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nf κb p65 rela  (Addgene inc)


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    Addgene inc nf κb p65 rela
    NF-κB signaling is required for the induction of BCL2A1 by hypoxia. ( A ) BCL2A1 promoter-luciferase assay showed that NF-κB <t>p65</t> (RELA) enhanced the BCL2A1 transcriptional activity dose-dependently in OVCA433 cells (** p < 0.005) as compared with control. ( B ) Western blot analysis showed that ectopic expression of NF-κB p65 (RELA) increased the expression level of BCL2A1, left. Depletion of RELA by siRNAs reduced the expression level of BCL2A1 as compared to the control cells when cultured in hypoxia (0.5% O 2 ) for 8 h. ( C ) Western blot analysis displayed that the expression levels of BCL2A1 and NF-κB p65 in a panel of ovarian cancer cells. HOSEs cell lines were used as normal control. ( D ) The induction of BCL2A1 is associated with the activation of NF-κB signaling pathway. OVCA433 cells were treated with hypoxia (0.5% O 2 ) for different time points within 0–24 h. ( E ) NF-κB luciferase assay showed that NF-κB transcription activity was increased by hypoxia at 8 h, while NF-κB inhibitor Bay 11-7082 (10 μM) abrogated such NF-κB induction in OVCA433 and A2780cp cells. ( F ) QPCR assay showed that Bay 11-7082 treatment (10 μM) abolished the upregulation of BCL2A1 mRNA level upon hypoxia treatment. For all, n = 3 technical replicates per sample. Data were represented as mean ± S.E.M.
    Nf κb P65 Rela, supplied by Addgene inc, used in various techniques. Bioz Stars score: 92/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/prsv+rela+p65/pmc08469659-39-1-9?v=Addgene+inc
    Average 92 stars, based on 5 article reviews
    nf κb p65 rela - by Bioz Stars, 2026-08
    92/100 stars

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    1) Product Images from "The Stress-Inducible BCL2A1 Is Required for Ovarian Cancer Metastatic Progression in the Peritoneal Microenvironment"

    Article Title: The Stress-Inducible BCL2A1 Is Required for Ovarian Cancer Metastatic Progression in the Peritoneal Microenvironment

    Journal: Cancers

    doi: 10.3390/cancers13184577

    NF-κB signaling is required for the induction of BCL2A1 by hypoxia. ( A ) BCL2A1 promoter-luciferase assay showed that NF-κB p65 (RELA) enhanced the BCL2A1 transcriptional activity dose-dependently in OVCA433 cells (** p < 0.005) as compared with control. ( B ) Western blot analysis showed that ectopic expression of NF-κB p65 (RELA) increased the expression level of BCL2A1, left. Depletion of RELA by siRNAs reduced the expression level of BCL2A1 as compared to the control cells when cultured in hypoxia (0.5% O 2 ) for 8 h. ( C ) Western blot analysis displayed that the expression levels of BCL2A1 and NF-κB p65 in a panel of ovarian cancer cells. HOSEs cell lines were used as normal control. ( D ) The induction of BCL2A1 is associated with the activation of NF-κB signaling pathway. OVCA433 cells were treated with hypoxia (0.5% O 2 ) for different time points within 0–24 h. ( E ) NF-κB luciferase assay showed that NF-κB transcription activity was increased by hypoxia at 8 h, while NF-κB inhibitor Bay 11-7082 (10 μM) abrogated such NF-κB induction in OVCA433 and A2780cp cells. ( F ) QPCR assay showed that Bay 11-7082 treatment (10 μM) abolished the upregulation of BCL2A1 mRNA level upon hypoxia treatment. For all, n = 3 technical replicates per sample. Data were represented as mean ± S.E.M.
    Figure Legend Snippet: NF-κB signaling is required for the induction of BCL2A1 by hypoxia. ( A ) BCL2A1 promoter-luciferase assay showed that NF-κB p65 (RELA) enhanced the BCL2A1 transcriptional activity dose-dependently in OVCA433 cells (** p < 0.005) as compared with control. ( B ) Western blot analysis showed that ectopic expression of NF-κB p65 (RELA) increased the expression level of BCL2A1, left. Depletion of RELA by siRNAs reduced the expression level of BCL2A1 as compared to the control cells when cultured in hypoxia (0.5% O 2 ) for 8 h. ( C ) Western blot analysis displayed that the expression levels of BCL2A1 and NF-κB p65 in a panel of ovarian cancer cells. HOSEs cell lines were used as normal control. ( D ) The induction of BCL2A1 is associated with the activation of NF-κB signaling pathway. OVCA433 cells were treated with hypoxia (0.5% O 2 ) for different time points within 0–24 h. ( E ) NF-κB luciferase assay showed that NF-κB transcription activity was increased by hypoxia at 8 h, while NF-κB inhibitor Bay 11-7082 (10 μM) abrogated such NF-κB induction in OVCA433 and A2780cp cells. ( F ) QPCR assay showed that Bay 11-7082 treatment (10 μM) abolished the upregulation of BCL2A1 mRNA level upon hypoxia treatment. For all, n = 3 technical replicates per sample. Data were represented as mean ± S.E.M.

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



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    nf κb p65 rela  (Addgene inc)
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    Addgene inc nf κb p65 rela
    NF-κB signaling is required for the induction of BCL2A1 by hypoxia. ( A ) BCL2A1 promoter-luciferase assay showed that NF-κB <t>p65</t> (RELA) enhanced the BCL2A1 transcriptional activity dose-dependently in OVCA433 cells (** p < 0.005) as compared with control. ( B ) Western blot analysis showed that ectopic expression of NF-κB p65 (RELA) increased the expression level of BCL2A1, left. Depletion of RELA by siRNAs reduced the expression level of BCL2A1 as compared to the control cells when cultured in hypoxia (0.5% O 2 ) for 8 h. ( C ) Western blot analysis displayed that the expression levels of BCL2A1 and NF-κB p65 in a panel of ovarian cancer cells. HOSEs cell lines were used as normal control. ( D ) The induction of BCL2A1 is associated with the activation of NF-κB signaling pathway. OVCA433 cells were treated with hypoxia (0.5% O 2 ) for different time points within 0–24 h. ( E ) NF-κB luciferase assay showed that NF-κB transcription activity was increased by hypoxia at 8 h, while NF-κB inhibitor Bay 11-7082 (10 μM) abrogated such NF-κB induction in OVCA433 and A2780cp cells. ( F ) QPCR assay showed that Bay 11-7082 treatment (10 μM) abolished the upregulation of BCL2A1 mRNA level upon hypoxia treatment. For all, n = 3 technical replicates per sample. Data were represented as mean ± S.E.M.
    Nf κb P65 Rela, supplied by Addgene inc, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/prsv+rela+p65/pmc08469659-39-1-9?v=Addgene+inc
    Average 92 stars, based on 1 article reviews
    nf κb p65 rela - by Bioz Stars, 2026-08
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    prsv rela p65  (Addgene inc)
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    Addgene inc prsv rela p65
    NF-κB signaling is required for the induction of BCL2A1 by hypoxia. ( A ) BCL2A1 promoter-luciferase assay showed that NF-κB <t>p65</t> (RELA) enhanced the BCL2A1 transcriptional activity dose-dependently in OVCA433 cells (** p < 0.005) as compared with control. ( B ) Western blot analysis showed that ectopic expression of NF-κB p65 (RELA) increased the expression level of BCL2A1, left. Depletion of RELA by siRNAs reduced the expression level of BCL2A1 as compared to the control cells when cultured in hypoxia (0.5% O 2 ) for 8 h. ( C ) Western blot analysis displayed that the expression levels of BCL2A1 and NF-κB p65 in a panel of ovarian cancer cells. HOSEs cell lines were used as normal control. ( D ) The induction of BCL2A1 is associated with the activation of NF-κB signaling pathway. OVCA433 cells were treated with hypoxia (0.5% O 2 ) for different time points within 0–24 h. ( E ) NF-κB luciferase assay showed that NF-κB transcription activity was increased by hypoxia at 8 h, while NF-κB inhibitor Bay 11-7082 (10 μM) abrogated such NF-κB induction in OVCA433 and A2780cp cells. ( F ) QPCR assay showed that Bay 11-7082 treatment (10 μM) abolished the upregulation of BCL2A1 mRNA level upon hypoxia treatment. For all, n = 3 technical replicates per sample. Data were represented as mean ± S.E.M.
    Prsv Rela P65, supplied by Addgene inc, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 92 stars, based on 1 article reviews
    prsv rela p65 - by Bioz Stars, 2026-08
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    expression plasmid prsv-nf- b (p65/rela)  (Sanofi)
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    NF-κB signaling is required for the induction of BCL2A1 by hypoxia. ( A ) BCL2A1 promoter-luciferase assay showed that NF-κB <t>p65</t> (RELA) enhanced the BCL2A1 transcriptional activity dose-dependently in OVCA433 cells (** p < 0.005) as compared with control. ( B ) Western blot analysis showed that ectopic expression of NF-κB p65 (RELA) increased the expression level of BCL2A1, left. Depletion of RELA by siRNAs reduced the expression level of BCL2A1 as compared to the control cells when cultured in hypoxia (0.5% O 2 ) for 8 h. ( C ) Western blot analysis displayed that the expression levels of BCL2A1 and NF-κB p65 in a panel of ovarian cancer cells. HOSEs cell lines were used as normal control. ( D ) The induction of BCL2A1 is associated with the activation of NF-κB signaling pathway. OVCA433 cells were treated with hypoxia (0.5% O 2 ) for different time points within 0–24 h. ( E ) NF-κB luciferase assay showed that NF-κB transcription activity was increased by hypoxia at 8 h, while NF-κB inhibitor Bay 11-7082 (10 μM) abrogated such NF-κB induction in OVCA433 and A2780cp cells. ( F ) QPCR assay showed that Bay 11-7082 treatment (10 μM) abolished the upregulation of BCL2A1 mRNA level upon hypoxia treatment. For all, n = 3 technical replicates per sample. Data were represented as mean ± S.E.M.
    Expression Plasmid Prsv Nf B (P65/Rela), supplied by Sanofi, 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/prsv+rela+p65/pm18768868-56-22-32?v=Sanofi
    Average 90 stars, based on 1 article reviews
    expression plasmid prsv-nf- b (p65/rela) - by Bioz Stars, 2026-08
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    NF-κB signaling is required for the induction of BCL2A1 by hypoxia. ( A ) BCL2A1 promoter-luciferase assay showed that NF-κB p65 (RELA) enhanced the BCL2A1 transcriptional activity dose-dependently in OVCA433 cells (** p < 0.005) as compared with control. ( B ) Western blot analysis showed that ectopic expression of NF-κB p65 (RELA) increased the expression level of BCL2A1, left. Depletion of RELA by siRNAs reduced the expression level of BCL2A1 as compared to the control cells when cultured in hypoxia (0.5% O 2 ) for 8 h. ( C ) Western blot analysis displayed that the expression levels of BCL2A1 and NF-κB p65 in a panel of ovarian cancer cells. HOSEs cell lines were used as normal control. ( D ) The induction of BCL2A1 is associated with the activation of NF-κB signaling pathway. OVCA433 cells were treated with hypoxia (0.5% O 2 ) for different time points within 0–24 h. ( E ) NF-κB luciferase assay showed that NF-κB transcription activity was increased by hypoxia at 8 h, while NF-κB inhibitor Bay 11-7082 (10 μM) abrogated such NF-κB induction in OVCA433 and A2780cp cells. ( F ) QPCR assay showed that Bay 11-7082 treatment (10 μM) abolished the upregulation of BCL2A1 mRNA level upon hypoxia treatment. For all, n = 3 technical replicates per sample. Data were represented as mean ± S.E.M.

    Journal: Cancers

    Article Title: The Stress-Inducible BCL2A1 Is Required for Ovarian Cancer Metastatic Progression in the Peritoneal Microenvironment

    doi: 10.3390/cancers13184577

    Figure Lengend Snippet: NF-κB signaling is required for the induction of BCL2A1 by hypoxia. ( A ) BCL2A1 promoter-luciferase assay showed that NF-κB p65 (RELA) enhanced the BCL2A1 transcriptional activity dose-dependently in OVCA433 cells (** p < 0.005) as compared with control. ( B ) Western blot analysis showed that ectopic expression of NF-κB p65 (RELA) increased the expression level of BCL2A1, left. Depletion of RELA by siRNAs reduced the expression level of BCL2A1 as compared to the control cells when cultured in hypoxia (0.5% O 2 ) for 8 h. ( C ) Western blot analysis displayed that the expression levels of BCL2A1 and NF-κB p65 in a panel of ovarian cancer cells. HOSEs cell lines were used as normal control. ( D ) The induction of BCL2A1 is associated with the activation of NF-κB signaling pathway. OVCA433 cells were treated with hypoxia (0.5% O 2 ) for different time points within 0–24 h. ( E ) NF-κB luciferase assay showed that NF-κB transcription activity was increased by hypoxia at 8 h, while NF-κB inhibitor Bay 11-7082 (10 μM) abrogated such NF-κB induction in OVCA433 and A2780cp cells. ( F ) QPCR assay showed that Bay 11-7082 treatment (10 μM) abolished the upregulation of BCL2A1 mRNA level upon hypoxia treatment. For all, n = 3 technical replicates per sample. Data were represented as mean ± S.E.M.

    Article Snippet: The NF-κB p65 (RELA)-expressing plasmid pRSV-p65 was obtained from Addgene (Plasmid #106453), the HIF-1α (RC202461)-expressing plasmid was purchased from OriGene (OriGene, Rockville, MD, USA), and RELA siRNA was ordered from Integrated DNA Technologies (IDT).

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