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plasmid p gl3-basic (Promega)

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Promega plasmid p gl3-basic
Plasmid P Gl3 Basic, 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/plasmid+p+gl3-basic/gl3+basic+vector/pmc11739467-458-21-24
Average 90 stars, based on 1 article reviews

plasmid p gl3-basic - by Bioz Stars, 2026-09

90/100 stars

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Article Title: An atlas of neuropathic pain-associated molecular pathological characteristics in the mouse spinal cord
Article Snippet: To identify the promoter activity of Penk , HEK293T cells cultured in the 12-well culture plates were transfected with 0.5 μg plasmid p GL3-basic (Promega, Madison, WI, USA) or p GL3- Penk -promoter constructed by Genecreate (Wuhan Genecreate Biotechnology Engineering Co., Ltd., Wuhan, China) that encompasses a 1500 bp region preceding the transcription start site.

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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 p GL3-basic-luc vector together with p RLTK 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).

Journal: International Journal of Molecular Sciences

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

doi: 10.3390/ijms24108608

Figure Lengend Snippet: 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 p GL3-basic-luc vector together with p RLTK 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).

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 [ , , , , ].

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

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 p GL3-b-hApoC3 ( A – C ) or p GL3-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.

Journal: International Journal of Molecular Sciences

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

doi: 10.3390/ijms24108608

Figure Lengend Snippet: 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 p GL3-b-hApoC3 ( A – C ) or p GL3-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: Mutagenesis, Ligand Binding Assay, Activation Assay, Transfection, Construct, Luciferase, Activity Assay

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 p GL3-b-hCYP26A1 ( A ) or p GL3-b-hRARβ ( B ) promoters, each with p RLTK 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.

Journal: International Journal of Molecular Sciences

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

doi: 10.3390/ijms24108608

Figure Lengend Snippet: 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 p GL3-b-hCYP26A1 ( A ) or p GL3-b-hRARβ ( B ) promoters, each with p RLTK 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: Mutagenesis, Ligand Binding Assay, Activation Assay, Transfection, Control, Luciferase, Activity Assay

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plasmid p gl3-basic (Promega)

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