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β-catenin/tcf firefly luciferase reporter vectors fop-flash  (Promega)

 
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    Structured Review

    Promega β-catenin/tcf firefly luciferase reporter vectors fop-flash
    β Catenin/Tcf Firefly Luciferase Reporter Vectors Fop Flash, supplied by Promega, 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/fop-flash+vector/%CE%B2+catenin+tcf+firefly+luciferase+reporter+vectors+fop+flash/pm32920660-65-1-18
    Average 90 stars, based on 1 article reviews
    β-catenin/tcf firefly luciferase reporter vectors fop-flash - by Bioz Stars, 2026-10
    90/100 stars

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    Related Articles

    Plasmid Preparation:

    Article Title: OIP5-AS1 contributes to tumorigenesis in hepatocellular carcinoma by miR-300/YY1-activated WNT pathway
    Article Snippet: Briefly, reporters containing TOP Flash or FOP Flash were synthesized and obtained from Addgene. .. Cells were placed in a 96-well plate, followed by co-transfection with indicated plasmids (GenePharma) and TOP Flash or FOP Flash vector (Promega). .. One day later, Promega Dual-Luciferase Reporter Assay System was applied for evaluating the luciferase activity, with activity of Renilla as normalizing control.

    other:

    Article Title: miR-140-3p enhances cisplatin sensitivity and attenuates stem cell-like properties through repressing Wnt/β-catenin signaling in lung adenocarcinoma cells
    Article Snippet: Subsequently, cells were co-transfected with 100 ng TOP/FOP flash vector (Promega Corporation), internal control pRL-TK Renilla luciferase vector (10 ng) and control mimic or miR-140-3p mimics (50 nM) using Lipofectamine ® 2000.



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    The suppressive effect of EFNA4 on dCK depends on the β-catenin signaling activation. A, protein level of β-catenin in in BxPC-3/GEM and PANC-1/GEM cells after hyperthermia examined by WB analysis (uncropped images of blots are provided as Supplementary material); B, transcriptional activity of β-catenin in cells after hyperthermia determined <t>by</t> <t>TOP</t> <t>Flash/FOP</t> Flash luciferase reporter assay; C, transcriptional activity of β-catenin in cells after EFNA4 overexpression and MSAB treatment determined by TOP Flash/FOP Flash luciferase reporter assay; D, protein levels of β-catenin and dCK in cells after EFNA4 overexpression and MSAB treatment determined by WB analysis (uncropped images of blots are provided as Supplementary material). Three biological replicates were performed. Differences were compared by the two-way ANOVA followed by Sidak's (A–B) or Tukey's (C–D) multiple comparison test. * p < 0.05.
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    The suppressive effect of EFNA4 on dCK depends on the β-catenin signaling activation. A, protein level of β-catenin in in BxPC-3/GEM and PANC-1/GEM cells after hyperthermia examined by WB analysis (uncropped images of blots are provided as Supplementary material); B, transcriptional activity of β-catenin in cells after hyperthermia determined <t>by</t> <t>TOP</t> <t>Flash/FOP</t> Flash luciferase reporter assay; C, transcriptional activity of β-catenin in cells after EFNA4 overexpression and MSAB treatment determined by TOP Flash/FOP Flash luciferase reporter assay; D, protein levels of β-catenin and dCK in cells after EFNA4 overexpression and MSAB treatment determined by WB analysis (uncropped images of blots are provided as Supplementary material). Three biological replicates were performed. Differences were compared by the two-way ANOVA followed by Sidak's (A–B) or Tukey's (C–D) multiple comparison test. * p < 0.05.
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    The suppressive effect of EFNA4 on dCK depends on the β-catenin signaling activation. A, protein level of β-catenin in in BxPC-3/GEM and PANC-1/GEM cells after hyperthermia examined by WB analysis (uncropped images of blots are provided as Supplementary material); B, transcriptional activity of β-catenin in cells after hyperthermia determined <t>by</t> <t>TOP</t> <t>Flash/FOP</t> Flash luciferase reporter assay; C, transcriptional activity of β-catenin in cells after EFNA4 overexpression and MSAB treatment determined by TOP Flash/FOP Flash luciferase reporter assay; D, protein levels of β-catenin and dCK in cells after EFNA4 overexpression and MSAB treatment determined by WB analysis (uncropped images of blots are provided as Supplementary material). Three biological replicates were performed. Differences were compared by the two-way ANOVA followed by Sidak's (A–B) or Tukey's (C–D) multiple comparison test. * p < 0.05.
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    EGFR-AS1 activates ACTN4-mediated WNT pathway in CC cells. a The knockdown efficacy of sh-ACTN4#1/2 on was tested by qRT-PCR in CC cells. b Expression levels of WNT pathway downstream genes in sh-ACTN4#1 transfected cells were detected by qRT-PCR in CC cells. c The effect of ACTN4 deficiency on the nuclear translocation of CTNNB1 (β-catenin) was detected by subcellular fractionation assay. d <t>TOP/FOP</t> flash assay was performed to measure the activity of WNT pathway upon ACTN4 knockdown. e , f Detection of mRNA and protein levels of WNT pathway downstream genes in CC cells transfected with sh-EGFR-AS1#1 was detected by qRT-PCR and western blot assays. g , h The nuclear translocation of CTNNB1 (β-catenin) was observed in sh-EGFR-AS1#1 group and sh-NC group. i Impact of EGFR-AS1 silencing on WNT pathway activity was detected. j – l Cell proliferation, apoptosis and invasion in cell transfected with sh-NC, sh-EGFR-AS1#1 and sh-EGFR-AS1#1 + LiCl were assessed by EdU, flow cytometry and transwell assays. **P < 0.01
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    EGFR-AS1 activates ACTN4-mediated WNT pathway in CC cells. a The knockdown efficacy of sh-ACTN4#1/2 on was tested by qRT-PCR in CC cells. b Expression levels of WNT pathway downstream genes in sh-ACTN4#1 transfected cells were detected by qRT-PCR in CC cells. c The effect of ACTN4 deficiency on the nuclear translocation of CTNNB1 (β-catenin) was detected by subcellular fractionation assay. d <t>TOP/FOP</t> flash assay was performed to measure the activity of WNT pathway upon ACTN4 knockdown. e , f Detection of mRNA and protein levels of WNT pathway downstream genes in CC cells transfected with sh-EGFR-AS1#1 was detected by qRT-PCR and western blot assays. g , h The nuclear translocation of CTNNB1 (β-catenin) was observed in sh-EGFR-AS1#1 group and sh-NC group. i Impact of EGFR-AS1 silencing on WNT pathway activity was detected. j – l Cell proliferation, apoptosis and invasion in cell transfected with sh-NC, sh-EGFR-AS1#1 and sh-EGFR-AS1#1 + LiCl were assessed by EdU, flow cytometry and transwell assays. **P < 0.01
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    EGFR-AS1 activates ACTN4-mediated WNT pathway in CC cells. a The knockdown efficacy of sh-ACTN4#1/2 on was tested by qRT-PCR in CC cells. b Expression levels of WNT pathway downstream genes in sh-ACTN4#1 transfected cells were detected by qRT-PCR in CC cells. c The effect of ACTN4 deficiency on the nuclear translocation of CTNNB1 (β-catenin) was detected by subcellular fractionation assay. d <t>TOP/FOP</t> flash assay was performed to measure the activity of WNT pathway upon ACTN4 knockdown. e , f Detection of mRNA and protein levels of WNT pathway downstream genes in CC cells transfected with sh-EGFR-AS1#1 was detected by qRT-PCR and western blot assays. g , h The nuclear translocation of CTNNB1 (β-catenin) was observed in sh-EGFR-AS1#1 group and sh-NC group. i Impact of EGFR-AS1 silencing on WNT pathway activity was detected. j – l Cell proliferation, apoptosis and invasion in cell transfected with sh-NC, sh-EGFR-AS1#1 and sh-EGFR-AS1#1 + LiCl were assessed by EdU, flow cytometry and transwell assays. **P < 0.01
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    Genechem fop flash luciferase reporter vector
    EGFR-AS1 activates ACTN4-mediated WNT pathway in CC cells. a The knockdown efficacy of sh-ACTN4#1/2 on was tested by qRT-PCR in CC cells. b Expression levels of WNT pathway downstream genes in sh-ACTN4#1 transfected cells were detected by qRT-PCR in CC cells. c The effect of ACTN4 deficiency on the nuclear translocation of CTNNB1 (β-catenin) was detected by subcellular fractionation assay. d <t>TOP/FOP</t> flash assay was performed to measure the activity of WNT pathway upon ACTN4 knockdown. e , f Detection of mRNA and protein levels of WNT pathway downstream genes in CC cells transfected with sh-EGFR-AS1#1 was detected by qRT-PCR and western blot assays. g , h The nuclear translocation of CTNNB1 (β-catenin) was observed in sh-EGFR-AS1#1 group and sh-NC group. i Impact of EGFR-AS1 silencing on WNT pathway activity was detected. j – l Cell proliferation, apoptosis and invasion in cell transfected with sh-NC, sh-EGFR-AS1#1 and sh-EGFR-AS1#1 + LiCl were assessed by EdU, flow cytometry and transwell assays. **P < 0.01
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    Image Search Results


    The suppressive effect of EFNA4 on dCK depends on the β-catenin signaling activation. A, protein level of β-catenin in in BxPC-3/GEM and PANC-1/GEM cells after hyperthermia examined by WB analysis (uncropped images of blots are provided as Supplementary material); B, transcriptional activity of β-catenin in cells after hyperthermia determined by TOP Flash/FOP Flash luciferase reporter assay; C, transcriptional activity of β-catenin in cells after EFNA4 overexpression and MSAB treatment determined by TOP Flash/FOP Flash luciferase reporter assay; D, protein levels of β-catenin and dCK in cells after EFNA4 overexpression and MSAB treatment determined by WB analysis (uncropped images of blots are provided as Supplementary material). Three biological replicates were performed. Differences were compared by the two-way ANOVA followed by Sidak's (A–B) or Tukey's (C–D) multiple comparison test. * p < 0.05.

    Journal: Heliyon

    Article Title: Hyperthermia improves gemcitabine sensitivity of pancreatic cancer cells by suppressing the EFNA4/β-catenin axis and activating dCK

    doi: 10.1016/j.heliyon.2024.e28488

    Figure Lengend Snippet: The suppressive effect of EFNA4 on dCK depends on the β-catenin signaling activation. A, protein level of β-catenin in in BxPC-3/GEM and PANC-1/GEM cells after hyperthermia examined by WB analysis (uncropped images of blots are provided as Supplementary material); B, transcriptional activity of β-catenin in cells after hyperthermia determined by TOP Flash/FOP Flash luciferase reporter assay; C, transcriptional activity of β-catenin in cells after EFNA4 overexpression and MSAB treatment determined by TOP Flash/FOP Flash luciferase reporter assay; D, protein levels of β-catenin and dCK in cells after EFNA4 overexpression and MSAB treatment determined by WB analysis (uncropped images of blots are provided as Supplementary material). Three biological replicates were performed. Differences were compared by the two-way ANOVA followed by Sidak's (A–B) or Tukey's (C–D) multiple comparison test. * p < 0.05.

    Article Snippet: To assess the β-catenin-mediated transcriptional activity of TCF/LEF, the TOP Flash reporter vector (D2501, Beyotime) was utilized, with the FOP Flash reporter vector containing mutant TCF/LEF binding sequences (D2503, Beyotime) serving as the NC.

    Techniques: Activation Assay, Activity Assay, Luciferase, Reporter Assay, Over Expression, Comparison

    EGFR-AS1 activates ACTN4-mediated WNT pathway in CC cells. a The knockdown efficacy of sh-ACTN4#1/2 on was tested by qRT-PCR in CC cells. b Expression levels of WNT pathway downstream genes in sh-ACTN4#1 transfected cells were detected by qRT-PCR in CC cells. c The effect of ACTN4 deficiency on the nuclear translocation of CTNNB1 (β-catenin) was detected by subcellular fractionation assay. d TOP/FOP flash assay was performed to measure the activity of WNT pathway upon ACTN4 knockdown. e , f Detection of mRNA and protein levels of WNT pathway downstream genes in CC cells transfected with sh-EGFR-AS1#1 was detected by qRT-PCR and western blot assays. g , h The nuclear translocation of CTNNB1 (β-catenin) was observed in sh-EGFR-AS1#1 group and sh-NC group. i Impact of EGFR-AS1 silencing on WNT pathway activity was detected. j – l Cell proliferation, apoptosis and invasion in cell transfected with sh-NC, sh-EGFR-AS1#1 and sh-EGFR-AS1#1 + LiCl were assessed by EdU, flow cytometry and transwell assays. **P < 0.01

    Journal: Biology Direct

    Article Title: H3K27ac-activated EGFR-AS1 promotes cell growth in cervical cancer through ACTN4-mediated WNT pathway

    doi: 10.1186/s13062-021-00315-5

    Figure Lengend Snippet: EGFR-AS1 activates ACTN4-mediated WNT pathway in CC cells. a The knockdown efficacy of sh-ACTN4#1/2 on was tested by qRT-PCR in CC cells. b Expression levels of WNT pathway downstream genes in sh-ACTN4#1 transfected cells were detected by qRT-PCR in CC cells. c The effect of ACTN4 deficiency on the nuclear translocation of CTNNB1 (β-catenin) was detected by subcellular fractionation assay. d TOP/FOP flash assay was performed to measure the activity of WNT pathway upon ACTN4 knockdown. e , f Detection of mRNA and protein levels of WNT pathway downstream genes in CC cells transfected with sh-EGFR-AS1#1 was detected by qRT-PCR and western blot assays. g , h The nuclear translocation of CTNNB1 (β-catenin) was observed in sh-EGFR-AS1#1 group and sh-NC group. i Impact of EGFR-AS1 silencing on WNT pathway activity was detected. j – l Cell proliferation, apoptosis and invasion in cell transfected with sh-NC, sh-EGFR-AS1#1 and sh-EGFR-AS1#1 + LiCl were assessed by EdU, flow cytometry and transwell assays. **P < 0.01

    Article Snippet: Besides, TOP/FOP-flash reporter vectors were available to assay the Wnt/β-catenin signaling activity as guided by manufacturer (Addgene, Cambridge, MA).

    Techniques: Quantitative RT-PCR, Expressing, Transfection, Translocation Assay, Fractionation, Activity Assay, Western Blot, Flow Cytometry