p 4e bp  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p 4e bp
    P 4e Bp, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    p 4e bp  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p 4e bp
    P 4e Bp, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    p 4ebp1 t37 46  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p 4ebp1 t37 46
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    anti p 4e bp1 37 42  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti p 4e bp1 37 42
    Anti P 4e Bp1 37 42, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    anti p 4e bp1  (Cell Signaling Technology Inc)


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    p 4e bp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p 4e bp1
    Sestrin2 overexpression inhibits TM-induced mTOR pathway activation. (a) Representative western-blot results of major proteins associated with mTOR pathway. (b) Statistical analysis of p-mTOR, mTOR and their ratio (unpaired two-tailed t -test; all P values >0.05). (c) Statistical results of p-P70S6K, P70S6K and their ratio (unpaired two-tailed t -test; for p-p70s6k/p70s6k: t (4) = 3.30, P =0.030). (d) Quantitative results <t>of</t> <t>p-4E-BP1,</t> 4E-BP1 and their ratio (unpaired two-tailed t -test; for 4E-BP1: t (4) = 3.62, P =0.022). ∗ P < 0.05.
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    1) Product Images from "Sestrin2 Overexpression Ameliorates Endoplasmic Reticulum Stress-Induced Apoptosis via Inhibiting mTOR Pathway in HepG2 Cells"

    Article Title: Sestrin2 Overexpression Ameliorates Endoplasmic Reticulum Stress-Induced Apoptosis via Inhibiting mTOR Pathway in HepG2 Cells

    Journal: International Journal of Endocrinology

    doi: 10.1155/2022/2009753

    Sestrin2 overexpression inhibits TM-induced mTOR pathway activation. (a) Representative western-blot results of major proteins associated with mTOR pathway. (b) Statistical analysis of p-mTOR, mTOR and their ratio (unpaired two-tailed t -test; all P values >0.05). (c) Statistical results of p-P70S6K, P70S6K and their ratio (unpaired two-tailed t -test; for p-p70s6k/p70s6k: t (4) = 3.30, P =0.030). (d) Quantitative results of p-4E-BP1, 4E-BP1 and their ratio (unpaired two-tailed t -test; for 4E-BP1: t (4) = 3.62, P =0.022). ∗ P < 0.05.
    Figure Legend Snippet: Sestrin2 overexpression inhibits TM-induced mTOR pathway activation. (a) Representative western-blot results of major proteins associated with mTOR pathway. (b) Statistical analysis of p-mTOR, mTOR and their ratio (unpaired two-tailed t -test; all P values >0.05). (c) Statistical results of p-P70S6K, P70S6K and their ratio (unpaired two-tailed t -test; for p-p70s6k/p70s6k: t (4) = 3.30, P =0.030). (d) Quantitative results of p-4E-BP1, 4E-BP1 and their ratio (unpaired two-tailed t -test; for 4E-BP1: t (4) = 3.62, P =0.022). ∗ P < 0.05.

    Techniques Used: Over Expression, Activation Assay, Western Blot, Two Tailed Test

    anti p 4ebp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc anti p 4ebp1
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    p 4ebp1 t37 46  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p 4ebp1 t37 46
    Seven-week-old Glul fl/fl Alb-Cre – (WT) and Glul fl/fl Alb-Cre + (KO) male mice were injected with vehicle or c-Met/ΔN90-β-catenin/SB10 plasmids, and livers were harvested 2 weeks later. ( A ) RNA-seq was performed, and the summary of significantly changed pathways identified by GSEA ( n = 4). NES, normalized enrichment score. ( B ) GSEA enrichment plots of mTORC1-mediated signaling (left panel) and ribosome biogenesis (right panel) that are positively enriched in KO livers ( n = 4). ( C ) Heatmap of the relative expression of the indicated genes related to the mTORC1-mediated signaling pathway ( n = 3–4). ( D ) Liver lysates were probed for the indicated proteins ( n = 3). Lowercase “t” indicates that the total protein was probed. ( E ) IHC was performed ( n = 3 mice for each group). The number of positive cells was quantified by ImageJ from 3–4 randomly selected fields. **** P < 0.0001 (2-tailed t test). ( F ) FFPE liver sections were costained for GS (green) and p-S6 S235/236 (red), <t>p-4EBP1</t> <t>T37/46</t> (red), or p-mTOR S2448 (red) ( n = 3). The portal vein (PV) and hepatic vein (HV) were judged by GS expression in healthy WT livers. ( G ) Fluorescence images in F were subjected to colocalization analyses using the Coloc2 plugin in ImageJ. The pixel intensity correlation of channels 1 and 2 over space is depicted as a 2D scatterplot. Scale bars: 100 μm ( E and F ). Kendall’s Tau-b correlation analysis was used to test the significance of correlation and was judged positively correlated when greater than 0.5.
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    1) Product Images from "Glutamine synthetase limits β-catenin–mutated liver cancer growth by maintaining nitrogen homeostasis and suppressing mTORC1"

    Article Title: Glutamine synthetase limits β-catenin–mutated liver cancer growth by maintaining nitrogen homeostasis and suppressing mTORC1

    Journal: The Journal of Clinical Investigation

    doi: 10.1172/JCI161408

    Seven-week-old Glul fl/fl Alb-Cre – (WT) and Glul fl/fl Alb-Cre + (KO) male mice were injected with vehicle or c-Met/ΔN90-β-catenin/SB10 plasmids, and livers were harvested 2 weeks later. ( A ) RNA-seq was performed, and the summary of significantly changed pathways identified by GSEA ( n = 4). NES, normalized enrichment score. ( B ) GSEA enrichment plots of mTORC1-mediated signaling (left panel) and ribosome biogenesis (right panel) that are positively enriched in KO livers ( n = 4). ( C ) Heatmap of the relative expression of the indicated genes related to the mTORC1-mediated signaling pathway ( n = 3–4). ( D ) Liver lysates were probed for the indicated proteins ( n = 3). Lowercase “t” indicates that the total protein was probed. ( E ) IHC was performed ( n = 3 mice for each group). The number of positive cells was quantified by ImageJ from 3–4 randomly selected fields. **** P < 0.0001 (2-tailed t test). ( F ) FFPE liver sections were costained for GS (green) and p-S6 S235/236 (red), p-4EBP1 T37/46 (red), or p-mTOR S2448 (red) ( n = 3). The portal vein (PV) and hepatic vein (HV) were judged by GS expression in healthy WT livers. ( G ) Fluorescence images in F were subjected to colocalization analyses using the Coloc2 plugin in ImageJ. The pixel intensity correlation of channels 1 and 2 over space is depicted as a 2D scatterplot. Scale bars: 100 μm ( E and F ). Kendall’s Tau-b correlation analysis was used to test the significance of correlation and was judged positively correlated when greater than 0.5.
    Figure Legend Snippet: Seven-week-old Glul fl/fl Alb-Cre – (WT) and Glul fl/fl Alb-Cre + (KO) male mice were injected with vehicle or c-Met/ΔN90-β-catenin/SB10 plasmids, and livers were harvested 2 weeks later. ( A ) RNA-seq was performed, and the summary of significantly changed pathways identified by GSEA ( n = 4). NES, normalized enrichment score. ( B ) GSEA enrichment plots of mTORC1-mediated signaling (left panel) and ribosome biogenesis (right panel) that are positively enriched in KO livers ( n = 4). ( C ) Heatmap of the relative expression of the indicated genes related to the mTORC1-mediated signaling pathway ( n = 3–4). ( D ) Liver lysates were probed for the indicated proteins ( n = 3). Lowercase “t” indicates that the total protein was probed. ( E ) IHC was performed ( n = 3 mice for each group). The number of positive cells was quantified by ImageJ from 3–4 randomly selected fields. **** P < 0.0001 (2-tailed t test). ( F ) FFPE liver sections were costained for GS (green) and p-S6 S235/236 (red), p-4EBP1 T37/46 (red), or p-mTOR S2448 (red) ( n = 3). The portal vein (PV) and hepatic vein (HV) were judged by GS expression in healthy WT livers. ( G ) Fluorescence images in F were subjected to colocalization analyses using the Coloc2 plugin in ImageJ. The pixel intensity correlation of channels 1 and 2 over space is depicted as a 2D scatterplot. Scale bars: 100 μm ( E and F ). Kendall’s Tau-b correlation analysis was used to test the significance of correlation and was judged positively correlated when greater than 0.5.

    Techniques Used: Injection, RNA Sequencing Assay, Expressing, Fluorescence

    ( A ) Relative GLUL mRNA levels in liver cancer patients with WT or mutated CTNNB1 (TCGA) were compared and are expressed as mean ± SEM. ( B ) Correlations between hepatic GLUL and UCE expression in patients with CTNNB1 mutations (TCGA) was calculated by Pearson’s correlation. ( C ) CTNNB1 mutation correlates positively with hepatic GS expression but inversely with GLUL CpG island methylation. ( D ) Two liver TMAs were costained for GS (green) and ARG1 (red) and quantified by ImageJ and normalized to the respective median (right panel). ( E ) TMAs with HCC tumors (T), adjacent normal tissue (N), or intrahepatic cholangiocarcinoma (ICC) were costained for GS (green) and p-4EBP1 T37/46 (red). ( F ) Ratios of p-4EBP1 T37/46 to GS intensities were plotted. Results are expressed as mean ± SEM. The cutoff value for GS-high ( n = 52) versus -low ( n = 372) was determined using the best separation between the 2 modes of a bimodal distribution. **** P < 0.0001 by 2-tailed t test ( A , D , and F ). ( G ) GSEA enrichment plots show that mTORC1 target genes correlate inversely with GS level in CTNNB1 -mutated patients (TCGA). The cutoff value for GS-high ( n = 62) versus -low ( n = 34) was determined using the best separation between the 2 modes of a bimodal distribution. P value was calculated by estimated score in GSEA. ( H ) The TCGA data of the indicated study were stratified into the RNA-seq results obtained from WT and Glul -KO mice 2 weeks after c-Met/ΔN90-β-catenin injection ( n = 4 in each group). GSEA plots show that high GS expression correlates with low recurrence. ( I ) Kaplan-Meier survival curves of patients with high ( n = 41) versus low ( n = 201) hepatic GS expression (GSE14520; P = 0.28, log rank). ( J ) In HCC patients harboring CTNNB1 mutations (TCGA) as shown in G , high GS expression tends to associate with better survival ( P = 0.09, log rank).
    Figure Legend Snippet: ( A ) Relative GLUL mRNA levels in liver cancer patients with WT or mutated CTNNB1 (TCGA) were compared and are expressed as mean ± SEM. ( B ) Correlations between hepatic GLUL and UCE expression in patients with CTNNB1 mutations (TCGA) was calculated by Pearson’s correlation. ( C ) CTNNB1 mutation correlates positively with hepatic GS expression but inversely with GLUL CpG island methylation. ( D ) Two liver TMAs were costained for GS (green) and ARG1 (red) and quantified by ImageJ and normalized to the respective median (right panel). ( E ) TMAs with HCC tumors (T), adjacent normal tissue (N), or intrahepatic cholangiocarcinoma (ICC) were costained for GS (green) and p-4EBP1 T37/46 (red). ( F ) Ratios of p-4EBP1 T37/46 to GS intensities were plotted. Results are expressed as mean ± SEM. The cutoff value for GS-high ( n = 52) versus -low ( n = 372) was determined using the best separation between the 2 modes of a bimodal distribution. **** P < 0.0001 by 2-tailed t test ( A , D , and F ). ( G ) GSEA enrichment plots show that mTORC1 target genes correlate inversely with GS level in CTNNB1 -mutated patients (TCGA). The cutoff value for GS-high ( n = 62) versus -low ( n = 34) was determined using the best separation between the 2 modes of a bimodal distribution. P value was calculated by estimated score in GSEA. ( H ) The TCGA data of the indicated study were stratified into the RNA-seq results obtained from WT and Glul -KO mice 2 weeks after c-Met/ΔN90-β-catenin injection ( n = 4 in each group). GSEA plots show that high GS expression correlates with low recurrence. ( I ) Kaplan-Meier survival curves of patients with high ( n = 41) versus low ( n = 201) hepatic GS expression (GSE14520; P = 0.28, log rank). ( J ) In HCC patients harboring CTNNB1 mutations (TCGA) as shown in G , high GS expression tends to associate with better survival ( P = 0.09, log rank).

    Techniques Used: Expressing, Mutagenesis, Methylation, RNA Sequencing Assay, Injection

    p 4e bp  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p 4e bp
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    rabbit anti p 4ebp1  (Cell Signaling Technology Inc)


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    p eif4ebp1 4e bp1  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p eif4ebp1 4e bp1
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    Sestrin2 overexpression inhibits TM-induced mTOR pathway activation. (a) Representative western-blot results of major proteins associated with mTOR pathway. (b) Statistical analysis of p-mTOR, mTOR and their ratio (unpaired two-tailed t -test; all P values >0.05). (c) Statistical results of p-P70S6K, P70S6K and their ratio (unpaired two-tailed t -test; for p-p70s6k/p70s6k: t (4) = 3.30, P =0.030). (d) Quantitative results <t>of</t> <t>p-4E-BP1,</t> 4E-BP1 and their ratio (unpaired two-tailed t -test; for 4E-BP1: t (4) = 3.62, P =0.022). ∗ P < 0.05.
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    Sestrin2 overexpression inhibits TM-induced mTOR pathway activation. (a) Representative western-blot results of major proteins associated with mTOR pathway. (b) Statistical analysis of p-mTOR, mTOR and their ratio (unpaired two-tailed t -test; all P values >0.05). (c) Statistical results of p-P70S6K, P70S6K and their ratio (unpaired two-tailed t -test; for p-p70s6k/p70s6k: t (4) = 3.30, P =0.030). (d) Quantitative results <t>of</t> <t>p-4E-BP1,</t> 4E-BP1 and their ratio (unpaired two-tailed t -test; for 4E-BP1: t (4) = 3.62, P =0.022). ∗ P < 0.05.
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    Sestrin2 overexpression inhibits TM-induced mTOR pathway activation. (a) Representative western-blot results of major proteins associated with mTOR pathway. (b) Statistical analysis of p-mTOR, mTOR and their ratio (unpaired two-tailed t -test; all P values >0.05). (c) Statistical results of p-P70S6K, P70S6K and their ratio (unpaired two-tailed t -test; for p-p70s6k/p70s6k: t (4) = 3.30, P =0.030). (d) Quantitative results of p-4E-BP1, 4E-BP1 and their ratio (unpaired two-tailed t -test; for 4E-BP1: t (4) = 3.62, P =0.022). ∗ P < 0.05.

    Journal: International Journal of Endocrinology

    Article Title: Sestrin2 Overexpression Ameliorates Endoplasmic Reticulum Stress-Induced Apoptosis via Inhibiting mTOR Pathway in HepG2 Cells

    doi: 10.1155/2022/2009753

    Figure Lengend Snippet: Sestrin2 overexpression inhibits TM-induced mTOR pathway activation. (a) Representative western-blot results of major proteins associated with mTOR pathway. (b) Statistical analysis of p-mTOR, mTOR and their ratio (unpaired two-tailed t -test; all P values >0.05). (c) Statistical results of p-P70S6K, P70S6K and their ratio (unpaired two-tailed t -test; for p-p70s6k/p70s6k: t (4) = 3.30, P =0.030). (d) Quantitative results of p-4E-BP1, 4E-BP1 and their ratio (unpaired two-tailed t -test; for 4E-BP1: t (4) = 3.62, P =0.022). ∗ P < 0.05.

    Article Snippet: We purchased the primary antibodies from Cell Signaling Technology (USA), and the antibodies include cleaved Caspase3 (Cat#9661s), Caspase3 (Cat#14220S) mTOR (Cat#2983s), p-mTOR ser2448 (Cat#5536s), 4E-BP1 (Cat#9644), p-4E-BP1 (Cat#2855), P70S6K (Cat#9202), and p-P70S6K (Cat#9205).

    Techniques: Over Expression, Activation Assay, Western Blot, Two Tailed Test