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rxr knockout hela cells  (AcceGen Biotechnology)


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    AcceGen Biotechnology rxr knockout hela cells
    FXR binds both IR1 motifs. (A) Schematic comparing FXR-RXR heterodimer and FXR homodimer, both bound to the two half-sites of IR1 DNA. Half sites are indicated in purple and orange. (B) Transcriptional activity of varying ratios of FXR-RXR using <t>RXR</t> <t>knockout</t> <t>HeLa</t> cells. Cells were treated with 10 µM OCA only and no RXR ligand. Data for luciferase assays are represented as the mean ± standard error of the mean of 2–3 independent experiments, where each experiment consists of three technical replicates. P values were calculated using two-way ANOVA with Dunnett’s multiple comparison test. GraphPad standard P -value statistical significance where present are: p > 0.1234 (ns); p < 0.032 (*); p < 0.0021 (**); p < 0.0002 (***); and p < 0.0001 (****). (C) IR1 DNA motif highlighting 5′ and 3′ half sites, as well as 5′ and 3′ IR1 motif sequences used in binding assays. (D) FP competition assay measuring binding of DNA motifs to FXR. 5′ and 3′ motifs are less efficient than the full IR1 motif in outcompeting fluorescein labeled IR1. N = 3, independent replicates, error bars represent the standard error of the mean. (E) Double-site and 5-site mutants of IR1 DNA, with substituted positions highlighted. (F) FP competition assay measuring binding of mutant DNA motifs to FXR. FXR binding to the 5′-site mutant is slightly reduced, but binding is abolished in the double-site mutant. (G) 5′-site and site-deletion mutants of IR1 DNA, with flanking nucleotides randomized ( r- 5′-site and r- site deletion). Substituted positions are highlighted, randomized nucleotides are represented by ‘NNN’. (H) FP competition assay measuring binding of mutant DNA motifs to FXR. The affinity for both motifs is reduced compared to IR1. (I) EMSA to assess binding of 5′ and 3′ motifs to FXR, RXR, and FXR-RXR. Lanes 2, 6, and 10 show that FXR binds all 3 DNA motifs. RXR binds the 5′ motif (Lane 7) and weakly to the 3′ motif . The experiment was performed twice; one replicate is shown here.
    Rxr Knockout Hela Cells, supplied by AcceGen Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rxr+knockout+hela+cells/HeLa/pmc12926912-111-0-6
    Average 94 stars, based on 2 article reviews
    rxr knockout hela cells - by Bioz Stars, 2026-08
    94/100 stars

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    1) Product Images from "DNA induces non-canonical dimerization of the farnesoid X receptor"

    Article Title: DNA induces non-canonical dimerization of the farnesoid X receptor

    Journal: Nucleic Acids Research

    doi: 10.1093/nar/gkag087

    FXR binds both IR1 motifs. (A) Schematic comparing FXR-RXR heterodimer and FXR homodimer, both bound to the two half-sites of IR1 DNA. Half sites are indicated in purple and orange. (B) Transcriptional activity of varying ratios of FXR-RXR using RXR knockout HeLa cells. Cells were treated with 10 µM OCA only and no RXR ligand. Data for luciferase assays are represented as the mean ± standard error of the mean of 2–3 independent experiments, where each experiment consists of three technical replicates. P values were calculated using two-way ANOVA with Dunnett’s multiple comparison test. GraphPad standard P -value statistical significance where present are: p > 0.1234 (ns); p < 0.032 (*); p < 0.0021 (**); p < 0.0002 (***); and p < 0.0001 (****). (C) IR1 DNA motif highlighting 5′ and 3′ half sites, as well as 5′ and 3′ IR1 motif sequences used in binding assays. (D) FP competition assay measuring binding of DNA motifs to FXR. 5′ and 3′ motifs are less efficient than the full IR1 motif in outcompeting fluorescein labeled IR1. N = 3, independent replicates, error bars represent the standard error of the mean. (E) Double-site and 5-site mutants of IR1 DNA, with substituted positions highlighted. (F) FP competition assay measuring binding of mutant DNA motifs to FXR. FXR binding to the 5′-site mutant is slightly reduced, but binding is abolished in the double-site mutant. (G) 5′-site and site-deletion mutants of IR1 DNA, with flanking nucleotides randomized ( r- 5′-site and r- site deletion). Substituted positions are highlighted, randomized nucleotides are represented by ‘NNN’. (H) FP competition assay measuring binding of mutant DNA motifs to FXR. The affinity for both motifs is reduced compared to IR1. (I) EMSA to assess binding of 5′ and 3′ motifs to FXR, RXR, and FXR-RXR. Lanes 2, 6, and 10 show that FXR binds all 3 DNA motifs. RXR binds the 5′ motif (Lane 7) and weakly to the 3′ motif . The experiment was performed twice; one replicate is shown here.
    Figure Legend Snippet: FXR binds both IR1 motifs. (A) Schematic comparing FXR-RXR heterodimer and FXR homodimer, both bound to the two half-sites of IR1 DNA. Half sites are indicated in purple and orange. (B) Transcriptional activity of varying ratios of FXR-RXR using RXR knockout HeLa cells. Cells were treated with 10 µM OCA only and no RXR ligand. Data for luciferase assays are represented as the mean ± standard error of the mean of 2–3 independent experiments, where each experiment consists of three technical replicates. P values were calculated using two-way ANOVA with Dunnett’s multiple comparison test. GraphPad standard P -value statistical significance where present are: p > 0.1234 (ns); p < 0.032 (*); p < 0.0021 (**); p < 0.0002 (***); and p < 0.0001 (****). (C) IR1 DNA motif highlighting 5′ and 3′ half sites, as well as 5′ and 3′ IR1 motif sequences used in binding assays. (D) FP competition assay measuring binding of DNA motifs to FXR. 5′ and 3′ motifs are less efficient than the full IR1 motif in outcompeting fluorescein labeled IR1. N = 3, independent replicates, error bars represent the standard error of the mean. (E) Double-site and 5-site mutants of IR1 DNA, with substituted positions highlighted. (F) FP competition assay measuring binding of mutant DNA motifs to FXR. FXR binding to the 5′-site mutant is slightly reduced, but binding is abolished in the double-site mutant. (G) 5′-site and site-deletion mutants of IR1 DNA, with flanking nucleotides randomized ( r- 5′-site and r- site deletion). Substituted positions are highlighted, randomized nucleotides are represented by ‘NNN’. (H) FP competition assay measuring binding of mutant DNA motifs to FXR. The affinity for both motifs is reduced compared to IR1. (I) EMSA to assess binding of 5′ and 3′ motifs to FXR, RXR, and FXR-RXR. Lanes 2, 6, and 10 show that FXR binds all 3 DNA motifs. RXR binds the 5′ motif (Lane 7) and weakly to the 3′ motif . The experiment was performed twice; one replicate is shown here.

    Techniques Used: Activity Assay, Knock-Out, Luciferase, Comparison, Binding Assay, Competitive Binding Assay, Labeling, Mutagenesis



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    rxr knockout hela cells  (AcceGen Biotechnology)
    94
    AcceGen Biotechnology rxr knockout hela cells
    FXR binds both IR1 motifs. (A) Schematic comparing FXR-RXR heterodimer and FXR homodimer, both bound to the two half-sites of IR1 DNA. Half sites are indicated in purple and orange. (B) Transcriptional activity of varying ratios of FXR-RXR using <t>RXR</t> <t>knockout</t> <t>HeLa</t> cells. Cells were treated with 10 µM OCA only and no RXR ligand. Data for luciferase assays are represented as the mean ± standard error of the mean of 2–3 independent experiments, where each experiment consists of three technical replicates. P values were calculated using two-way ANOVA with Dunnett’s multiple comparison test. GraphPad standard P -value statistical significance where present are: p > 0.1234 (ns); p < 0.032 (*); p < 0.0021 (**); p < 0.0002 (***); and p < 0.0001 (****). (C) IR1 DNA motif highlighting 5′ and 3′ half sites, as well as 5′ and 3′ IR1 motif sequences used in binding assays. (D) FP competition assay measuring binding of DNA motifs to FXR. 5′ and 3′ motifs are less efficient than the full IR1 motif in outcompeting fluorescein labeled IR1. N = 3, independent replicates, error bars represent the standard error of the mean. (E) Double-site and 5-site mutants of IR1 DNA, with substituted positions highlighted. (F) FP competition assay measuring binding of mutant DNA motifs to FXR. FXR binding to the 5′-site mutant is slightly reduced, but binding is abolished in the double-site mutant. (G) 5′-site and site-deletion mutants of IR1 DNA, with flanking nucleotides randomized ( r- 5′-site and r- site deletion). Substituted positions are highlighted, randomized nucleotides are represented by ‘NNN’. (H) FP competition assay measuring binding of mutant DNA motifs to FXR. The affinity for both motifs is reduced compared to IR1. (I) EMSA to assess binding of 5′ and 3′ motifs to FXR, RXR, and FXR-RXR. Lanes 2, 6, and 10 show that FXR binds all 3 DNA motifs. RXR binds the 5′ motif (Lane 7) and weakly to the 3′ motif . The experiment was performed twice; one replicate is shown here.
    Rxr Knockout Hela Cells, supplied by AcceGen Biotechnology, 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/rxr+knockout+hela+cells/HeLa/pmc12926912-111-0-6
    Average 94 stars, based on 1 article reviews
    rxr knockout hela cells - by Bioz Stars, 2026-08
    94/100 stars
    		  Buy from Supplier

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    FXR binds both IR1 motifs. (A) Schematic comparing FXR-RXR heterodimer and FXR homodimer, both bound to the two half-sites of IR1 DNA. Half sites are indicated in purple and orange. (B) Transcriptional activity of varying ratios of FXR-RXR using RXR knockout HeLa cells. Cells were treated with 10 µM OCA only and no RXR ligand. Data for luciferase assays are represented as the mean ± standard error of the mean of 2–3 independent experiments, where each experiment consists of three technical replicates. P values were calculated using two-way ANOVA with Dunnett’s multiple comparison test. GraphPad standard P -value statistical significance where present are: p > 0.1234 (ns); p < 0.032 (*); p < 0.0021 (**); p < 0.0002 (***); and p < 0.0001 (****). (C) IR1 DNA motif highlighting 5′ and 3′ half sites, as well as 5′ and 3′ IR1 motif sequences used in binding assays. (D) FP competition assay measuring binding of DNA motifs to FXR. 5′ and 3′ motifs are less efficient than the full IR1 motif in outcompeting fluorescein labeled IR1. N = 3, independent replicates, error bars represent the standard error of the mean. (E) Double-site and 5-site mutants of IR1 DNA, with substituted positions highlighted. (F) FP competition assay measuring binding of mutant DNA motifs to FXR. FXR binding to the 5′-site mutant is slightly reduced, but binding is abolished in the double-site mutant. (G) 5′-site and site-deletion mutants of IR1 DNA, with flanking nucleotides randomized ( r- 5′-site and r- site deletion). Substituted positions are highlighted, randomized nucleotides are represented by ‘NNN’. (H) FP competition assay measuring binding of mutant DNA motifs to FXR. The affinity for both motifs is reduced compared to IR1. (I) EMSA to assess binding of 5′ and 3′ motifs to FXR, RXR, and FXR-RXR. Lanes 2, 6, and 10 show that FXR binds all 3 DNA motifs. RXR binds the 5′ motif (Lane 7) and weakly to the 3′ motif . The experiment was performed twice; one replicate is shown here.

    Journal: Nucleic Acids Research

    Article Title: DNA induces non-canonical dimerization of the farnesoid X receptor

    doi: 10.1093/nar/gkag087

    Figure Lengend Snippet: FXR binds both IR1 motifs. (A) Schematic comparing FXR-RXR heterodimer and FXR homodimer, both bound to the two half-sites of IR1 DNA. Half sites are indicated in purple and orange. (B) Transcriptional activity of varying ratios of FXR-RXR using RXR knockout HeLa cells. Cells were treated with 10 µM OCA only and no RXR ligand. Data for luciferase assays are represented as the mean ± standard error of the mean of 2–3 independent experiments, where each experiment consists of three technical replicates. P values were calculated using two-way ANOVA with Dunnett’s multiple comparison test. GraphPad standard P -value statistical significance where present are: p > 0.1234 (ns); p < 0.032 (*); p < 0.0021 (**); p < 0.0002 (***); and p < 0.0001 (****). (C) IR1 DNA motif highlighting 5′ and 3′ half sites, as well as 5′ and 3′ IR1 motif sequences used in binding assays. (D) FP competition assay measuring binding of DNA motifs to FXR. 5′ and 3′ motifs are less efficient than the full IR1 motif in outcompeting fluorescein labeled IR1. N = 3, independent replicates, error bars represent the standard error of the mean. (E) Double-site and 5-site mutants of IR1 DNA, with substituted positions highlighted. (F) FP competition assay measuring binding of mutant DNA motifs to FXR. FXR binding to the 5′-site mutant is slightly reduced, but binding is abolished in the double-site mutant. (G) 5′-site and site-deletion mutants of IR1 DNA, with flanking nucleotides randomized ( r- 5′-site and r- site deletion). Substituted positions are highlighted, randomized nucleotides are represented by ‘NNN’. (H) FP competition assay measuring binding of mutant DNA motifs to FXR. The affinity for both motifs is reduced compared to IR1. (I) EMSA to assess binding of 5′ and 3′ motifs to FXR, RXR, and FXR-RXR. Lanes 2, 6, and 10 show that FXR binds all 3 DNA motifs. RXR binds the 5′ motif (Lane 7) and weakly to the 3′ motif . The experiment was performed twice; one replicate is shown here.

    Article Snippet: RXR-Knockout HeLa cells created using CRISPR-Cas (Accegen, NJ, USA) were grown and maintained in DMEM supplemented with 10% charcoal stripped FBS.

    Techniques: Activity Assay, Knock-Out, Luciferase, Comparison, Binding Assay, Competitive Binding Assay, Labeling, Mutagenesis