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phospho bad ser155  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc phospho bad ser155
    Phospho Bad Ser155, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/phospho+bad+ser155/pm41423011-49-28-50?v=Cell+Signaling+Technology+Inc
    Average 86 stars, based on 1 article reviews
    phospho bad ser155 - by Bioz Stars, 2026-07
    86/100 stars

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    Cell Signaling Technology Inc antibodies h3k4me3
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    Cell Signaling Technology Inc phospho bad antibody ser155
    Differentially phosphorylated proteins in hyperammonemia are shared with those in skeletal muscle from exercised mice and humans (A) Venn diagrams of differentially expressed phosphoproteins (DEpP) and differentially phosphorylated phosphosites (DPPS) present in at least one of the 6h/24h ammonium acetate (AmAc) treated C2C12 myotube datasets compared to DEpP and DPPS, respectively, from at least one of the exercise (mouse or human) datasets. (B) Canonical pathways enriched in DEpP unique to the hyperammonemia datasets compared to the exercise datasets. (C) Representative immunoblots and densitometry of a protein kinase A (PKA) substrate motif (RRXS∗/T∗) phosphorylation in murine C2C12 myotubes treated with 10mM AmAc, 50uM H89 (PKA activator), and 20uM forskolin (Fsk; PKA inhibitor). Separate membranes with the same samples were used to generate loading controls for this panel. (D) Representative immunoblots and densitometry of <t>p-BAD(Ser155)</t> in myotubes treated with 10mM AmAc, 50uM H89, and 20uM Fsk. (E) Heatmap of enriched canonical pathways in DEpP unique to the exercise datasets and not found in the hyperammonemic datasets. (F) UpSet plot showing unique and shared DEpP and DPPS among the 6hAmAc and 24hAmAc, mouse exercise, and human exercise datasets. (G) Bar graph of enriched canonical pathways from the subset of DEpP that are shared between at least one hyperammonemia and at least one exercise dataset. (H) Correlation matrix of shared DPPS between any exercise dataset and any hyperammonemic dataset (Blue = positive correlation and Red = negative correlation).Myotube experiments were done in n = 3 biological replicates (one 24hAmAc replicate was removed from downstream analyses because of outlier status). Densitometry data are mean ± SD. ∗p<0.05; ∗∗p<0.01; ∗∗∗p<0.001 ANOVA with Bonferroni post-hoc analysis. Statistical significance cutoff for DEpP/DPPS was padj<0.05 for ammonia and mouse data and padj<0.05 and expression fold change >|1.5| for human data. Significance for canonical pathways was-log(p value) ≥1.3 using a right-sided Fisher exact test. Daytime exercise = mice that underwent high-intensity treadmill running during the zeitgeber time (ZT)0 period of “lights on”; MIC = maximal intensity contraction; Nighttime exercise = mice that underwent high-intensity treadmill running during the ZT12 period of “lights off”, Treadmill (65% max.) exercise = mice exercised at 65% of their maximal running speed on a treadmill.
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    Image Search Results


    Comparison of H3K4me3, H3K27me3, and Pol II occupancy. The signal intensity diagram of H3K4me3 (A) , H3K27me3, (B) and Pol II (C) at gene promoters (TSS flanking 2 kb) of upregulated genes in the Mdivi-1-treated group compared to the control group (upper) and the heatmap of upregulated genes at gene promoter regions (lower).

    Journal: Frontiers in Cell and Developmental Biology

    Article Title: Regulation of cleavage embryo genes upon DRP1 inhibition in mouse embryonic stem cells

    doi: 10.3389/fcell.2023.1191797

    Figure Lengend Snippet: Comparison of H3K4me3, H3K27me3, and Pol II occupancy. The signal intensity diagram of H3K4me3 (A) , H3K27me3, (B) and Pol II (C) at gene promoters (TSS flanking 2 kb) of upregulated genes in the Mdivi-1-treated group compared to the control group (upper) and the heatmap of upregulated genes at gene promoter regions (lower).

    Article Snippet: ChIP-seq was performed using a Hyperactive In-Situ ChIP Library Prep Kit for Illumina (pG-Tn5) (Vazyme, Nanjing, China), according to the manufacturer’s procedure with the appropriate antibodies H3K4me3 (9297, CST, United States), H3K27me3 (ab6002, Abcam, United Kingdom), and Pol II (39097, Active motif, United States).

    Techniques: Comparison, Control

    Differentially phosphorylated proteins in hyperammonemia are shared with those in skeletal muscle from exercised mice and humans (A) Venn diagrams of differentially expressed phosphoproteins (DEpP) and differentially phosphorylated phosphosites (DPPS) present in at least one of the 6h/24h ammonium acetate (AmAc) treated C2C12 myotube datasets compared to DEpP and DPPS, respectively, from at least one of the exercise (mouse or human) datasets. (B) Canonical pathways enriched in DEpP unique to the hyperammonemia datasets compared to the exercise datasets. (C) Representative immunoblots and densitometry of a protein kinase A (PKA) substrate motif (RRXS∗/T∗) phosphorylation in murine C2C12 myotubes treated with 10mM AmAc, 50uM H89 (PKA activator), and 20uM forskolin (Fsk; PKA inhibitor). Separate membranes with the same samples were used to generate loading controls for this panel. (D) Representative immunoblots and densitometry of p-BAD(Ser155) in myotubes treated with 10mM AmAc, 50uM H89, and 20uM Fsk. (E) Heatmap of enriched canonical pathways in DEpP unique to the exercise datasets and not found in the hyperammonemic datasets. (F) UpSet plot showing unique and shared DEpP and DPPS among the 6hAmAc and 24hAmAc, mouse exercise, and human exercise datasets. (G) Bar graph of enriched canonical pathways from the subset of DEpP that are shared between at least one hyperammonemia and at least one exercise dataset. (H) Correlation matrix of shared DPPS between any exercise dataset and any hyperammonemic dataset (Blue = positive correlation and Red = negative correlation).Myotube experiments were done in n = 3 biological replicates (one 24hAmAc replicate was removed from downstream analyses because of outlier status). Densitometry data are mean ± SD. ∗p<0.05; ∗∗p<0.01; ∗∗∗p<0.001 ANOVA with Bonferroni post-hoc analysis. Statistical significance cutoff for DEpP/DPPS was padj<0.05 for ammonia and mouse data and padj<0.05 and expression fold change >|1.5| for human data. Significance for canonical pathways was-log(p value) ≥1.3 using a right-sided Fisher exact test. Daytime exercise = mice that underwent high-intensity treadmill running during the zeitgeber time (ZT)0 period of “lights on”; MIC = maximal intensity contraction; Nighttime exercise = mice that underwent high-intensity treadmill running during the ZT12 period of “lights off”, Treadmill (65% max.) exercise = mice exercised at 65% of their maximal running speed on a treadmill.

    Journal: iScience

    Article Title: Shared and unique phosphoproteomics responses in skeletal muscle from exercise models and in hyperammonemic myotubes

    doi: 10.1016/j.isci.2022.105325

    Figure Lengend Snippet: Differentially phosphorylated proteins in hyperammonemia are shared with those in skeletal muscle from exercised mice and humans (A) Venn diagrams of differentially expressed phosphoproteins (DEpP) and differentially phosphorylated phosphosites (DPPS) present in at least one of the 6h/24h ammonium acetate (AmAc) treated C2C12 myotube datasets compared to DEpP and DPPS, respectively, from at least one of the exercise (mouse or human) datasets. (B) Canonical pathways enriched in DEpP unique to the hyperammonemia datasets compared to the exercise datasets. (C) Representative immunoblots and densitometry of a protein kinase A (PKA) substrate motif (RRXS∗/T∗) phosphorylation in murine C2C12 myotubes treated with 10mM AmAc, 50uM H89 (PKA activator), and 20uM forskolin (Fsk; PKA inhibitor). Separate membranes with the same samples were used to generate loading controls for this panel. (D) Representative immunoblots and densitometry of p-BAD(Ser155) in myotubes treated with 10mM AmAc, 50uM H89, and 20uM Fsk. (E) Heatmap of enriched canonical pathways in DEpP unique to the exercise datasets and not found in the hyperammonemic datasets. (F) UpSet plot showing unique and shared DEpP and DPPS among the 6hAmAc and 24hAmAc, mouse exercise, and human exercise datasets. (G) Bar graph of enriched canonical pathways from the subset of DEpP that are shared between at least one hyperammonemia and at least one exercise dataset. (H) Correlation matrix of shared DPPS between any exercise dataset and any hyperammonemic dataset (Blue = positive correlation and Red = negative correlation).Myotube experiments were done in n = 3 biological replicates (one 24hAmAc replicate was removed from downstream analyses because of outlier status). Densitometry data are mean ± SD. ∗p<0.05; ∗∗p<0.01; ∗∗∗p<0.001 ANOVA with Bonferroni post-hoc analysis. Statistical significance cutoff for DEpP/DPPS was padj<0.05 for ammonia and mouse data and padj<0.05 and expression fold change >|1.5| for human data. Significance for canonical pathways was-log(p value) ≥1.3 using a right-sided Fisher exact test. Daytime exercise = mice that underwent high-intensity treadmill running during the zeitgeber time (ZT)0 period of “lights on”; MIC = maximal intensity contraction; Nighttime exercise = mice that underwent high-intensity treadmill running during the ZT12 period of “lights off”, Treadmill (65% max.) exercise = mice exercised at 65% of their maximal running speed on a treadmill.

    Article Snippet: Phospho-Bad antibody (Ser155) (rabbit polyclonal) , Cell Signaling , Cat# 9297; RRID: AB_2062131.

    Techniques: Western Blot, Phospho-proteomics, Expressing

    Journal: iScience

    Article Title: Shared and unique phosphoproteomics responses in skeletal muscle from exercise models and in hyperammonemic myotubes

    doi: 10.1016/j.isci.2022.105325

    Figure Lengend Snippet:

    Article Snippet: Phospho-Bad antibody (Ser155) (rabbit polyclonal) , Cell Signaling , Cat# 9297; RRID: AB_2062131.

    Techniques: Recombinant, Activity Assay, Phospho-proteomics, Software