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  • 99
    New England Biolabs standard immunoblotting protocol
    Standard Immunoblotting Protocol, supplied by New England Biolabs, used in various techniques. Bioz Stars score: 99/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Millipore apc western blot
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    Upstate Biotechnology Inc immunoblot protocol
    Immunoblot Protocol, supplied by Upstate Biotechnology Inc, used in various techniques. Bioz Stars score: 85/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc western immunoblotting protocol
    Transcriptional regulation of the Glc-6-Pase promoter by apoA-IV acting through NR1D1. A , protein-protein interaction between exogenous apoA-IV-GFP and endogenous NR1D1 in nuclei of HepG2 cells. HepG2 cells were treated with r-h-apoA-IV-GFP (50 μg/ml) for 6 h. Nuclear proteins from the cells were then isolated and immunoprecipitated ( IP ) with anti-GFP and assayed for apoA-IV-GFP and NR1D1by <t>immunoblotting.</t> GFP not conjugated to apoA-IV was used as the negative control. B , ChIP assays to detect association of exogenous apoA-IV and endogenous NR1D1 with the proximal region of the human Glc-6-Pase promoter as described under “Experimental Procedures.” The mean ± S.E. of four samples is shown. *, p
    Western Immunoblotting Protocol, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 85/100, based on 19 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    MIKROGEN immunoblot protocol
    Transcriptional regulation of the Glc-6-Pase promoter by apoA-IV acting through NR1D1. A , protein-protein interaction between exogenous apoA-IV-GFP and endogenous NR1D1 in nuclei of HepG2 cells. HepG2 cells were treated with r-h-apoA-IV-GFP (50 μg/ml) for 6 h. Nuclear proteins from the cells were then isolated and immunoprecipitated ( IP ) with anti-GFP and assayed for apoA-IV-GFP and NR1D1by <t>immunoblotting.</t> GFP not conjugated to apoA-IV was used as the negative control. B , ChIP assays to detect association of exogenous apoA-IV and endogenous NR1D1 with the proximal region of the human Glc-6-Pase promoter as described under “Experimental Procedures.” The mean ± S.E. of four samples is shown. *, p
    Immunoblot Protocol, supplied by MIKROGEN, used in various techniques. Bioz Stars score: 85/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc immunoblotting protocol
    Transcriptional regulation of the Glc-6-Pase promoter by apoA-IV acting through NR1D1. A , protein-protein interaction between exogenous apoA-IV-GFP and endogenous NR1D1 in nuclei of HepG2 cells. HepG2 cells were treated with r-h-apoA-IV-GFP (50 μg/ml) for 6 h. Nuclear proteins from the cells were then isolated and immunoprecipitated ( IP ) with anti-GFP and assayed for apoA-IV-GFP and NR1D1by <t>immunoblotting.</t> GFP not conjugated to apoA-IV was used as the negative control. B , ChIP assays to detect association of exogenous apoA-IV and endogenous NR1D1 with the proximal region of the human Glc-6-Pase promoter as described under “Experimental Procedures.” The mean ± S.E. of four samples is shown. *, p
    Immunoblotting Protocol, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 88/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    MitoSciences immunoblotting protocol
    Transcriptional regulation of the Glc-6-Pase promoter by apoA-IV acting through NR1D1. A , protein-protein interaction between exogenous apoA-IV-GFP and endogenous NR1D1 in nuclei of HepG2 cells. HepG2 cells were treated with r-h-apoA-IV-GFP (50 μg/ml) for 6 h. Nuclear proteins from the cells were then isolated and immunoprecipitated ( IP ) with anti-GFP and assayed for apoA-IV-GFP and NR1D1by <t>immunoblotting.</t> GFP not conjugated to apoA-IV was used as the negative control. B , ChIP assays to detect association of exogenous apoA-IV and endogenous NR1D1 with the proximal region of the human Glc-6-Pase promoter as described under “Experimental Procedures.” The mean ± S.E. of four samples is shown. *, p
    Immunoblotting Protocol, supplied by MitoSciences, used in various techniques. Bioz Stars score: 88/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc mapk immunoblotting protocol
    Transcriptional regulation of the Glc-6-Pase promoter by apoA-IV acting through NR1D1. A , protein-protein interaction between exogenous apoA-IV-GFP and endogenous NR1D1 in nuclei of HepG2 cells. HepG2 cells were treated with r-h-apoA-IV-GFP (50 μg/ml) for 6 h. Nuclear proteins from the cells were then isolated and immunoprecipitated ( IP ) with anti-GFP and assayed for apoA-IV-GFP and NR1D1by <t>immunoblotting.</t> GFP not conjugated to apoA-IV was used as the negative control. B , ChIP assays to detect association of exogenous apoA-IV and endogenous NR1D1 with the proximal region of the human Glc-6-Pase promoter as described under “Experimental Procedures.” The mean ± S.E. of four samples is shown. *, p
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    GE Healthcare ecl western blotting protocol
    Transcriptional regulation of the Glc-6-Pase promoter by apoA-IV acting through NR1D1. A , protein-protein interaction between exogenous apoA-IV-GFP and endogenous NR1D1 in nuclei of HepG2 cells. HepG2 cells were treated with r-h-apoA-IV-GFP (50 μg/ml) for 6 h. Nuclear proteins from the cells were then isolated and immunoprecipitated ( IP ) with anti-GFP and assayed for apoA-IV-GFP and NR1D1by <t>immunoblotting.</t> GFP not conjugated to apoA-IV was used as the negative control. B , ChIP assays to detect association of exogenous apoA-IV and endogenous NR1D1 with the proximal region of the human Glc-6-Pase promoter as described under “Experimental Procedures.” The mean ± S.E. of four samples is shown. *, p
    Ecl Western Blotting Protocol, supplied by GE Healthcare, used in various techniques. Bioz Stars score: 89/100, based on 203 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    GE Healthcare ecl western blotting detection kit
    Transcriptional regulation of the Glc-6-Pase promoter by apoA-IV acting through NR1D1. A , protein-protein interaction between exogenous apoA-IV-GFP and endogenous NR1D1 in nuclei of HepG2 cells. HepG2 cells were treated with r-h-apoA-IV-GFP (50 μg/ml) for 6 h. Nuclear proteins from the cells were then isolated and immunoprecipitated ( IP ) with anti-GFP and assayed for apoA-IV-GFP and NR1D1by <t>immunoblotting.</t> GFP not conjugated to apoA-IV was used as the negative control. B , ChIP assays to detect association of exogenous apoA-IV and endogenous NR1D1 with the proximal region of the human Glc-6-Pase promoter as described under “Experimental Procedures.” The mean ± S.E. of four samples is shown. *, p
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    Bio-Rad ecl western blotting protocol
    Transcriptional regulation of the Glc-6-Pase promoter by apoA-IV acting through NR1D1. A , protein-protein interaction between exogenous apoA-IV-GFP and endogenous NR1D1 in nuclei of HepG2 cells. HepG2 cells were treated with r-h-apoA-IV-GFP (50 μg/ml) for 6 h. Nuclear proteins from the cells were then isolated and immunoprecipitated ( IP ) with anti-GFP and assayed for apoA-IV-GFP and NR1D1by <t>immunoblotting.</t> GFP not conjugated to apoA-IV was used as the negative control. B , ChIP assays to detect association of exogenous apoA-IV and endogenous NR1D1 with the proximal region of the human Glc-6-Pase promoter as described under “Experimental Procedures.” The mean ± S.E. of four samples is shown. *, p
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    Bio-Rad tesee western blot protocol
    Transcriptional regulation of the Glc-6-Pase promoter by apoA-IV acting through NR1D1. A , protein-protein interaction between exogenous apoA-IV-GFP and endogenous NR1D1 in nuclei of HepG2 cells. HepG2 cells were treated with r-h-apoA-IV-GFP (50 μg/ml) for 6 h. Nuclear proteins from the cells were then isolated and immunoprecipitated ( IP ) with anti-GFP and assayed for apoA-IV-GFP and NR1D1by <t>immunoblotting.</t> GFP not conjugated to apoA-IV was used as the negative control. B , ChIP assays to detect association of exogenous apoA-IV and endogenous NR1D1 with the proximal region of the human Glc-6-Pase promoter as described under “Experimental Procedures.” The mean ± S.E. of four samples is shown. *, p
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    Transcriptional regulation of the Glc-6-Pase promoter by apoA-IV acting through NR1D1. A , protein-protein interaction between exogenous apoA-IV-GFP and endogenous NR1D1 in nuclei of HepG2 cells. HepG2 cells were treated with r-h-apoA-IV-GFP (50 μg/ml) for 6 h. Nuclear proteins from the cells were then isolated and immunoprecipitated ( IP ) with anti-GFP and assayed for apoA-IV-GFP and NR1D1by <t>immunoblotting.</t> GFP not conjugated to apoA-IV was used as the negative control. B , ChIP assays to detect association of exogenous apoA-IV and endogenous NR1D1 with the proximal region of the human Glc-6-Pase promoter as described under “Experimental Procedures.” The mean ± S.E. of four samples is shown. *, p
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    Valiant htlv blot 2 4 western blot assay protocol
    Transcriptional regulation of the Glc-6-Pase promoter by apoA-IV acting through NR1D1. A , protein-protein interaction between exogenous apoA-IV-GFP and endogenous NR1D1 in nuclei of HepG2 cells. HepG2 cells were treated with r-h-apoA-IV-GFP (50 μg/ml) for 6 h. Nuclear proteins from the cells were then isolated and immunoprecipitated ( IP ) with anti-GFP and assayed for apoA-IV-GFP and NR1D1by <t>immunoblotting.</t> GFP not conjugated to apoA-IV was used as the negative control. B , ChIP assays to detect association of exogenous apoA-IV and endogenous NR1D1 with the proximal region of the human Glc-6-Pase promoter as described under “Experimental Procedures.” The mean ± S.E. of four samples is shown. *, p
    Htlv Blot 2 4 Western Blot Assay Protocol, supplied by Valiant, used in various techniques. Bioz Stars score: 93/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    GE Healthcare ecl plus western blotting detection system
    Transcriptional regulation of the Glc-6-Pase promoter by apoA-IV acting through NR1D1. A , protein-protein interaction between exogenous apoA-IV-GFP and endogenous NR1D1 in nuclei of HepG2 cells. HepG2 cells were treated with r-h-apoA-IV-GFP (50 μg/ml) for 6 h. Nuclear proteins from the cells were then isolated and immunoprecipitated ( IP ) with anti-GFP and assayed for apoA-IV-GFP and NR1D1by <t>immunoblotting.</t> GFP not conjugated to apoA-IV was used as the negative control. B , ChIP assays to detect association of exogenous apoA-IV and endogenous NR1D1 with the proximal region of the human Glc-6-Pase promoter as described under “Experimental Procedures.” The mean ± S.E. of four samples is shown. *, p
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    Beyotime ecl western blot protocol
    Transcriptional regulation of the Glc-6-Pase promoter by apoA-IV acting through NR1D1. A , protein-protein interaction between exogenous apoA-IV-GFP and endogenous NR1D1 in nuclei of HepG2 cells. HepG2 cells were treated with r-h-apoA-IV-GFP (50 μg/ml) for 6 h. Nuclear proteins from the cells were then isolated and immunoprecipitated ( IP ) with anti-GFP and assayed for apoA-IV-GFP and NR1D1by <t>immunoblotting.</t> GFP not conjugated to apoA-IV was used as the negative control. B , ChIP assays to detect association of exogenous apoA-IV and endogenous NR1D1 with the proximal region of the human Glc-6-Pase promoter as described under “Experimental Procedures.” The mean ± S.E. of four samples is shown. *, p
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    GE Healthcare ecltm western blotting detection reagents
    Transcriptional regulation of the Glc-6-Pase promoter by apoA-IV acting through NR1D1. A , protein-protein interaction between exogenous apoA-IV-GFP and endogenous NR1D1 in nuclei of HepG2 cells. HepG2 cells were treated with r-h-apoA-IV-GFP (50 μg/ml) for 6 h. Nuclear proteins from the cells were then isolated and immunoprecipitated ( IP ) with anti-GFP and assayed for apoA-IV-GFP and NR1D1by <t>immunoblotting.</t> GFP not conjugated to apoA-IV was used as the negative control. B , ChIP assays to detect association of exogenous apoA-IV and endogenous NR1D1 with the proximal region of the human Glc-6-Pase promoter as described under “Experimental Procedures.” The mean ± S.E. of four samples is shown. *, p
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    Millipore m2 α flag
    Transcriptional regulation of the Glc-6-Pase promoter by apoA-IV acting through NR1D1. A , protein-protein interaction between exogenous apoA-IV-GFP and endogenous NR1D1 in nuclei of HepG2 cells. HepG2 cells were treated with r-h-apoA-IV-GFP (50 μg/ml) for 6 h. Nuclear proteins from the cells were then isolated and immunoprecipitated ( IP ) with anti-GFP and assayed for apoA-IV-GFP and NR1D1by <t>immunoblotting.</t> GFP not conjugated to apoA-IV was used as the negative control. B , ChIP assays to detect association of exogenous apoA-IV and endogenous NR1D1 with the proximal region of the human Glc-6-Pase promoter as described under “Experimental Procedures.” The mean ± S.E. of four samples is shown. *, p
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    GE Healthcare chemiluminescence ecl western blotting protocol
    Transcriptional regulation of the Glc-6-Pase promoter by apoA-IV acting through NR1D1. A , protein-protein interaction between exogenous apoA-IV-GFP and endogenous NR1D1 in nuclei of HepG2 cells. HepG2 cells were treated with r-h-apoA-IV-GFP (50 μg/ml) for 6 h. Nuclear proteins from the cells were then isolated and immunoprecipitated ( IP ) with anti-GFP and assayed for apoA-IV-GFP and NR1D1by <t>immunoblotting.</t> GFP not conjugated to apoA-IV was used as the negative control. B , ChIP assays to detect association of exogenous apoA-IV and endogenous NR1D1 with the proximal region of the human Glc-6-Pase promoter as described under “Experimental Procedures.” The mean ± S.E. of four samples is shown. *, p
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    GE Healthcare ecl western blotting detection kit protocol
    Transcriptional regulation of the Glc-6-Pase promoter by apoA-IV acting through NR1D1. A , protein-protein interaction between exogenous apoA-IV-GFP and endogenous NR1D1 in nuclei of HepG2 cells. HepG2 cells were treated with r-h-apoA-IV-GFP (50 μg/ml) for 6 h. Nuclear proteins from the cells were then isolated and immunoprecipitated ( IP ) with anti-GFP and assayed for apoA-IV-GFP and NR1D1by <t>immunoblotting.</t> GFP not conjugated to apoA-IV was used as the negative control. B , ChIP assays to detect association of exogenous apoA-IV and endogenous NR1D1 with the proximal region of the human Glc-6-Pase promoter as described under “Experimental Procedures.” The mean ± S.E. of four samples is shown. *, p
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    Thermo Fisher westernbreeze chromogenic western blot immunodetection kit protocol
    Transcriptional regulation of the Glc-6-Pase promoter by apoA-IV acting through NR1D1. A , protein-protein interaction between exogenous apoA-IV-GFP and endogenous NR1D1 in nuclei of HepG2 cells. HepG2 cells were treated with r-h-apoA-IV-GFP (50 μg/ml) for 6 h. Nuclear proteins from the cells were then isolated and immunoprecipitated ( IP ) with anti-GFP and assayed for apoA-IV-GFP and NR1D1by <t>immunoblotting.</t> GFP not conjugated to apoA-IV was used as the negative control. B , ChIP assays to detect association of exogenous apoA-IV and endogenous NR1D1 with the proximal region of the human Glc-6-Pase promoter as described under “Experimental Procedures.” The mean ± S.E. of four samples is shown. *, p
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    Image Search Results


    Transcriptional regulation of the Glc-6-Pase promoter by apoA-IV acting through NR1D1. A , protein-protein interaction between exogenous apoA-IV-GFP and endogenous NR1D1 in nuclei of HepG2 cells. HepG2 cells were treated with r-h-apoA-IV-GFP (50 μg/ml) for 6 h. Nuclear proteins from the cells were then isolated and immunoprecipitated ( IP ) with anti-GFP and assayed for apoA-IV-GFP and NR1D1by immunoblotting. GFP not conjugated to apoA-IV was used as the negative control. B , ChIP assays to detect association of exogenous apoA-IV and endogenous NR1D1 with the proximal region of the human Glc-6-Pase promoter as described under “Experimental Procedures.” The mean ± S.E. of four samples is shown. *, p

    Journal: The Journal of Biological Chemistry

    Article Title: Apolipoprotein A-IV Reduces Hepatic Gluconeogenesis through Nuclear Receptor NR1D1 *

    doi: 10.1074/jbc.M113.511766

    Figure Lengend Snippet: Transcriptional regulation of the Glc-6-Pase promoter by apoA-IV acting through NR1D1. A , protein-protein interaction between exogenous apoA-IV-GFP and endogenous NR1D1 in nuclei of HepG2 cells. HepG2 cells were treated with r-h-apoA-IV-GFP (50 μg/ml) for 6 h. Nuclear proteins from the cells were then isolated and immunoprecipitated ( IP ) with anti-GFP and assayed for apoA-IV-GFP and NR1D1by immunoblotting. GFP not conjugated to apoA-IV was used as the negative control. B , ChIP assays to detect association of exogenous apoA-IV and endogenous NR1D1 with the proximal region of the human Glc-6-Pase promoter as described under “Experimental Procedures.” The mean ± S.E. of four samples is shown. *, p

    Article Snippet: Western blotting was performed as described in the Western immunoblotting protocol from Cell Signaling Technology.

    Techniques: Gas Chromatography, Isolation, Immunoprecipitation, Negative Control, Chromatin Immunoprecipitation

    ApoA-IV induces NR1D1 expression in primary mouse hepatocytes and HepG2 and HEK-293 cells. The cells were starved in DMEM with 1% BSA overnight and then treated with or without 20 μg/ml r-m-apoA-IV in mouse hepatocytes for the indicated times or 50 μg/ml r-h-apoA-IV in HepG2 and HEK-293 for 2 h. mRNA levels in primary mouse hepatocytes were quantitated by real-time RT-PCR and normalized to cyclophilin. NR1D1 protein levels were detected by Western immunoblotting with anti-NR1D1 antibody and then standardized against actin. The results are from three independent experiments with at least three samples each time. Data are presented as mean ± S.E. *, p

    Journal: The Journal of Biological Chemistry

    Article Title: Apolipoprotein A-IV Reduces Hepatic Gluconeogenesis through Nuclear Receptor NR1D1 *

    doi: 10.1074/jbc.M113.511766

    Figure Lengend Snippet: ApoA-IV induces NR1D1 expression in primary mouse hepatocytes and HepG2 and HEK-293 cells. The cells were starved in DMEM with 1% BSA overnight and then treated with or without 20 μg/ml r-m-apoA-IV in mouse hepatocytes for the indicated times or 50 μg/ml r-h-apoA-IV in HepG2 and HEK-293 for 2 h. mRNA levels in primary mouse hepatocytes were quantitated by real-time RT-PCR and normalized to cyclophilin. NR1D1 protein levels were detected by Western immunoblotting with anti-NR1D1 antibody and then standardized against actin. The results are from three independent experiments with at least three samples each time. Data are presented as mean ± S.E. *, p

    Article Snippet: Western blotting was performed as described in the Western immunoblotting protocol from Cell Signaling Technology.

    Techniques: Expressing, Quantitative RT-PCR, Western Blot