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pcmx iκbα mt  (Addgene inc)


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    Structured Review

    Addgene inc pcmx iκbα mt
    Blockade of the NF-κB pathway activates p53 in a ROS-dependent manner. A–D, overexpression of dominant-negative mutant of <t>IκBα</t> <t>(IκBαM)</t> in A549 cells inhibits NF-κB activity (A); decreases Nrf2, Nqo1, and SLC7A11 mRNA levels (B); increases the level of intracellular ROS (C); and increases the levels of p53 phosphorylation (P-p53), p53, and p21Waf1/cip1 in a ROS-dependent manner (D). Treatment with NAC rescues from the effects of IκBαM. E–H, the IKK inhibitor BAY 11-7085 (20 μm) inhibits NF-κB activity (E); decreases Nrf2, Nqo1, and SLC7A11 mRNA levels (F); increases the level of intracellular ROS (G); and increases the levels of P-p53, p53, and p21Waf1/cip1 in a ROS-dependent manner (H). Treatment with NAC rescues from the effects of BAY 11-7085. DCF, dichlorofluorescein; EV, empty vector.
    Pcmx Iκbα Mt, supplied by Addgene inc, used in various techniques. Bioz Stars score: 91/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/pcmx iκbα mt/product/Addgene inc
    Average 91 stars, based on 7 article reviews
    pcmx iκbα mt - by Bioz Stars, 2026-03
    91/100 stars

    Images

    1) Product Images from "The GTPase KRAS suppresses the p53 tumor suppressor by activating the NRF2-regulated antioxidant defense system in cancer cells"

    Article Title: The GTPase KRAS suppresses the p53 tumor suppressor by activating the NRF2-regulated antioxidant defense system in cancer cells

    Journal: The Journal of Biological Chemistry

    doi: 10.1074/jbc.RA119.011930

    Blockade of the NF-κB pathway activates p53 in a ROS-dependent manner. A–D, overexpression of dominant-negative mutant of IκBα (IκBαM) in A549 cells inhibits NF-κB activity (A); decreases Nrf2, Nqo1, and SLC7A11 mRNA levels (B); increases the level of intracellular ROS (C); and increases the levels of p53 phosphorylation (P-p53), p53, and p21Waf1/cip1 in a ROS-dependent manner (D). Treatment with NAC rescues from the effects of IκBαM. E–H, the IKK inhibitor BAY 11-7085 (20 μm) inhibits NF-κB activity (E); decreases Nrf2, Nqo1, and SLC7A11 mRNA levels (F); increases the level of intracellular ROS (G); and increases the levels of P-p53, p53, and p21Waf1/cip1 in a ROS-dependent manner (H). Treatment with NAC rescues from the effects of BAY 11-7085. DCF, dichlorofluorescein; EV, empty vector.
    Figure Legend Snippet: Blockade of the NF-κB pathway activates p53 in a ROS-dependent manner. A–D, overexpression of dominant-negative mutant of IκBα (IκBαM) in A549 cells inhibits NF-κB activity (A); decreases Nrf2, Nqo1, and SLC7A11 mRNA levels (B); increases the level of intracellular ROS (C); and increases the levels of p53 phosphorylation (P-p53), p53, and p21Waf1/cip1 in a ROS-dependent manner (D). Treatment with NAC rescues from the effects of IκBαM. E–H, the IKK inhibitor BAY 11-7085 (20 μm) inhibits NF-κB activity (E); decreases Nrf2, Nqo1, and SLC7A11 mRNA levels (F); increases the level of intracellular ROS (G); and increases the levels of P-p53, p53, and p21Waf1/cip1 in a ROS-dependent manner (H). Treatment with NAC rescues from the effects of BAY 11-7085. DCF, dichlorofluorescein; EV, empty vector.

    Techniques Used: Over Expression, Dominant Negative Mutation, Activity Assay, Phospho-proteomics, Plasmid Preparation



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    Blockade of the NF-κB pathway activates p53 in a ROS-dependent manner. A–D, overexpression of dominant-negative mutant of <t>IκBα</t> <t>(IκBαM)</t> in A549 cells inhibits NF-κB activity (A); decreases Nrf2, Nqo1, and SLC7A11 mRNA levels (B); increases the level of intracellular ROS (C); and increases the levels of p53 phosphorylation (P-p53), p53, and p21Waf1/cip1 in a ROS-dependent manner (D). Treatment with NAC rescues from the effects of IκBαM. E–H, the IKK inhibitor BAY 11-7085 (20 μm) inhibits NF-κB activity (E); decreases Nrf2, Nqo1, and SLC7A11 mRNA levels (F); increases the level of intracellular ROS (G); and increases the levels of P-p53, p53, and p21Waf1/cip1 in a ROS-dependent manner (H). Treatment with NAC rescues from the effects of BAY 11-7085. DCF, dichlorofluorescein; EV, empty vector.
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    Blockade of the NF-κB pathway activates p53 in a ROS-dependent manner. A–D, overexpression of dominant-negative mutant of <t>IκBα</t> <t>(IκBαM)</t> in A549 cells inhibits NF-κB activity (A); decreases Nrf2, Nqo1, and SLC7A11 mRNA levels (B); increases the level of intracellular ROS (C); and increases the levels of p53 phosphorylation (P-p53), p53, and p21Waf1/cip1 in a ROS-dependent manner (D). Treatment with NAC rescues from the effects of IκBαM. E–H, the IKK inhibitor BAY 11-7085 (20 μm) inhibits NF-κB activity (E); decreases Nrf2, Nqo1, and SLC7A11 mRNA levels (F); increases the level of intracellular ROS (G); and increases the levels of P-p53, p53, and p21Waf1/cip1 in a ROS-dependent manner (H). Treatment with NAC rescues from the effects of BAY 11-7085. DCF, dichlorofluorescein; EV, empty vector.
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    Blockade of the NF-κB pathway activates p53 in a ROS-dependent manner. A–D, overexpression of dominant-negative mutant of <t>IκBα</t> <t>(IκBαM)</t> in A549 cells inhibits NF-κB activity (A); decreases Nrf2, Nqo1, and SLC7A11 mRNA levels (B); increases the level of intracellular ROS (C); and increases the levels of p53 phosphorylation (P-p53), p53, and p21Waf1/cip1 in a ROS-dependent manner (D). Treatment with NAC rescues from the effects of IκBαM. E–H, the IKK inhibitor BAY 11-7085 (20 μm) inhibits NF-κB activity (E); decreases Nrf2, Nqo1, and SLC7A11 mRNA levels (F); increases the level of intracellular ROS (G); and increases the levels of P-p53, p53, and p21Waf1/cip1 in a ROS-dependent manner (H). Treatment with NAC rescues from the effects of BAY 11-7085. DCF, dichlorofluorescein; EV, empty vector.
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    Blockade of the NF-κB pathway activates p53 in a ROS-dependent manner. A–D, overexpression of dominant-negative mutant of IκBα (IκBαM) in A549 cells inhibits NF-κB activity (A); decreases Nrf2, Nqo1, and SLC7A11 mRNA levels (B); increases the level of intracellular ROS (C); and increases the levels of p53 phosphorylation (P-p53), p53, and p21Waf1/cip1 in a ROS-dependent manner (D). Treatment with NAC rescues from the effects of IκBαM. E–H, the IKK inhibitor BAY 11-7085 (20 μm) inhibits NF-κB activity (E); decreases Nrf2, Nqo1, and SLC7A11 mRNA levels (F); increases the level of intracellular ROS (G); and increases the levels of P-p53, p53, and p21Waf1/cip1 in a ROS-dependent manner (H). Treatment with NAC rescues from the effects of BAY 11-7085. DCF, dichlorofluorescein; EV, empty vector.

    Journal: The Journal of Biological Chemistry

    Article Title: The GTPase KRAS suppresses the p53 tumor suppressor by activating the NRF2-regulated antioxidant defense system in cancer cells

    doi: 10.1074/jbc.RA119.011930

    Figure Lengend Snippet: Blockade of the NF-κB pathway activates p53 in a ROS-dependent manner. A–D, overexpression of dominant-negative mutant of IκBα (IκBαM) in A549 cells inhibits NF-κB activity (A); decreases Nrf2, Nqo1, and SLC7A11 mRNA levels (B); increases the level of intracellular ROS (C); and increases the levels of p53 phosphorylation (P-p53), p53, and p21Waf1/cip1 in a ROS-dependent manner (D). Treatment with NAC rescues from the effects of IκBαM. E–H, the IKK inhibitor BAY 11-7085 (20 μm) inhibits NF-κB activity (E); decreases Nrf2, Nqo1, and SLC7A11 mRNA levels (F); increases the level of intracellular ROS (G); and increases the levels of P-p53, p53, and p21Waf1/cip1 in a ROS-dependent manner (H). Treatment with NAC rescues from the effects of BAY 11-7085. DCF, dichlorofluorescein; EV, empty vector.

    Article Snippet: DNA transfection The cells were plated overnight to reach 70–80% confluency and were then transfected with plasmid DNA of pCMX IκBα mt (IκBαM, Addgene, 12329) using Lipofectamine 2000 (11668-027, Invitrogen) transfection reagent according to the manufacturer's instructions.

    Techniques: Over Expression, Dominant Negative Mutation, Activity Assay, Phospho-proteomics, Plasmid Preparation