in the media with rapamycin had more CD133+ cells than those in rapamycin-free media. Single CD133+ LPC-H12 cells were sorted into 96-well plates and cultured with or without rapamycin (10 nM). Each symbol represents an individual single-cell-derived colony; small horizontal lines indicate the means (n = 8). D The percentage of CD133+ cells in each colony derived from single CD133+ LPC-H12 stably expressing mTOR-sh2 was higher than that from single CD133+ LPC-H12 infected with control retrovirus. Data are shown as the means±SD (n = 8).

    Techniques Used: Inhibition, Expressing, FACS, Cell Culture, Derivative Assay, Stable Transfection, Infection

    A The percentage of CD133+ cells in GFP+ cells harvested from xenograft tumors with mTOR-sh2 expression was higher than that from control ones. LPC-H cells with GFP infected with control or mTOR-sh2 retroviral vector were subcutaneously implanted into nude BALB/c mice (n = 3 per group). The animals were euthanized on day 24. The percentage of CD133+ cells in GFP+ tumor cells with expression of mTOR shRNA and control shRNA are shown as the means±SD (n = 3). B There was no significant effect of knockdown mTOR on tumor growth of LPC-H cells in vivo. Differences in tumor size in mm 3 between control and mTOR-knockdown groups are reported as means±SD. C The xenografts of LPC-H cells contained a high proportion of CD133+ cells in the mice after rapamycin treatment for 10 days. FACS analysis profile (left). Percentages of CD133+ cells in LPC-H cells in vivo are presented as means±SD (n = 5) (right).
    Figure Legend Snippet: A The percentage of CD133+ cells in GFP+ cells harvested from xenograft tumors with mTOR-sh2 expression was higher than that from control ones. LPC-H cells with GFP infected with control or mTOR-sh2 retroviral vector were subcutaneously implanted into nude BALB/c mice (n = 3 per group). The animals were euthanized on day 24. The percentage of CD133+ cells in GFP+ tumor cells with expression of mTOR shRNA and control shRNA are shown as the means±SD (n = 3). B There was no significant effect of knockdown mTOR on tumor growth of LPC-H cells in vivo. Differences in tumor size in mm 3 between control and mTOR-knockdown groups are reported as means±SD. C The xenografts of LPC-H cells contained a high proportion of CD133+ cells in the mice after rapamycin treatment for 10 days. FACS analysis profile (left). Percentages of CD133+ cells in LPC-H cells in vivo are presented as means±SD (n = 5) (right).

    Techniques Used: Expressing, Infection, Plasmid Preparation, shRNA, In Vivo

    A Serial xenograft strategy. LPC-H cells were subcutaneously injected into nude BALB/c mice (n = 5 per group). After 3 weeks of tumor growth, the animals were treated with rapamycin (1.5 mg/kg/day) or diluents for 10 days, and then euthanized. Tumor cells were dissociated, and GFP+ tumor cells were then implanted into secondary recipients. B, C Subcutaneous tumors grew more slowly in nude BALB/c mice after treatment with rapamycin than did tumors without rapamycin treatment. Original magnification (B) and growth curve of xenograft tumors in nude mice (C). D Continuous tumorigenesis of LPC-H cells with exposure to rapamycin in vivo was more efficient than that without rapamycin treatment. The tumor cells from nude BALB/c mice with or without treatment with rapamycin (1.5 mg/kg/day) for 10 days were secondarily implanted into the right or left flanks of the mice, respectively. Arrows indicate tumor formation (2.5×10 3 GFP+ tumor cells implanted). E The secondary tumor-initiating ability of LPC-H cells treated with or without rapamycin in the nude BALB/c xenograft transplant model. Tumor initiation was monitored for 4 wk after implantation.
    Figure Legend Snippet: A Serial xenograft strategy. LPC-H cells were subcutaneously injected into nude BALB/c mice (n = 5 per group). After 3 weeks of tumor growth, the animals were treated with rapamycin (1.5 mg/kg/day) or diluents for 10 days, and then euthanized. Tumor cells were dissociated, and GFP+ tumor cells were then implanted into secondary recipients. B, C Subcutaneous tumors grew more slowly in nude BALB/c mice after treatment with rapamycin than did tumors without rapamycin treatment. Original magnification (B) and growth curve of xenograft tumors in nude mice (C). D Continuous tumorigenesis of LPC-H cells with exposure to rapamycin in vivo was more efficient than that without rapamycin treatment. The tumor cells from nude BALB/c mice with or without treatment with rapamycin (1.5 mg/kg/day) for 10 days were secondarily implanted into the right or left flanks of the mice, respectively. Arrows indicate tumor formation (2.5×10 3 GFP+ tumor cells implanted). E The secondary tumor-initiating ability of LPC-H cells treated with or without rapamycin in the nude BALB/c xenograft transplant model. Tumor initiation was monitored for 4 wk after implantation.

    Techniques Used: Injection, In Vivo

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    NGF treatment reverses impairment of angiogenesis in aging GECs through PI3 kinase/Akt and <t>mTOR</t> pathways. ( A ) NGF treatment dose-dependently increases in vitro angiogenesis in aging GECs. Aging GECs were treated with either PBS (control) or exogenous NGF (10, 50, 100, or 1000 ng/mL) and in vitro angiogenesis on Matrigel was examined. Data are means ± SD (N = 6). Treatment of aging GECs with NGF dose-dependently increased angiogenesis with the maximal threshold stimulating dose of 100 ng/mL at 6 hours ( P < .001). There was no significant difference in angiogenesis between cells treated with NGF 100 ng/mL and 1000 ng/mL. † P > .05 (NS). ( B ) In vitro angiogenesis on Matrigel at 6 hours in aging GECs treated with PBS or recombinant rat NGF (100 ng/mL) with or without pretreatment with specific PI3 kinase inhibitor (LY294002; 50 μmol/L for 30 minutes), or mTOR inhibitor <t>(rapamycin;</t> 10 nmol/L for 60 minutes). Short-term (6 hours) treatment with exogenous NGF significantly increased in vitro angiogenesis and in aging GECs by 1.5-fold and pretreatment with LY294002, and rapamycin abolished the NGF-induced increase in angiogenesis. Data are means ± SD (N = 6). ( C ) Representative Western blots for phosphorylated Akt (pAkt) and Akt expression in aging GECs treated with exogenous NGF (0.1 μg/mL) for 4 and 24 hours. Treatment of aging GECs with exogenous NGF significantly increased Akt phosphorylation at 4 and 24 hours. Data are means ± SD (N = 3). The Student t test and 1-way analysis of variance with the Tukey multiple comparison test were used to determine statistical significance between 2 or multiple groups, respectively.
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    Curcumin enhanced <t>the</t> <t>SIRT1-AMPK/mTOR</t> signal pathway. (a) Representative western blot for SIRT1 p-AMPK and p-mTOR levels in cardiomyocyte lysates ( n = 5). (b) Quantitation results of p-mTOR. (c) Quantitation results of SIRT1. (d). Quantitation results of p-AMPK. ∗∗ P < 0.01 vs. control. # P < 0.05, # # P < 0.01, vs. D-gal. The data are expressed as the mean ± SEM.
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    NGF treatment reverses impairment of angiogenesis in aging GECs through PI3 kinase/Akt and mTOR pathways. ( A ) NGF treatment dose-dependently increases in vitro angiogenesis in aging GECs. Aging GECs were treated with either PBS (control) or exogenous NGF (10, 50, 100, or 1000 ng/mL) and in vitro angiogenesis on Matrigel was examined. Data are means ± SD (N = 6). Treatment of aging GECs with NGF dose-dependently increased angiogenesis with the maximal threshold stimulating dose of 100 ng/mL at 6 hours ( P < .001). There was no significant difference in angiogenesis between cells treated with NGF 100 ng/mL and 1000 ng/mL. † P > .05 (NS). ( B ) In vitro angiogenesis on Matrigel at 6 hours in aging GECs treated with PBS or recombinant rat NGF (100 ng/mL) with or without pretreatment with specific PI3 kinase inhibitor (LY294002; 50 μmol/L for 30 minutes), or mTOR inhibitor (rapamycin; 10 nmol/L for 60 minutes). Short-term (6 hours) treatment with exogenous NGF significantly increased in vitro angiogenesis and in aging GECs by 1.5-fold and pretreatment with LY294002, and rapamycin abolished the NGF-induced increase in angiogenesis. Data are means ± SD (N = 6). ( C ) Representative Western blots for phosphorylated Akt (pAkt) and Akt expression in aging GECs treated with exogenous NGF (0.1 μg/mL) for 4 and 24 hours. Treatment of aging GECs with exogenous NGF significantly increased Akt phosphorylation at 4 and 24 hours. Data are means ± SD (N = 3). The Student t test and 1-way analysis of variance with the Tukey multiple comparison test were used to determine statistical significance between 2 or multiple groups, respectively.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Reduced NGF in Gastric Endothelial Cells Is One of the Main Causes of Impaired Angiogenesis in Aging Gastric Mucosa

    doi: 10.1016/j.jcmgh.2018.05.003

    Figure Lengend Snippet: NGF treatment reverses impairment of angiogenesis in aging GECs through PI3 kinase/Akt and mTOR pathways. ( A ) NGF treatment dose-dependently increases in vitro angiogenesis in aging GECs. Aging GECs were treated with either PBS (control) or exogenous NGF (10, 50, 100, or 1000 ng/mL) and in vitro angiogenesis on Matrigel was examined. Data are means ± SD (N = 6). Treatment of aging GECs with NGF dose-dependently increased angiogenesis with the maximal threshold stimulating dose of 100 ng/mL at 6 hours ( P < .001). There was no significant difference in angiogenesis between cells treated with NGF 100 ng/mL and 1000 ng/mL. † P > .05 (NS). ( B ) In vitro angiogenesis on Matrigel at 6 hours in aging GECs treated with PBS or recombinant rat NGF (100 ng/mL) with or without pretreatment with specific PI3 kinase inhibitor (LY294002; 50 μmol/L for 30 minutes), or mTOR inhibitor (rapamycin; 10 nmol/L for 60 minutes). Short-term (6 hours) treatment with exogenous NGF significantly increased in vitro angiogenesis and in aging GECs by 1.5-fold and pretreatment with LY294002, and rapamycin abolished the NGF-induced increase in angiogenesis. Data are means ± SD (N = 6). ( C ) Representative Western blots for phosphorylated Akt (pAkt) and Akt expression in aging GECs treated with exogenous NGF (0.1 μg/mL) for 4 and 24 hours. Treatment of aging GECs with exogenous NGF significantly increased Akt phosphorylation at 4 and 24 hours. Data are means ± SD (N = 3). The Student t test and 1-way analysis of variance with the Tukey multiple comparison test were used to determine statistical significance between 2 or multiple groups, respectively.

    Article Snippet: For some studies, GECs were treated with the specific PI3 kinase inhibitor 50 μmol/L for 30 minutes; Cell Signaling Technology, Danvers, MA), the mTOR inhibitor rapamycin (10 nmol/L for 60 minutes; Cell Signaling Technology), Latrunculin B (0.5 μmol/L for 30 minutes; Invitrogen, Carlsbad, CA; inhibitor of actin polymerization), or recombinant rat NGF (10–1000 ng/mL; R&D Systems, Minneapolis, MN).

    Techniques: In Vitro, Recombinant, Western Blot, Expressing

    Curcumin enhanced the SIRT1-AMPK/mTOR signal pathway. (a) Representative western blot for SIRT1 p-AMPK and p-mTOR levels in cardiomyocyte lysates ( n = 5). (b) Quantitation results of p-mTOR. (c) Quantitation results of SIRT1. (d). Quantitation results of p-AMPK. ∗∗ P < 0.01 vs. control. # P < 0.05, # # P < 0.01, vs. D-gal. The data are expressed as the mean ± SEM.

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Curcumin Alleviates D-Galactose-Induced Cardiomyocyte Senescence by Promoting Autophagy via the SIRT1/AMPK/mTOR Pathway

    doi: 10.1155/2022/2990843

    Figure Lengend Snippet: Curcumin enhanced the SIRT1-AMPK/mTOR signal pathway. (a) Representative western blot for SIRT1 p-AMPK and p-mTOR levels in cardiomyocyte lysates ( n = 5). (b) Quantitation results of p-mTOR. (c) Quantitation results of SIRT1. (d). Quantitation results of p-AMPK. ∗∗ P < 0.01 vs. control. # P < 0.05, # # P < 0.01, vs. D-gal. The data are expressed as the mean ± SEM.

    Article Snippet: The membranes were washed three times with TBST and incubated with a secondary antibody labeled with horseradish peroxidase (1 : 5000; Abclonal, China) at room temperature for 1 h. The primary rabbit antibodies included mTOR (1 : 1000; Cell Signaling Technology, USA), phospho-mTOR (1 : 1000; Cell Signaling Technology, USA), AMPK (1 : 1000; Cell Signaling Technology, USA), phospho-AMPK (1 : 1000; Cell Signaling Technology, USA), SIRT1 (1 : 1000; Cell Signaling Technology, USA), P53 (1 : 500; Abclonal, China, A19585), P16 (1 : 2000; Abcam, USA), LC3I/II (1 : 2000; Abcam, USA), P62 (1 : 1000; Cell Signaling Technology, USA), and GAPDH (1 : 1000; Cell Signaling Technology, USA).

    Techniques: Western Blot, Quantitation Assay

    (a) Representative western blot of the levels of SIRT1 p-AMPK and p-mTOR. siSIRT1-mediated knockdown blocked the inducing effect of curcumin on the SIRT1/AMPK/mTOR pathway in cardiac aging ( n = 5). (b) The quantitation results of SIRT1. (c) The quantitation results of p-AMPK. (d) The quantitation results of p-mTOR. # P < 0.05, # # P < 0.01, vs. control. The data are expressed as the mean ± SEM.

    Journal: Evidence-based Complementary and Alternative Medicine : eCAM

    Article Title: Curcumin Alleviates D-Galactose-Induced Cardiomyocyte Senescence by Promoting Autophagy via the SIRT1/AMPK/mTOR Pathway

    doi: 10.1155/2022/2990843

    Figure Lengend Snippet: (a) Representative western blot of the levels of SIRT1 p-AMPK and p-mTOR. siSIRT1-mediated knockdown blocked the inducing effect of curcumin on the SIRT1/AMPK/mTOR pathway in cardiac aging ( n = 5). (b) The quantitation results of SIRT1. (c) The quantitation results of p-AMPK. (d) The quantitation results of p-mTOR. # P < 0.05, # # P < 0.01, vs. control. The data are expressed as the mean ± SEM.

    Article Snippet: The membranes were washed three times with TBST and incubated with a secondary antibody labeled with horseradish peroxidase (1 : 5000; Abclonal, China) at room temperature for 1 h. The primary rabbit antibodies included mTOR (1 : 1000; Cell Signaling Technology, USA), phospho-mTOR (1 : 1000; Cell Signaling Technology, USA), AMPK (1 : 1000; Cell Signaling Technology, USA), phospho-AMPK (1 : 1000; Cell Signaling Technology, USA), SIRT1 (1 : 1000; Cell Signaling Technology, USA), P53 (1 : 500; Abclonal, China, A19585), P16 (1 : 2000; Abcam, USA), LC3I/II (1 : 2000; Abcam, USA), P62 (1 : 1000; Cell Signaling Technology, USA), and GAPDH (1 : 1000; Cell Signaling Technology, USA).

    Techniques: Western Blot, Quantitation Assay

    List of antibodies used for western blot analyses.

    Journal: Neural Plasticity

    Article Title: Growth Hormone Increases BDNF and mTOR Expression in Specific Brain Regions after Photothrombotic Stroke in Mice

    doi: 10.1155/2022/9983042

    Figure Lengend Snippet: List of antibodies used for western blot analyses.

    Article Snippet: T-mTOR , Cell Signalling, monoclonal mouse anti-total- mTOR, #4517 , 1 : 1000.

    Techniques: Western Blot

    t -test and Pearson's results summary table.

    Journal: Neural Plasticity

    Article Title: Growth Hormone Increases BDNF and mTOR Expression in Specific Brain Regions after Photothrombotic Stroke in Mice

    doi: 10.1155/2022/9983042

    Figure Lengend Snippet: t -test and Pearson's results summary table.

    Article Snippet: T-mTOR , Cell Signalling, monoclonal mouse anti-total- mTOR, #4517 , 1 : 1000.

    Techniques:

    The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the peri-infarct region. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70S6-kinase P-p70S6K), and total-p70S6k (T-p70S6K). (b) T-mTOR and T-p70S6K levels were normalized to β -actin. P-mTOR and P-p70S6K levels were normalized to T-mTOR and T-p70S6K, respectively. Levels were expressed as a fold change (FC) of mean ± SD for each group relative to the mean of the Sham+Saline group (dotted line). We found a significant increase in T-mTOR protein expression within the peri-infarct region in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗ p < 0.05, 2-tailed t -test.

    Journal: Neural Plasticity

    Article Title: Growth Hormone Increases BDNF and mTOR Expression in Specific Brain Regions after Photothrombotic Stroke in Mice

    doi: 10.1155/2022/9983042

    Figure Lengend Snippet: The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the peri-infarct region. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70S6-kinase P-p70S6K), and total-p70S6k (T-p70S6K). (b) T-mTOR and T-p70S6K levels were normalized to β -actin. P-mTOR and P-p70S6K levels were normalized to T-mTOR and T-p70S6K, respectively. Levels were expressed as a fold change (FC) of mean ± SD for each group relative to the mean of the Sham+Saline group (dotted line). We found a significant increase in T-mTOR protein expression within the peri-infarct region in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗ p < 0.05, 2-tailed t -test.

    Article Snippet: T-mTOR , Cell Signalling, monoclonal mouse anti-total- mTOR, #4517 , 1 : 1000.

    Techniques: Recombinant, Expressing

    The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the hippocampus. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70s6-kinase (P-p70S6K), and total-p70s6k (T-p70S6K). (b) Data are presented as in . We found a significant increase in T-p70S6K protein expression within the hippocampus in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗ p < 0.05, 2-tailed t -test.

    Journal: Neural Plasticity

    Article Title: Growth Hormone Increases BDNF and mTOR Expression in Specific Brain Regions after Photothrombotic Stroke in Mice

    doi: 10.1155/2022/9983042

    Figure Lengend Snippet: The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the hippocampus. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70s6-kinase (P-p70S6K), and total-p70s6k (T-p70S6K). (b) Data are presented as in . We found a significant increase in T-p70S6K protein expression within the hippocampus in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗ p < 0.05, 2-tailed t -test.

    Article Snippet: T-mTOR , Cell Signalling, monoclonal mouse anti-total- mTOR, #4517 , 1 : 1000.

    Techniques: Recombinant, Expressing

    The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the thalamus. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70S6-kinase (P-p70S6K), and total-p70S6K (T-p70S6K). (b) Data are presented as in . We found a significant increase in T-mTOR protein expression within the thalamus in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗∗ p < 0.01, 2-tailed t -test.

    Journal: Neural Plasticity

    Article Title: Growth Hormone Increases BDNF and mTOR Expression in Specific Brain Regions after Photothrombotic Stroke in Mice

    doi: 10.1155/2022/9983042

    Figure Lengend Snippet: The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the thalamus. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70S6-kinase (P-p70S6K), and total-p70S6K (T-p70S6K). (b) Data are presented as in . We found a significant increase in T-mTOR protein expression within the thalamus in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗∗ p < 0.01, 2-tailed t -test.

    Article Snippet: T-mTOR , Cell Signalling, monoclonal mouse anti-total- mTOR, #4517 , 1 : 1000.

    Techniques: Recombinant, Expressing

    Correlation of uncleaved immature form of BDNF (pro-BDNF) with mammalian target of rapamycin (mTOR) and markers of neuroplasticity. Correlation of pro-BDNF, with T-mTOR (top panel), α -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-receptor subunit GluR1 (marker of synaptic plasticity, second from top panel), NeuN (neuronal marker, third from top panel), and doublecortin (DCX, neuronal migration marker, bottom panel) in the peri-infarct region (a), hippocampus (b), and thalamus (c). Dataset GluR1, NeuN, and DCX was an excerpt from previous study [ , ]. Correlations contain all three experimental groups, Sham+Saline (black crosses), Stroke+Saline (red circles), and Stroke+r-hGH (blue squares) and analyzed using Pearson's correlation. Pearson's r and associated p values for each correlation are reported on the corresponding graph.

    Journal: Neural Plasticity

    Article Title: Growth Hormone Increases BDNF and mTOR Expression in Specific Brain Regions after Photothrombotic Stroke in Mice

    doi: 10.1155/2022/9983042

    Figure Lengend Snippet: Correlation of uncleaved immature form of BDNF (pro-BDNF) with mammalian target of rapamycin (mTOR) and markers of neuroplasticity. Correlation of pro-BDNF, with T-mTOR (top panel), α -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-receptor subunit GluR1 (marker of synaptic plasticity, second from top panel), NeuN (neuronal marker, third from top panel), and doublecortin (DCX, neuronal migration marker, bottom panel) in the peri-infarct region (a), hippocampus (b), and thalamus (c). Dataset GluR1, NeuN, and DCX was an excerpt from previous study [ , ]. Correlations contain all three experimental groups, Sham+Saline (black crosses), Stroke+Saline (red circles), and Stroke+r-hGH (blue squares) and analyzed using Pearson's correlation. Pearson's r and associated p values for each correlation are reported on the corresponding graph.

    Article Snippet: T-mTOR , Cell Signalling, monoclonal mouse anti-total- mTOR, #4517 , 1 : 1000.

    Techniques: Marker, Migration

    List of antibodies used for western blot analyses.

    Journal: Neural Plasticity

    Article Title: Growth Hormone Increases BDNF and mTOR Expression in Specific Brain Regions after Photothrombotic Stroke in Mice

    doi: 10.1155/2022/9983042

    Figure Lengend Snippet: List of antibodies used for western blot analyses.

    Article Snippet: P-mTOR , Cell Signalling, monoclonal rabbit anti-phospho-mTOR (Ser2448), #5536 , 1 : 500.

    Techniques: Western Blot

    t -test and Pearson's results summary table.

    Journal: Neural Plasticity

    Article Title: Growth Hormone Increases BDNF and mTOR Expression in Specific Brain Regions after Photothrombotic Stroke in Mice

    doi: 10.1155/2022/9983042

    Figure Lengend Snippet: t -test and Pearson's results summary table.

    Article Snippet: P-mTOR , Cell Signalling, monoclonal rabbit anti-phospho-mTOR (Ser2448), #5536 , 1 : 500.

    Techniques:

    The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the peri-infarct region. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70S6-kinase P-p70S6K), and total-p70S6k (T-p70S6K). (b) T-mTOR and T-p70S6K levels were normalized to β -actin. P-mTOR and P-p70S6K levels were normalized to T-mTOR and T-p70S6K, respectively. Levels were expressed as a fold change (FC) of mean ± SD for each group relative to the mean of the Sham+Saline group (dotted line). We found a significant increase in T-mTOR protein expression within the peri-infarct region in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗ p < 0.05, 2-tailed t -test.

    Journal: Neural Plasticity

    Article Title: Growth Hormone Increases BDNF and mTOR Expression in Specific Brain Regions after Photothrombotic Stroke in Mice

    doi: 10.1155/2022/9983042

    Figure Lengend Snippet: The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the peri-infarct region. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70S6-kinase P-p70S6K), and total-p70S6k (T-p70S6K). (b) T-mTOR and T-p70S6K levels were normalized to β -actin. P-mTOR and P-p70S6K levels were normalized to T-mTOR and T-p70S6K, respectively. Levels were expressed as a fold change (FC) of mean ± SD for each group relative to the mean of the Sham+Saline group (dotted line). We found a significant increase in T-mTOR protein expression within the peri-infarct region in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗ p < 0.05, 2-tailed t -test.

    Article Snippet: P-mTOR , Cell Signalling, monoclonal rabbit anti-phospho-mTOR (Ser2448), #5536 , 1 : 500.

    Techniques: Recombinant, Expressing

    The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the hippocampus. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70s6-kinase (P-p70S6K), and total-p70s6k (T-p70S6K). (b) Data are presented as in . We found a significant increase in T-p70S6K protein expression within the hippocampus in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗ p < 0.05, 2-tailed t -test.

    Journal: Neural Plasticity

    Article Title: Growth Hormone Increases BDNF and mTOR Expression in Specific Brain Regions after Photothrombotic Stroke in Mice

    doi: 10.1155/2022/9983042

    Figure Lengend Snippet: The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the hippocampus. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70s6-kinase (P-p70S6K), and total-p70s6k (T-p70S6K). (b) Data are presented as in . We found a significant increase in T-p70S6K protein expression within the hippocampus in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗ p < 0.05, 2-tailed t -test.

    Article Snippet: P-mTOR , Cell Signalling, monoclonal rabbit anti-phospho-mTOR (Ser2448), #5536 , 1 : 500.

    Techniques: Recombinant, Expressing

    The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the thalamus. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70S6-kinase (P-p70S6K), and total-p70S6K (T-p70S6K). (b) Data are presented as in . We found a significant increase in T-mTOR protein expression within the thalamus in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗∗ p < 0.01, 2-tailed t -test.

    Journal: Neural Plasticity

    Article Title: Growth Hormone Increases BDNF and mTOR Expression in Specific Brain Regions after Photothrombotic Stroke in Mice

    doi: 10.1155/2022/9983042

    Figure Lengend Snippet: The effect of recombinant human growth factor (r-hGH) treatment poststroke on mammalian target of rapamycin (mTOR) in the thalamus. (a) Representative blots of phosphorylated-mTOR (P-mTOR, active form), total-mTOR (T-mTOR), phosphorylated-p70S6-kinase (P-p70S6K), and total-p70S6K (T-p70S6K). (b) Data are presented as in . We found a significant increase in T-mTOR protein expression within the thalamus in stroked mice treated with r-hGH (blue squares) compared with saline (red circles). ∗∗ p < 0.01, 2-tailed t -test.

    Article Snippet: P-mTOR , Cell Signalling, monoclonal rabbit anti-phospho-mTOR (Ser2448), #5536 , 1 : 500.

    Techniques: Recombinant, Expressing