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nf 174 e2 related factor 2 nrf2  (Proteintech)


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    Proteintech nf 174 e2 related factor 2 nrf2
    Nf 174 E2 Related Factor 2 Nrf2, supplied by Proteintech, used in various techniques. Bioz Stars score: 99/100, based on 162 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/nf+e2/NRF2%2C+NFE2L2+Fusion+Protein/pm41554468-97-16-23
    Average 99 stars, based on 162 article reviews
    nf 174 e2 related factor 2 nrf2 - by Bioz Stars, 2026-09
    99/100 stars

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    Article Snippet: .. Add primary antibody and incubate overnight, then wash three times with PBST (PBS with 2% Tween-20), the secondary antibody was added and incubated at 37°C for 1 h. Antibodies against RAS (Abmart, T56672S), p-MEK1/2 (CST, 9154S), MEK1/2 (CST, 8727 S), p-ERK1/2 (Abmart, TA1015S), ERK1/2 (Abmart, TA0155), p-AMPK (Abmart, T55608F), AMPK (Abmart, T55326F), NF-E2 (Proteintech, United States, 11089-1-AP), GATA1 (Proteintech, United States, 10917-2-AP), FOS (Proteintech, United States, 66590-1-Ig), GAPDH (Proteintech, United States, 10494-1-AP). ..

    other:

    Article Title: Ginkgolic acid: a novel IL1R1 agonist facilitating megakaryocyte differentiation and platelet production via the SRC/MEK/ERK pathway.
    Article Snippet: Thrombocytopenia, a common complication of prolonged radiotherapy in cancer patients, presents significant clinical management challenges due to limitations of current therapies.. In this study, we screened Ginkgolic acid (GA) and elucidated its mechanisms in regulating the differentiation of Megakaryocytes (MKs) and thrombopoiesis, as well as its therapeutic potential for thrombocytopenia.. Firstly, Initial validation studies conducted in vitro using K562, Meg-01 cell lines and mouse primary MK showed that GA promoted MK differentiation, which evidenced by increased cell size, enhanced polyploidization, and upregulation of specific markers.



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    RDV stimulates HO-1 promoter activity via the <t>Nrf2/ARE</t> complex in rat aortic SMCs. ( A ) RDV-mediated HO-1 mRNA expression is dependent on de novo RNA synthesis. SMCs were treated with actinomycin D (ActD; 1 µg/mL) for 8 h in the absence or presence of RDV (50 µM). ( B ) RDV stimulates HO-1 promoter activity. Cells were transfected with a HO-1 promoter construct (E1) or a mutated HO-1 construct (M739) and a Renilla luciferase construct, treated with RDV (50 µM) for 8 h, and then analyzed for luciferase activity. In some instances, a dominant-negative Nrf2 (dnNrf2) construct was co-transfected into cells. ( C ) RDV (50 µM), but not MPR (50 µM) or NTV (50 µM), exposure for 24 h increases ROS production in SMCs. ( D ) RDV (50 µM) exposure for 24 h stimulates ROS production that is blocked by the antioxidant N-acetyl-L-cysteine (NAC; 10 mM). ( E ) ChIP assays demonstrate that RDV (50 µM) exposure for 8 h increases Nrf2 binding to the HO-1 enhancer E1 that is blocked by NAC (10 mM). ( F ) NAC (10 mM) inhibits RDV (50 µM for 24 h)-mediated HO-1 protein expression. Statistical analysis was performed using an analysis of variance with the Holm–Sidak post hoc test. * Statistically significant effect of RDV.
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    RDV stimulates HO-1 promoter activity via the <t>Nrf2/ARE</t> complex in rat aortic SMCs. ( A ) RDV-mediated HO-1 mRNA expression is dependent on de novo RNA synthesis. SMCs were treated with actinomycin D (ActD; 1 µg/mL) for 8 h in the absence or presence of RDV (50 µM). ( B ) RDV stimulates HO-1 promoter activity. Cells were transfected with a HO-1 promoter construct (E1) or a mutated HO-1 construct (M739) and a Renilla luciferase construct, treated with RDV (50 µM) for 8 h, and then analyzed for luciferase activity. In some instances, a dominant-negative Nrf2 (dnNrf2) construct was co-transfected into cells. ( C ) RDV (50 µM), but not MPR (50 µM) or NTV (50 µM), exposure for 24 h increases ROS production in SMCs. ( D ) RDV (50 µM) exposure for 24 h stimulates ROS production that is blocked by the antioxidant N-acetyl-L-cysteine (NAC; 10 mM). ( E ) ChIP assays demonstrate that RDV (50 µM) exposure for 8 h increases Nrf2 binding to the HO-1 enhancer E1 that is blocked by NAC (10 mM). ( F ) NAC (10 mM) inhibits RDV (50 µM for 24 h)-mediated HO-1 protein expression. Statistical analysis was performed using an analysis of variance with the Holm–Sidak post hoc test. * Statistically significant effect of RDV.
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    RDV stimulates HO-1 promoter activity via the Nrf2/ARE complex in rat aortic SMCs. ( A ) RDV-mediated HO-1 mRNA expression is dependent on de novo RNA synthesis. SMCs were treated with actinomycin D (ActD; 1 µg/mL) for 8 h in the absence or presence of RDV (50 µM). ( B ) RDV stimulates HO-1 promoter activity. Cells were transfected with a HO-1 promoter construct (E1) or a mutated HO-1 construct (M739) and a Renilla luciferase construct, treated with RDV (50 µM) for 8 h, and then analyzed for luciferase activity. In some instances, a dominant-negative Nrf2 (dnNrf2) construct was co-transfected into cells. ( C ) RDV (50 µM), but not MPR (50 µM) or NTV (50 µM), exposure for 24 h increases ROS production in SMCs. ( D ) RDV (50 µM) exposure for 24 h stimulates ROS production that is blocked by the antioxidant N-acetyl-L-cysteine (NAC; 10 mM). ( E ) ChIP assays demonstrate that RDV (50 µM) exposure for 8 h increases Nrf2 binding to the HO-1 enhancer E1 that is blocked by NAC (10 mM). ( F ) NAC (10 mM) inhibits RDV (50 µM for 24 h)-mediated HO-1 protein expression. Statistical analysis was performed using an analysis of variance with the Holm–Sidak post hoc test. * Statistically significant effect of RDV.

    Journal: Antioxidants

    Article Title: Selective Inhibition of Vascular Smooth Muscle Cell Function by COVID-19 Antiviral Drugs: Impact of Heme Oxygenase-1

    doi: 10.3390/antiox14080945

    Figure Lengend Snippet: RDV stimulates HO-1 promoter activity via the Nrf2/ARE complex in rat aortic SMCs. ( A ) RDV-mediated HO-1 mRNA expression is dependent on de novo RNA synthesis. SMCs were treated with actinomycin D (ActD; 1 µg/mL) for 8 h in the absence or presence of RDV (50 µM). ( B ) RDV stimulates HO-1 promoter activity. Cells were transfected with a HO-1 promoter construct (E1) or a mutated HO-1 construct (M739) and a Renilla luciferase construct, treated with RDV (50 µM) for 8 h, and then analyzed for luciferase activity. In some instances, a dominant-negative Nrf2 (dnNrf2) construct was co-transfected into cells. ( C ) RDV (50 µM), but not MPR (50 µM) or NTV (50 µM), exposure for 24 h increases ROS production in SMCs. ( D ) RDV (50 µM) exposure for 24 h stimulates ROS production that is blocked by the antioxidant N-acetyl-L-cysteine (NAC; 10 mM). ( E ) ChIP assays demonstrate that RDV (50 µM) exposure for 8 h increases Nrf2 binding to the HO-1 enhancer E1 that is blocked by NAC (10 mM). ( F ) NAC (10 mM) inhibits RDV (50 µM for 24 h)-mediated HO-1 protein expression. Statistical analysis was performed using an analysis of variance with the Holm–Sidak post hoc test. * Statistically significant effect of RDV.

    Article Snippet: Polyclonal antibodies against HO-1 and HO-2 were from Enzo Life Sciences (Farmingdale, NY, USA) while antibodies directed against NF-E2-related factor-2 (Nrf2) and β-actin were from Santa Cruz Biotechnology (Santa Cruz, CA, USA).

    Techniques: Activity Assay, Expressing, Transfection, Construct, Luciferase, Dominant Negative Mutation, Binding Assay