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nf κb reporter luc hek293 cell line  (BPS Bioscience)


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    BPS Bioscience nf κb reporter luc hek293 cell line
    a C273 increases resistance to oxidative stress induced by H 2 O 2 in MC65 Tet-Off cells expressing Aβ. Cells were pretreated with C273 prior to H 2 O 2 exposure, and cell viability was assessed to determine LD 50 values. LD 50 values were calculated by nonlinear regression using GraphPad Prism. b, c C273 restores intracellular NADPH ( b ) and GSH ( c ) levels in MC65 Tet-Off cells. d C273 suppresses IL-1β-induced NF-κB activation. NF-κB reporter <t>HEK293</t> cells were pretreated for 24 h with C273 (50 nM, 500 nM, or 5 μM), AICAR (0.5 mM), or metformin (0.5 mM), followed by stimulation with IL-1β (1 ng/ml) for 6 h. NF-κB luciferase activity was measured using the Luciferase Assay System (Promega, E1501). n = 4 independent experiments. e C273 restores mitochondrial biogenesis, expression of ETC complexes, autophagy markers, and antioxidant proteins in MC65 Tet-Off cells. MC65 cells were cultured under Tet-On (Aβ-) or Tet-Off (Aβ+) conditions and treated with vehicle or C273 (5 nM, 50 nM, or 500 nM) for 24 h. Protein levels were analyzed by Western blot. Statistical analysis was performed via one-way ANOVA to compare the vehicle-, metformin-, AICAR- and C273-treated groups. Data are presented as mean ± SD. * P < 0.05; ** P < 0.01.
    Nf κb Reporter Luc Hek293 Cell Line, supplied by BPS Bioscience, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/nf+%CE%BAb+reporter+luc+hek293+cell+line/RANK+%2F+NF-%CE%BAB+Reporter+-+HEK293+Recombinant+Cell+Line/bio_rxiv__64898__2026__04__10__717554-222-0-21
    Average 94 stars, based on 1 article reviews
    nf κb reporter luc hek293 cell line - by Bioz Stars, 2026-09
    94/100 stars

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    1) Product Images from "Discovery and Preclinical Validation of a Clinically Optimized Mitochondrial Complex I Modulator for Alzheimer’s Disease"

    Article Title: Discovery and Preclinical Validation of a Clinically Optimized Mitochondrial Complex I Modulator for Alzheimer’s Disease

    Journal: bioRxiv

    doi: 10.64898/2026.04.10.717554

    a C273 increases resistance to oxidative stress induced by H 2 O 2 in MC65 Tet-Off cells expressing Aβ. Cells were pretreated with C273 prior to H 2 O 2 exposure, and cell viability was assessed to determine LD 50 values. LD 50 values were calculated by nonlinear regression using GraphPad Prism. b, c C273 restores intracellular NADPH ( b ) and GSH ( c ) levels in MC65 Tet-Off cells. d C273 suppresses IL-1β-induced NF-κB activation. NF-κB reporter HEK293 cells were pretreated for 24 h with C273 (50 nM, 500 nM, or 5 μM), AICAR (0.5 mM), or metformin (0.5 mM), followed by stimulation with IL-1β (1 ng/ml) for 6 h. NF-κB luciferase activity was measured using the Luciferase Assay System (Promega, E1501). n = 4 independent experiments. e C273 restores mitochondrial biogenesis, expression of ETC complexes, autophagy markers, and antioxidant proteins in MC65 Tet-Off cells. MC65 cells were cultured under Tet-On (Aβ-) or Tet-Off (Aβ+) conditions and treated with vehicle or C273 (5 nM, 50 nM, or 500 nM) for 24 h. Protein levels were analyzed by Western blot. Statistical analysis was performed via one-way ANOVA to compare the vehicle-, metformin-, AICAR- and C273-treated groups. Data are presented as mean ± SD. * P < 0.05; ** P < 0.01.
    Figure Legend Snippet: a C273 increases resistance to oxidative stress induced by H 2 O 2 in MC65 Tet-Off cells expressing Aβ. Cells were pretreated with C273 prior to H 2 O 2 exposure, and cell viability was assessed to determine LD 50 values. LD 50 values were calculated by nonlinear regression using GraphPad Prism. b, c C273 restores intracellular NADPH ( b ) and GSH ( c ) levels in MC65 Tet-Off cells. d C273 suppresses IL-1β-induced NF-κB activation. NF-κB reporter HEK293 cells were pretreated for 24 h with C273 (50 nM, 500 nM, or 5 μM), AICAR (0.5 mM), or metformin (0.5 mM), followed by stimulation with IL-1β (1 ng/ml) for 6 h. NF-κB luciferase activity was measured using the Luciferase Assay System (Promega, E1501). n = 4 independent experiments. e C273 restores mitochondrial biogenesis, expression of ETC complexes, autophagy markers, and antioxidant proteins in MC65 Tet-Off cells. MC65 cells were cultured under Tet-On (Aβ-) or Tet-Off (Aβ+) conditions and treated with vehicle or C273 (5 nM, 50 nM, or 500 nM) for 24 h. Protein levels were analyzed by Western blot. Statistical analysis was performed via one-way ANOVA to compare the vehicle-, metformin-, AICAR- and C273-treated groups. Data are presented as mean ± SD. * P < 0.05; ** P < 0.01.

    Techniques Used: Expressing, Activation Assay, Luciferase, Activity Assay, Cell Culture, Western Blot



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    a C273 increases resistance to oxidative stress induced by H 2 O 2 in MC65 Tet-Off cells expressing Aβ. Cells were pretreated with C273 prior to H 2 O 2 exposure, and cell viability was assessed to determine LD 50 values. LD 50 values were calculated by nonlinear regression using GraphPad Prism. b, c C273 restores intracellular NADPH ( b ) and GSH ( c ) levels in MC65 Tet-Off cells. d C273 suppresses IL-1β-induced NF-κB activation. NF-κB reporter <t>HEK293</t> cells were pretreated for 24 h with C273 (50 nM, 500 nM, or 5 μM), AICAR (0.5 mM), or metformin (0.5 mM), followed by stimulation with IL-1β (1 ng/ml) for 6 h. NF-κB luciferase activity was measured using the Luciferase Assay System (Promega, E1501). n = 4 independent experiments. e C273 restores mitochondrial biogenesis, expression of ETC complexes, autophagy markers, and antioxidant proteins in MC65 Tet-Off cells. MC65 cells were cultured under Tet-On (Aβ-) or Tet-Off (Aβ+) conditions and treated with vehicle or C273 (5 nM, 50 nM, or 500 nM) for 24 h. Protein levels were analyzed by Western blot. Statistical analysis was performed via one-way ANOVA to compare the vehicle-, metformin-, AICAR- and C273-treated groups. Data are presented as mean ± SD. * P < 0.05; ** P < 0.01.
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    a C273 increases resistance to oxidative stress induced by H 2 O 2 in MC65 Tet-Off cells expressing Aβ. Cells were pretreated with C273 prior to H 2 O 2 exposure, and cell viability was assessed to determine LD 50 values. LD 50 values were calculated by nonlinear regression using GraphPad Prism. b, c C273 restores intracellular NADPH ( b ) and GSH ( c ) levels in MC65 Tet-Off cells. d C273 suppresses IL-1β-induced NF-κB activation. NF-κB reporter <t>HEK293</t> cells were pretreated for 24 h with C273 (50 nM, 500 nM, or 5 μM), AICAR (0.5 mM), or metformin (0.5 mM), followed by stimulation with IL-1β (1 ng/ml) for 6 h. NF-κB luciferase activity was measured using the Luciferase Assay System (Promega, E1501). n = 4 independent experiments. e C273 restores mitochondrial biogenesis, expression of ETC complexes, autophagy markers, and antioxidant proteins in MC65 Tet-Off cells. MC65 cells were cultured under Tet-On (Aβ-) or Tet-Off (Aβ+) conditions and treated with vehicle or C273 (5 nM, 50 nM, or 500 nM) for 24 h. Protein levels were analyzed by Western blot. Statistical analysis was performed via one-way ANOVA to compare the vehicle-, metformin-, AICAR- and C273-treated groups. Data are presented as mean ± SD. * P < 0.05; ** P < 0.01.
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    Image Search Results


    a C273 increases resistance to oxidative stress induced by H 2 O 2 in MC65 Tet-Off cells expressing Aβ. Cells were pretreated with C273 prior to H 2 O 2 exposure, and cell viability was assessed to determine LD 50 values. LD 50 values were calculated by nonlinear regression using GraphPad Prism. b, c C273 restores intracellular NADPH ( b ) and GSH ( c ) levels in MC65 Tet-Off cells. d C273 suppresses IL-1β-induced NF-κB activation. NF-κB reporter HEK293 cells were pretreated for 24 h with C273 (50 nM, 500 nM, or 5 μM), AICAR (0.5 mM), or metformin (0.5 mM), followed by stimulation with IL-1β (1 ng/ml) for 6 h. NF-κB luciferase activity was measured using the Luciferase Assay System (Promega, E1501). n = 4 independent experiments. e C273 restores mitochondrial biogenesis, expression of ETC complexes, autophagy markers, and antioxidant proteins in MC65 Tet-Off cells. MC65 cells were cultured under Tet-On (Aβ-) or Tet-Off (Aβ+) conditions and treated with vehicle or C273 (5 nM, 50 nM, or 500 nM) for 24 h. Protein levels were analyzed by Western blot. Statistical analysis was performed via one-way ANOVA to compare the vehicle-, metformin-, AICAR- and C273-treated groups. Data are presented as mean ± SD. * P < 0.05; ** P < 0.01.

    Journal: bioRxiv

    Article Title: Discovery and Preclinical Validation of a Clinically Optimized Mitochondrial Complex I Modulator for Alzheimer’s Disease

    doi: 10.64898/2026.04.10.717554

    Figure Lengend Snippet: a C273 increases resistance to oxidative stress induced by H 2 O 2 in MC65 Tet-Off cells expressing Aβ. Cells were pretreated with C273 prior to H 2 O 2 exposure, and cell viability was assessed to determine LD 50 values. LD 50 values were calculated by nonlinear regression using GraphPad Prism. b, c C273 restores intracellular NADPH ( b ) and GSH ( c ) levels in MC65 Tet-Off cells. d C273 suppresses IL-1β-induced NF-κB activation. NF-κB reporter HEK293 cells were pretreated for 24 h with C273 (50 nM, 500 nM, or 5 μM), AICAR (0.5 mM), or metformin (0.5 mM), followed by stimulation with IL-1β (1 ng/ml) for 6 h. NF-κB luciferase activity was measured using the Luciferase Assay System (Promega, E1501). n = 4 independent experiments. e C273 restores mitochondrial biogenesis, expression of ETC complexes, autophagy markers, and antioxidant proteins in MC65 Tet-Off cells. MC65 cells were cultured under Tet-On (Aβ-) or Tet-Off (Aβ+) conditions and treated with vehicle or C273 (5 nM, 50 nM, or 500 nM) for 24 h. Protein levels were analyzed by Western blot. Statistical analysis was performed via one-way ANOVA to compare the vehicle-, metformin-, AICAR- and C273-treated groups. Data are presented as mean ± SD. * P < 0.05; ** P < 0.01.

    Article Snippet: NF-κB Reporter (Luc) HEK293 cell line and the antioxidant response element (ARE) Luciferase Reporter HepG2 hepatic cell line were purchased from BPS Bioscience (CA, USA) and were cultured in accordance of manufacturer instructions.

    Techniques: Expressing, Activation Assay, Luciferase, Activity Assay, Cell Culture, Western Blot