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pgl3  (Addgene inc)


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    Addgene inc pgl3
    Figure 2. HNF4α regulates the promoter of the RARβ gene in HepG2 cells. HepG2 cells in 24-well plates were co-transfected for 24 h with a fragment of the human RARβ promoter expanding from −1.7 kbp from transcription start site to +0.217 kpb, as the full length promoter construct, in <t>pGL3-</t> basic-luc vector together with pRLTK plasmid containing Renilla-luc, as the control, and with either human HNF4α, RARα/RXRα, or all three transcription factors, and then treated further either without (A) or with RA for 1 to 24 h, after which the cells were collected to assay for luciferase activity. HNF4α alone or with RARα/RXRα suppressed the promoter activity of the human RARβ gene in the cells treated without RA (A), but upregulated the promoter when the cells were treated with RA following transfection (B). HNF4α regulates the promoter of the mouse RARβ gene in HepG2 cells (C). It suppresses the promoter activity of the mouse gene (empty bars in C) in HepG2 cells treated with the vehicle, but it increases the promoter activity in the cells treated with RA (black bar in C).
    Pgl3, supplied by Addgene inc, used in various techniques. Bioz Stars score: 92/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Hepatocyte Nuclear Factor 4α (HNF4α) Plays a Controlling Role in Expression of the Retinoic Acid Receptor β ( RARβ ) Gene in Hepatocytes."

    Article Title: Hepatocyte Nuclear Factor 4α (HNF4α) Plays a Controlling Role in Expression of the Retinoic Acid Receptor β ( RARβ ) Gene in Hepatocytes.

    Journal: International journal of molecular sciences

    doi: 10.3390/ijms24108608

    Figure 2. HNF4α regulates the promoter of the RARβ gene in HepG2 cells. HepG2 cells in 24-well plates were co-transfected for 24 h with a fragment of the human RARβ promoter expanding from −1.7 kbp from transcription start site to +0.217 kpb, as the full length promoter construct, in pGL3- basic-luc vector together with pRLTK plasmid containing Renilla-luc, as the control, and with either human HNF4α, RARα/RXRα, or all three transcription factors, and then treated further either without (A) or with RA for 1 to 24 h, after which the cells were collected to assay for luciferase activity. HNF4α alone or with RARα/RXRα suppressed the promoter activity of the human RARβ gene in the cells treated without RA (A), but upregulated the promoter when the cells were treated with RA following transfection (B). HNF4α regulates the promoter of the mouse RARβ gene in HepG2 cells (C). It suppresses the promoter activity of the mouse gene (empty bars in C) in HepG2 cells treated with the vehicle, but it increases the promoter activity in the cells treated with RA (black bar in C).
    Figure Legend Snippet: Figure 2. HNF4α regulates the promoter of the RARβ gene in HepG2 cells. HepG2 cells in 24-well plates were co-transfected for 24 h with a fragment of the human RARβ promoter expanding from −1.7 kbp from transcription start site to +0.217 kpb, as the full length promoter construct, in pGL3- basic-luc vector together with pRLTK plasmid containing Renilla-luc, as the control, and with either human HNF4α, RARα/RXRα, or all three transcription factors, and then treated further either without (A) or with RA for 1 to 24 h, after which the cells were collected to assay for luciferase activity. HNF4α alone or with RARα/RXRα suppressed the promoter activity of the human RARβ gene in the cells treated without RA (A), but upregulated the promoter when the cells were treated with RA following transfection (B). HNF4α regulates the promoter of the mouse RARβ gene in HepG2 cells (C). It suppresses the promoter activity of the mouse gene (empty bars in C) in HepG2 cells treated with the vehicle, but it increases the promoter activity in the cells treated with RA (black bar in C).

    Techniques Used: Transfection, Construct, Plasmid Preparation, Control, Luciferase, Activity Assay

    Figure 6. Mutation of the critical residues present in the ligand binding domain of human HNF4α suppresses transcription activation of the promoters of human APOC3 and CYP2C9 genes. HepG2 cells were co-transfected with either the pGL3-b-hApoC3 (A–C) or pGL3-b-hCYP2C9 (D–F) promoter construct together with either hHNF4α, RARα/RXRα, or all three transcription factors, and then treated with either vehicle or 1 µM RA for 24 h, after which the cells were assayed for their luciferase activity. The effects of the individual mutant residues in the ligand binding domain of the human HNF4α compared with WT HNF4α on the promoter activity of APOC3 (B) or CYP2C9 (E) in HepG2 cells treated with either vehicle or 1 µM RA for 24 h. The endogenous HNF4α transcriptional activity toward APOC3 (C) and CYP2C9 (F) promoters was assessed in HepG2 cells with or without the addition of human HNF4α mutants. Data from each bar represent the mean of n = 3 wells ± SD. HNF4α mutant #’s are as follows: (1) S190K, (2) 191MK, (3) R221G, (4) L228K, (5) L229K, (6) R235G, (7) I347K, and (8) I355K.
    Figure Legend Snippet: Figure 6. Mutation of the critical residues present in the ligand binding domain of human HNF4α suppresses transcription activation of the promoters of human APOC3 and CYP2C9 genes. HepG2 cells were co-transfected with either the pGL3-b-hApoC3 (A–C) or pGL3-b-hCYP2C9 (D–F) promoter construct together with either hHNF4α, RARα/RXRα, or all three transcription factors, and then treated with either vehicle or 1 µM RA for 24 h, after which the cells were assayed for their luciferase activity. The effects of the individual mutant residues in the ligand binding domain of the human HNF4α compared with WT HNF4α on the promoter activity of APOC3 (B) or CYP2C9 (E) in HepG2 cells treated with either vehicle or 1 µM RA for 24 h. The endogenous HNF4α transcriptional activity toward APOC3 (C) and CYP2C9 (F) promoters was assessed in HepG2 cells with or without the addition of human HNF4α mutants. Data from each bar represent the mean of n = 3 wells ± SD. HNF4α mutant #’s are as follows: (1) S190K, (2) 191MK, (3) R221G, (4) L228K, (5) L229K, (6) R235G, (7) I347K, and (8) I355K.

    Techniques Used: Mutagenesis, Ligand Binding Assay, Activation Assay, Transfection, Construct, Luciferase, Activity Assay

    Figure 7. Mutation of the critical amino acid residues present in the ligand binding domain of human HNF4α suppresses transcription activation of the promoters of human CYP26A1 and RARβ genes in HepG2 cells treated with RA. HepG2 cells grown in 24-well plates were co-transfected with either pGL3-b-hCYP26A1 (A) or pGL3-b-hRARβ (B) promoters, each with pRLTK as the control, together with either wildtype (WT) HNF4α or its individual mutants (Mutant # 1 to 8), and then treated with either vehicle or 1 µM RA for 24 h, after which the cells were assayed for luciferase activity. Data from each bar represent the mean of n = 3 wells ± SD. HNF4α mutant #’s are as follows: (1) S190K, (2) 191MK, (3) R221G, (4) L228K, (5) L229K, (6) R235G, (7) I347K, and (8) I355K.
    Figure Legend Snippet: Figure 7. Mutation of the critical amino acid residues present in the ligand binding domain of human HNF4α suppresses transcription activation of the promoters of human CYP26A1 and RARβ genes in HepG2 cells treated with RA. HepG2 cells grown in 24-well plates were co-transfected with either pGL3-b-hCYP26A1 (A) or pGL3-b-hRARβ (B) promoters, each with pRLTK as the control, together with either wildtype (WT) HNF4α or its individual mutants (Mutant # 1 to 8), and then treated with either vehicle or 1 µM RA for 24 h, after which the cells were assayed for luciferase activity. Data from each bar represent the mean of n = 3 wells ± SD. HNF4α mutant #’s are as follows: (1) S190K, (2) 191MK, (3) R221G, (4) L228K, (5) L229K, (6) R235G, (7) I347K, and (8) I355K.

    Techniques Used: Mutagenesis, Ligand Binding Assay, Activation Assay, Transfection, Control, Luciferase, Activity Assay

    Related Articles

    Luciferase:

    Article Title: Single Cell Multimodal Analyses Reveal Epigenomic and Transcriptomic Basis for Birth Defects in Maternal Diabetes
    Article Snippet: Luciferase assays were conducted 8 hours after stimulation using a dual luciferase kit (Dual-Luciferase ® Reporter Assay System, Promega) according to manufacturer’s protocol. .. Luciferase activity was measured in SpectraMax MiniMax 300 imaging cytometer with SoftMax Pro6, Version 6.4 (Molecular Devices). pGL3-Basic-hCYP26A1-FL-luciferase (Addgene, #135566) 52 was used as a positive control in the assay system. ..

    Article Title: Transcriptional Inhibition of MicroRNA miR-122 by Small Molecules Reduces Hepatitis C Virus Replication in Liver Cells.
    Article Snippet: MicroRNAs (miRNAs) are noncoding RNA molecules of 22−24 nucleotides that are estimated to regulate thousands of genes in humans, and their dysregulation has been implicated in many diseases.. MicroRNA-122 (miR-122) is the most abundant miRNA in the liver and has been linked to the development of hepatocellular carcinoma and hepatitis C virus (HCV) infection.. Its role in these diseases renders miR-122 a potential target for small-molecule therapeutics.

    Activity Assay:

    Article Title: Single Cell Multimodal Analyses Reveal Epigenomic and Transcriptomic Basis for Birth Defects in Maternal Diabetes
    Article Snippet: Luciferase assays were conducted 8 hours after stimulation using a dual luciferase kit (Dual-Luciferase ® Reporter Assay System, Promega) according to manufacturer’s protocol. .. Luciferase activity was measured in SpectraMax MiniMax 300 imaging cytometer with SoftMax Pro6, Version 6.4 (Molecular Devices). pGL3-Basic-hCYP26A1-FL-luciferase (Addgene, #135566) 52 was used as a positive control in the assay system. ..

    Article Title: Single Cell Multimodal Analyses Reveal Epigenomic and Transcriptomic Basis for Birth Defects in Maternal Diabetes
    Article Snippet: Luciferase assays were conducted 8 hours after stimulation using a dual luciferase kit (Dual-Luciferase® Reporter Assay System, Promega) according to manufacturer’s protocol. .. Luciferase activity was measured in SpectraMax MiniMax 300 imaging cytometer with SoftMax Pro6, Version 6.4 (Molecular Devices). pGL3-Basic-hCYP26A1-FL-luciferase (Addgene, #135566) was used as a positive control in the assay system. ..

    Imaging:

    Article Title: Single Cell Multimodal Analyses Reveal Epigenomic and Transcriptomic Basis for Birth Defects in Maternal Diabetes
    Article Snippet: Luciferase assays were conducted 8 hours after stimulation using a dual luciferase kit (Dual-Luciferase ® Reporter Assay System, Promega) according to manufacturer’s protocol. .. Luciferase activity was measured in SpectraMax MiniMax 300 imaging cytometer with SoftMax Pro6, Version 6.4 (Molecular Devices). pGL3-Basic-hCYP26A1-FL-luciferase (Addgene, #135566) 52 was used as a positive control in the assay system. ..

    Article Title: Single Cell Multimodal Analyses Reveal Epigenomic and Transcriptomic Basis for Birth Defects in Maternal Diabetes
    Article Snippet: Luciferase assays were conducted 8 hours after stimulation using a dual luciferase kit (Dual-Luciferase® Reporter Assay System, Promega) according to manufacturer’s protocol. .. Luciferase activity was measured in SpectraMax MiniMax 300 imaging cytometer with SoftMax Pro6, Version 6.4 (Molecular Devices). pGL3-Basic-hCYP26A1-FL-luciferase (Addgene, #135566) was used as a positive control in the assay system. ..

    Cytometry:

    Article Title: Single Cell Multimodal Analyses Reveal Epigenomic and Transcriptomic Basis for Birth Defects in Maternal Diabetes
    Article Snippet: Luciferase assays were conducted 8 hours after stimulation using a dual luciferase kit (Dual-Luciferase ® Reporter Assay System, Promega) according to manufacturer’s protocol. .. Luciferase activity was measured in SpectraMax MiniMax 300 imaging cytometer with SoftMax Pro6, Version 6.4 (Molecular Devices). pGL3-Basic-hCYP26A1-FL-luciferase (Addgene, #135566) 52 was used as a positive control in the assay system. ..

    Article Title: Single Cell Multimodal Analyses Reveal Epigenomic and Transcriptomic Basis for Birth Defects in Maternal Diabetes
    Article Snippet: Luciferase assays were conducted 8 hours after stimulation using a dual luciferase kit (Dual-Luciferase® Reporter Assay System, Promega) according to manufacturer’s protocol. .. Luciferase activity was measured in SpectraMax MiniMax 300 imaging cytometer with SoftMax Pro6, Version 6.4 (Molecular Devices). pGL3-Basic-hCYP26A1-FL-luciferase (Addgene, #135566) was used as a positive control in the assay system. ..

    Positive Control:

    Article Title: Single Cell Multimodal Analyses Reveal Epigenomic and Transcriptomic Basis for Birth Defects in Maternal Diabetes
    Article Snippet: Luciferase assays were conducted 8 hours after stimulation using a dual luciferase kit (Dual-Luciferase ® Reporter Assay System, Promega) according to manufacturer’s protocol. .. Luciferase activity was measured in SpectraMax MiniMax 300 imaging cytometer with SoftMax Pro6, Version 6.4 (Molecular Devices). pGL3-Basic-hCYP26A1-FL-luciferase (Addgene, #135566) 52 was used as a positive control in the assay system. ..

    Article Title: Single Cell Multimodal Analyses Reveal Epigenomic and Transcriptomic Basis for Birth Defects in Maternal Diabetes
    Article Snippet: Luciferase assays were conducted 8 hours after stimulation using a dual luciferase kit (Dual-Luciferase® Reporter Assay System, Promega) according to manufacturer’s protocol. .. Luciferase activity was measured in SpectraMax MiniMax 300 imaging cytometer with SoftMax Pro6, Version 6.4 (Molecular Devices). pGL3-Basic-hCYP26A1-FL-luciferase (Addgene, #135566) was used as a positive control in the assay system. ..

    Plasmid Preparation:

    Article Title: Hepatocyte Nuclear Factor 4α (HNF4α) Plays a Controlling Role in Expression of the Retinoic Acid Receptor β ( RARβ ) Gene in Hepatocytes.
    Article Snippet: .. Construction of the plasmid vectors including pGL3-Basic-hCYP26A1-E4-luc (submitted to addgene.org), pGL3-Basic-hRARβp-luc (human RARβ2 promoter), pGL3-BasichCYP2C9p-luc, pcDNNA3.1-hRARα.hRXRα (submitted to addgene.org), and pcDNA3.1hHNF4α were reported previously [18,20,33,34,43]. ..

    Article Title: Hepatocyte Nuclear Factor 4α (HNF4α) Plays a Controlling Role in Expression of the Retinoic Acid Receptor β ( RARβ ) Gene in Hepatocytes
    Article Snippet: .. Construction of the plasmid vectors including p GL3-Basic-hCYP26A1-E4-luc (submitted to addgene.org), p GL3-Basic-hRARβp-luc (human RARβ2 promoter), p GL3-Basic-hCYP2C9p-luc, p cDNNA3.1-hRARα.hRXRα (submitted to addgene.org), and p cDNA3.1-hHNF4α were reported previously [ , , , , ]. ..

    Incubation:

    Article Title: Transcriptional Inhibition of MicroRNA miR-122 by Small Molecules Reduces Hepatitis C Virus Replication in Liver Cells.
    Article Snippet: MicroRNAs (miRNAs) are noncoding RNA molecules of 22−24 nucleotides that are estimated to regulate thousands of genes in humans, and their dysregulation has been implicated in many diseases.. MicroRNA-122 (miR-122) is the most abundant miRNA in the liver and has been linked to the development of hepatocellular carcinoma and hepatitis C virus (HCV) infection.. Its role in these diseases renders miR-122 a potential target for small-molecule therapeutics.

    Transfection:

    Article Title: Transcriptional Inhibition of MicroRNA miR-122 by Small Molecules Reduces Hepatitis C Virus Replication in Liver Cells.
    Article Snippet: MicroRNAs (miRNAs) are noncoding RNA molecules of 22−24 nucleotides that are estimated to regulate thousands of genes in humans, and their dysregulation has been implicated in many diseases.. MicroRNA-122 (miR-122) is the most abundant miRNA in the liver and has been linked to the development of hepatocellular carcinoma and hepatitis C virus (HCV) infection.. Its role in these diseases renders miR-122 a potential target for small-molecule therapeutics.

    Expressing:

    Article Title: Transcriptional Inhibition of MicroRNA miR-122 by Small Molecules Reduces Hepatitis C Virus Replication in Liver Cells.
    Article Snippet: MicroRNAs (miRNAs) are noncoding RNA molecules of 22−24 nucleotides that are estimated to regulate thousands of genes in humans, and their dysregulation has been implicated in many diseases.. MicroRNA-122 (miR-122) is the most abundant miRNA in the liver and has been linked to the development of hepatocellular carcinoma and hepatitis C virus (HCV) infection.. Its role in these diseases renders miR-122 a potential target for small-molecule therapeutics.

    Control:

    Article Title: Transcriptional Inhibition of MicroRNA miR-122 by Small Molecules Reduces Hepatitis C Virus Replication in Liver Cells.
    Article Snippet: MicroRNAs (miRNAs) are noncoding RNA molecules of 22−24 nucleotides that are estimated to regulate thousands of genes in humans, and their dysregulation has been implicated in many diseases.. MicroRNA-122 (miR-122) is the most abundant miRNA in the liver and has been linked to the development of hepatocellular carcinoma and hepatitis C virus (HCV) infection.. Its role in these diseases renders miR-122 a potential target for small-molecule therapeutics.

    Concentration Assay:

    Article Title: Transcriptional Inhibition of MicroRNA miR-122 by Small Molecules Reduces Hepatitis C Virus Replication in Liver Cells.
    Article Snippet: MicroRNAs (miRNAs) are noncoding RNA molecules of 22−24 nucleotides that are estimated to regulate thousands of genes in humans, and their dysregulation has been implicated in many diseases.. MicroRNA-122 (miR-122) is the most abundant miRNA in the liver and has been linked to the development of hepatocellular carcinoma and hepatitis C virus (HCV) infection.. Its role in these diseases renders miR-122 a potential target for small-molecule therapeutics.



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    Estrogen promotes HNRNPAB expression via SP1. (A) Immunoblot assessment of HNRNPAB in 2 human normal breast epithelial cell lines and 11 human BC cell lines. (B) CPTAC database analyzed the relative HNRNPAB and ERα protein level in 105 BC patients. P value was determined by Pearson correlation analysis. (C) The relative expression of TFF1 and HNRNPAB mRNAs after stimulated with 10 nM E 2 in estrogen-deprived MCF-7 cells for 48 h analyzed by qRT-PCR. (D) Immunoblot assessment of HNRNPAB expression in MCF-7 with or without 10 nM E 2 in estrogen-deprived MCF-7 cells for 72 h, or in short-term oestrogen deprivation (STED) MCF-7 cells for 7 days and parental cells. (E) The schematic of HNRNPAB promoter region sequence selected from the transcription start site of -2 kb~+100 bp. (F) MCF-7 cells were transfected with <t>pGL3</t> basic reporter vector containing HNRNPAB promoter, and pRL-TK reporter control vector containing luciferase activity, as well as control siRNA or different siRNA sequences of JUN , FOS , FOXA1 and SP1 . The relative fluorescence activity was measured. (G) CPTAC database analyzed the relative HNRNPAB and SP1 protein level in 68 ER+ BC patients. P value was determined by Pearson correlation analysis. (H) 293T cells were transfected with control or SP1 vector, and pRL-TK reporter control vector containing luciferase activity, as well as pGL3 basic reporter vector containing different regions of HNRNPAB promoter. The relative fluorescence activity was measured. (I) The schematic of three predicted conserved SP1 binding sites on the upstream -425 bp~+100 bp regions of the human HNRNPAB gene. Red boxes represent the predicted SP1 binding sites. (J) The DNA regions enriched by SP1 in ChIP assay were verified by PCR. (K) 293T cells were transfected with control or SP1 vector, and pRL-TK reporter control vector containing luciferase activity, as well as pGL3 basic reporter vector or containing “b” or “b” mutant regions. The relative fluorescence activity was measured. (L) The relative expression of SP1 and HNRNPAB mRNAs in MCF-7 cells bearing control or SP1 shRNAs analyzed by qRT-PCR. (M) Immunoblot assessment of SP1 and HNRNPAB expression in MCF-7 cells with or without SP1 shRNAs in the presence or absence of 10 nM E 2 for 48 h. Data was shown as mean ± S.D. from three independent experiments. Unpaired two-tailed Student's t test (C, H, K) and one-way ANOVA followed by Tukey's multiple comparisons test (F, L). ns, P >0.05; ***, P <0.001; ****, P <0.0001.
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    Image Search Results


    Estrogen promotes HNRNPAB expression via SP1. (A) Immunoblot assessment of HNRNPAB in 2 human normal breast epithelial cell lines and 11 human BC cell lines. (B) CPTAC database analyzed the relative HNRNPAB and ERα protein level in 105 BC patients. P value was determined by Pearson correlation analysis. (C) The relative expression of TFF1 and HNRNPAB mRNAs after stimulated with 10 nM E 2 in estrogen-deprived MCF-7 cells for 48 h analyzed by qRT-PCR. (D) Immunoblot assessment of HNRNPAB expression in MCF-7 with or without 10 nM E 2 in estrogen-deprived MCF-7 cells for 72 h, or in short-term oestrogen deprivation (STED) MCF-7 cells for 7 days and parental cells. (E) The schematic of HNRNPAB promoter region sequence selected from the transcription start site of -2 kb~+100 bp. (F) MCF-7 cells were transfected with pGL3 basic reporter vector containing HNRNPAB promoter, and pRL-TK reporter control vector containing luciferase activity, as well as control siRNA or different siRNA sequences of JUN , FOS , FOXA1 and SP1 . The relative fluorescence activity was measured. (G) CPTAC database analyzed the relative HNRNPAB and SP1 protein level in 68 ER+ BC patients. P value was determined by Pearson correlation analysis. (H) 293T cells were transfected with control or SP1 vector, and pRL-TK reporter control vector containing luciferase activity, as well as pGL3 basic reporter vector containing different regions of HNRNPAB promoter. The relative fluorescence activity was measured. (I) The schematic of three predicted conserved SP1 binding sites on the upstream -425 bp~+100 bp regions of the human HNRNPAB gene. Red boxes represent the predicted SP1 binding sites. (J) The DNA regions enriched by SP1 in ChIP assay were verified by PCR. (K) 293T cells were transfected with control or SP1 vector, and pRL-TK reporter control vector containing luciferase activity, as well as pGL3 basic reporter vector or containing “b” or “b” mutant regions. The relative fluorescence activity was measured. (L) The relative expression of SP1 and HNRNPAB mRNAs in MCF-7 cells bearing control or SP1 shRNAs analyzed by qRT-PCR. (M) Immunoblot assessment of SP1 and HNRNPAB expression in MCF-7 cells with or without SP1 shRNAs in the presence or absence of 10 nM E 2 for 48 h. Data was shown as mean ± S.D. from three independent experiments. Unpaired two-tailed Student's t test (C, H, K) and one-way ANOVA followed by Tukey's multiple comparisons test (F, L). ns, P >0.05; ***, P <0.001; ****, P <0.0001.

    Journal: International Journal of Biological Sciences

    Article Title: The Interaction of CircESR1 and HNRNPAB Regulates Cell Cycle Transition of Breast Cancer Cell

    doi: 10.7150/ijbs.126014

    Figure Lengend Snippet: Estrogen promotes HNRNPAB expression via SP1. (A) Immunoblot assessment of HNRNPAB in 2 human normal breast epithelial cell lines and 11 human BC cell lines. (B) CPTAC database analyzed the relative HNRNPAB and ERα protein level in 105 BC patients. P value was determined by Pearson correlation analysis. (C) The relative expression of TFF1 and HNRNPAB mRNAs after stimulated with 10 nM E 2 in estrogen-deprived MCF-7 cells for 48 h analyzed by qRT-PCR. (D) Immunoblot assessment of HNRNPAB expression in MCF-7 with or without 10 nM E 2 in estrogen-deprived MCF-7 cells for 72 h, or in short-term oestrogen deprivation (STED) MCF-7 cells for 7 days and parental cells. (E) The schematic of HNRNPAB promoter region sequence selected from the transcription start site of -2 kb~+100 bp. (F) MCF-7 cells were transfected with pGL3 basic reporter vector containing HNRNPAB promoter, and pRL-TK reporter control vector containing luciferase activity, as well as control siRNA or different siRNA sequences of JUN , FOS , FOXA1 and SP1 . The relative fluorescence activity was measured. (G) CPTAC database analyzed the relative HNRNPAB and SP1 protein level in 68 ER+ BC patients. P value was determined by Pearson correlation analysis. (H) 293T cells were transfected with control or SP1 vector, and pRL-TK reporter control vector containing luciferase activity, as well as pGL3 basic reporter vector containing different regions of HNRNPAB promoter. The relative fluorescence activity was measured. (I) The schematic of three predicted conserved SP1 binding sites on the upstream -425 bp~+100 bp regions of the human HNRNPAB gene. Red boxes represent the predicted SP1 binding sites. (J) The DNA regions enriched by SP1 in ChIP assay were verified by PCR. (K) 293T cells were transfected with control or SP1 vector, and pRL-TK reporter control vector containing luciferase activity, as well as pGL3 basic reporter vector or containing “b” or “b” mutant regions. The relative fluorescence activity was measured. (L) The relative expression of SP1 and HNRNPAB mRNAs in MCF-7 cells bearing control or SP1 shRNAs analyzed by qRT-PCR. (M) Immunoblot assessment of SP1 and HNRNPAB expression in MCF-7 cells with or without SP1 shRNAs in the presence or absence of 10 nM E 2 for 48 h. Data was shown as mean ± S.D. from three independent experiments. Unpaired two-tailed Student's t test (C, H, K) and one-way ANOVA followed by Tukey's multiple comparisons test (F, L). ns, P >0.05; ***, P <0.001; ****, P <0.0001.

    Article Snippet: For transcription factor mediated HNRNPAB expression, 0.2 μg pGL3 Basic luciferase reporter (RRID: Addgene_48743), 50 nmol JUN or FOS or FOXA1 or SP1 siRNAs and 0.02 μg pRL-TK plasmid (RRID: Addgene_11313) were transfected into cells using Lipofectamine 2000 (Invitrogen, Carlsbad, USA).

    Techniques: Expressing, Western Blot, Quantitative RT-PCR, Sequencing, Transfection, Plasmid Preparation, Control, Luciferase, Activity Assay, Fluorescence, Binding Assay, Mutagenesis, Two Tailed Test