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p bad s112 mab  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc p bad s112 mab
    P Bad S112 Mab, 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/p+bad+s112+mab/pm27096050__ml5b00403_si_001-304-9-12
    Average 86 stars, based on 1 article reviews
    p bad s112 mab - by Bioz Stars, 2026-10
    86/100 stars

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    Article Title: Discovery and Optimization of Macrocyclic Quinoxaline-Pyrrolo-dihydropiperidinones as Potent Pim-1/2 Kinase Inhibitors
    Article Snippet: .. Biotinylated BAD peptide (Biopeptide), 10 mM ATP (Sigma), Labeled p-BAD (S112) mAb (Cell Signalling and Perkin Elmer) [with 0.05% BSA and 2 mM DTT added] streptavidin:Allophycocyanin [Perkin Elmer]. ..



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    A Western blot analysis of <t>BAD,</t> p-BAD <t>S112</t> , p-BAD S136 and β-actin in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 12 h. B Western blot analysis of AKT, p-AKT T308 and β-actin in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 12 h. C Time-course analysis of p-AKT T308 levels in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment. D HepG2 cells with or without PID1 overexpression were pretreated with Sorafenib (10 μM) for 3 h and then treated with insulin (10 nM) for 0.25 h. Western blot analysis of AKT, p-AKT T308 and β-actin was performed. E Hep3B cells with or without PID1 deficiency were pretreated with Sorafenib (10 μM) for 3 h and then treated with IGF-1 (50 ng/mL) treatment for 0.25 h. Western blot analysis of AKT, p-AKT T308 , BAD, p-BAD S136 and β-actin was performed. F Cell apoptosis in Hep3B with or without PID1 knockout upon Sorafenib (10 μM) treatment for 24 h in the presence of AKT inhibitor VIII (10 μM) was examined by cytometry analysis. Data are expressed as mean ± SD ( n = 3). * p < 0.05; ** p < 0.01; *** p < 0.001; ns not significant.
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    labeled p-bad (s112) mab cell signalling antibody  (Cell Signaling Technology Inc)
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    A Western blot analysis of <t>BAD,</t> p-BAD <t>S112</t> , p-BAD S136 and β-actin in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 12 h. B Western blot analysis of AKT, p-AKT T308 and β-actin in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 12 h. C Time-course analysis of p-AKT T308 levels in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment. D HepG2 cells with or without PID1 overexpression were pretreated with Sorafenib (10 μM) for 3 h and then treated with insulin (10 nM) for 0.25 h. Western blot analysis of AKT, p-AKT T308 and β-actin was performed. E Hep3B cells with or without PID1 deficiency were pretreated with Sorafenib (10 μM) for 3 h and then treated with IGF-1 (50 ng/mL) treatment for 0.25 h. Western blot analysis of AKT, p-AKT T308 , BAD, p-BAD S136 and β-actin was performed. F Cell apoptosis in Hep3B with or without PID1 knockout upon Sorafenib (10 μM) treatment for 24 h in the presence of AKT inhibitor VIII (10 μM) was examined by cytometry analysis. Data are expressed as mean ± SD ( n = 3). * p < 0.05; ** p < 0.01; *** p < 0.001; ns not significant.
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    labeled p-bad (s112) mab  (Cell Signaling Technology Inc)
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    Cell Signaling Technology Inc labeled p-bad (s112) mab
    A Western blot analysis of <t>BAD,</t> p-BAD <t>S112</t> , p-BAD S136 and β-actin in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 12 h. B Western blot analysis of AKT, p-AKT T308 and β-actin in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 12 h. C Time-course analysis of p-AKT T308 levels in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment. D HepG2 cells with or without PID1 overexpression were pretreated with Sorafenib (10 μM) for 3 h and then treated with insulin (10 nM) for 0.25 h. Western blot analysis of AKT, p-AKT T308 and β-actin was performed. E Hep3B cells with or without PID1 deficiency were pretreated with Sorafenib (10 μM) for 3 h and then treated with IGF-1 (50 ng/mL) treatment for 0.25 h. Western blot analysis of AKT, p-AKT T308 , BAD, p-BAD S136 and β-actin was performed. F Cell apoptosis in Hep3B with or without PID1 knockout upon Sorafenib (10 μM) treatment for 24 h in the presence of AKT inhibitor VIII (10 μM) was examined by cytometry analysis. Data are expressed as mean ± SD ( n = 3). * p < 0.05; ** p < 0.01; *** p < 0.001; ns not significant.
    Labeled P Bad (S112) Mab, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/p+bad+s112+mab/human+pbad+s112+elisa+kit/us09394297-5077-9-12
    Average 90 stars, based on 1 article reviews
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    A Western blot analysis of BAD, p-BAD S112 , p-BAD S136 and β-actin in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 12 h. B Western blot analysis of AKT, p-AKT T308 and β-actin in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 12 h. C Time-course analysis of p-AKT T308 levels in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment. D HepG2 cells with or without PID1 overexpression were pretreated with Sorafenib (10 μM) for 3 h and then treated with insulin (10 nM) for 0.25 h. Western blot analysis of AKT, p-AKT T308 and β-actin was performed. E Hep3B cells with or without PID1 deficiency were pretreated with Sorafenib (10 μM) for 3 h and then treated with IGF-1 (50 ng/mL) treatment for 0.25 h. Western blot analysis of AKT, p-AKT T308 , BAD, p-BAD S136 and β-actin was performed. F Cell apoptosis in Hep3B with or without PID1 knockout upon Sorafenib (10 μM) treatment for 24 h in the presence of AKT inhibitor VIII (10 μM) was examined by cytometry analysis. Data are expressed as mean ± SD ( n = 3). * p < 0.05; ** p < 0.01; *** p < 0.001; ns not significant.

    Journal: Cell Death Discovery

    Article Title: Dual role of PID1 in regulating apoptosis induced by distinct anticancer-agents through AKT/Raf-1-dependent pathway in hepatocellular carcinoma

    doi: 10.1038/s41420-023-01405-1

    Figure Lengend Snippet: A Western blot analysis of BAD, p-BAD S112 , p-BAD S136 and β-actin in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 12 h. B Western blot analysis of AKT, p-AKT T308 and β-actin in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment for 12 h. C Time-course analysis of p-AKT T308 levels in HepG2 cells with or without PID1 overexpression upon Sorafenib (10 μM) treatment. D HepG2 cells with or without PID1 overexpression were pretreated with Sorafenib (10 μM) for 3 h and then treated with insulin (10 nM) for 0.25 h. Western blot analysis of AKT, p-AKT T308 and β-actin was performed. E Hep3B cells with or without PID1 deficiency were pretreated with Sorafenib (10 μM) for 3 h and then treated with IGF-1 (50 ng/mL) treatment for 0.25 h. Western blot analysis of AKT, p-AKT T308 , BAD, p-BAD S136 and β-actin was performed. F Cell apoptosis in Hep3B with or without PID1 knockout upon Sorafenib (10 μM) treatment for 24 h in the presence of AKT inhibitor VIII (10 μM) was examined by cytometry analysis. Data are expressed as mean ± SD ( n = 3). * p < 0.05; ** p < 0.01; *** p < 0.001; ns not significant.

    Article Snippet: Antibodies used to determine the protein expression were the following: PID1 (#27951; Signalway Antibody, Greenbelt, Maryland, USA), β-actin (#66009-1-lg; Proteintech, USA), Bcl-xL (#2764; Cell Signaling Technology, USA), Bcl2 (#12789-1-AP; Proteintech), BAD (#sc-8044 Santa Cruz Technology, Texas, USA), p-BAD S112 (#5284; Cell Signaling Technology), p-BAD S136 (#4366; Cell Signaling Technology), cytochrome c (#sc-13156; Santa Cruz Technology), cleaved caspase-3 (#9664; Cell Signaling Technology), Tom20 (#42406; Cell Signaling Technology), Raf-1 (#9422; Cell Signaling Technology), p-Raf-1 S259 (#9421; Cell Signaling Technology), p-Raf-1 S338 (#9427; Cell Signaling Technology), AKT (#4691; Cell Signaling Technology), p-AKT T308 (#13038; Cell Signaling Technology), HA-tag (#sc-7392; Santa Cruz Technology), His-tag (#sc-8036; Santa Cruz Technology), HA-tag (#14793; Cell Signaling Technology), His-tag (#12698; Cell Signal Technology), FLAG-tag (#3724; Cell Signaling Technology), FLAG-tag (#8146; Cell Signaling Technology), ERK1/2 (#4695; Cell Signaling Technology), p-ERK1/2 T202/Y204 (#4370; Cell Signaling Technology), MEK1 (#9122; Cell Signaling Technology), p-MEK1 T292 (#07-852; Upstate, Darmstadt, Germany), BRAF (#sc-5284; Santa Cruz Technology), p-BRAF S445 (#2696; Cell Signaling Technology).

    Techniques: Western Blot, Over Expression, Knock-Out, Cytometry