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empty pgl3 c vector (New England Biolabs)

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New England Biolabs empty pgl3 c vector
Empty Pgl3 C Vector, supplied by New England Biolabs, used in various techniques. Bioz Stars score: 99/100, based on 9085 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pgl3+empty+vector/XhoI/pm38740892-243-6-32
Average 99 stars, based on 9085 article reviews

empty pgl3 c vector - by Bioz Stars, 2026-10

99/100 stars

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Article Title: Deciphering the role of a SINE-VNTR-Alu retrotransposon polymorphism as a biomarker of Parkinson’s disease progression
Article Snippet: .. For this, SVA-containing pGL3-P constructs and empty pGL3-C vector were digested with SacI and XhoI to clone full-length SVA-F (from INPP5F locus) and truncated SVA_67 allele 3 into pGL3-C. T4 DNA ligase (NEB) was used to complete the ligation process. .. All corresponding cloning steps were performed using Subcloning E ciencyTM DH5α Competent Cells (Invitrogen), grown in LB medium supplemented with the appropriate antibiotic (100 μg/mL ampicillin for pGL3-P/-C or 50 μg/mL kanamycin for pCR-Blunt).

Article Title: Deciphering the role of a SINE-VNTR-Alu retrotransposon polymorphism as a biomarker of Parkinson's disease progression.
Article Snippet: .. For this, SVA-containing pGL3-P constructs and empty pGL3-C vector were digested with SacI and XhoI to clone full-length SVA-F (from INPP5F locus) and truncated SVA_67 allele 3 into pGL3-C. T4 DNA ligase (NEB) was used to complete the ligation process. .. All corresponding cloning steps were performed using Subcloning EfficiencyTM DH5α Competent Cells (Invitrogen), grown in LB medium supplemented with the appropriate 11 Vol.

Article Title: Deciphering the role of a SINE-VNTR- Alu retrotransposon polymorphism as a biomarker of Parkinson’s disease progression
Article Snippet: .. For this, SVA-containing pGL3-P constructs and empty pGL3-C vector were digested with SacI and XhoI to clone full-length SVA-F (from INPP5F locus) and truncated SVA_67 allele 3 into pGL3-C. T4 DNA ligase (NEB) was used to complete the ligation process. .. All corresponding cloning steps were performed using Subcloning EfficiencyTM DH5α Competent Cells (Invitrogen), grown in LB medium supplemented with the appropriate antibiotic (100 μg/mL ampicillin for pGL3-P/-C or 50 μg/mL kanamycin for pCR-Blunt).

Ligation:

Article Title: Deciphering the role of a SINE-VNTR- Alu retrotransposon polymorphism as a biomarker of Parkinson’s disease progression
Article Snippet: .. For this, SVA-containing pGL3-P constructs and empty pGL3-C vector were digested with SacI and XhoI to clone full-length SVA-F (from INPP5F locus) and truncated SVA_67 allele 3 into pGL3-C. T4 DNA ligase (NEB) was used to complete the ligation process. .. All corresponding cloning steps were performed using Subcloning EfficiencyTM DH5α Competent Cells (Invitrogen), grown in LB medium supplemented with the appropriate antibiotic (100 μg/mL ampicillin for pGL3-P/-C or 50 μg/mL kanamycin for pCR-Blunt).

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$(A.i.) Giemsa-stained images of LD-S, LD-R, in murine peritoneal MФs with or without the presence of suboptimal dose of SbV (1.52µg/ml). In some experimental condition LD infection was performed in the presence of N-acetyl-L-cysteine (NAC), while in some experimental conditions, LDs are pre-treated with H 2 O 2 + 6-AN. All the infections were performed for 24hrs (A.ii.) Bar graph showing amastigotes/100MФs in all the experimental sets mentioned in A.i. (B.) Western blot of whole cell lysate showing significant high expression of Heme-oxygenase 1 (HO1) in LD-R infected MФs while no significant change in expression level was observed for Ferritin (FTH1) at 4hrs pi. β-actin is used as the positive control. (C.) Schematic representation of HO-1 promoter region with p50 and c-Rel binding sites. Site A (−4/−635) was demarcated as green, and Site B (−636/−1377) was demarcated as red. (D.i.) Western blot of nuclear fraction showing significant high expression of p50 and c-Rel in LD-R infected MФs 4hrs pi with Histone (H3) as loading control. (D.ii.) Confocal images representing the localization of p50 and c-Rel, in MФs, with DAPI representing the nucleus. The right-most panel shows the RGB-profile plot with grey regions demarcating the region where p50 and cRel are colocalized with DAPI. p50 and c-Rel were found to be localized in the nucleus of LD-R-infected MФs. One representative small nucleus of LD has been marked in ( * ) to show the infected MФs. (E.) Fold luciferase activity of RAW264.7 cell lysate transfected either with HO1+PGL3 promoter, or Site A ( −/− ), Site B( −/− ) deleted constructs followed by infection with LD-S and LD-R for 4hrs. PGL3 enhancer empty vector is used for normalization for each transfected set. Each experiment was performed in 3 biological replicates and graphical data are represented as Mean with SEM. P ≤ 0.05 is marked as *, P ≤ 0.01 is marked as **, P ≤ 0.001 is marked as ***, and P ≤ 0.0001 is marked as ****.$

Journal: bioRxiv

Article Title: Addressing anemia severity in antimony-resistant Leishmania donovani infection at the nexus of oxidative outburst and iron transit

doi: 10.1101/2024.03.04.583250

Figure Lengend Snippet: (A.i.) Giemsa-stained images of LD-S, LD-R, in murine peritoneal MФs with or without the presence of suboptimal dose of SbV (1.52µg/ml). In some experimental condition LD infection was performed in the presence of N-acetyl-L-cysteine (NAC), while in some experimental conditions, LDs are pre-treated with H 2 O 2 + 6-AN. All the infections were performed for 24hrs (A.ii.) Bar graph showing amastigotes/100MФs in all the experimental sets mentioned in A.i. (B.) Western blot of whole cell lysate showing significant high expression of Heme-oxygenase 1 (HO1) in LD-R infected MФs while no significant change in expression level was observed for Ferritin (FTH1) at 4hrs pi. β-actin is used as the positive control. (C.) Schematic representation of HO-1 promoter region with p50 and c-Rel binding sites. Site A (−4/−635) was demarcated as green, and Site B (−636/−1377) was demarcated as red. (D.i.) Western blot of nuclear fraction showing significant high expression of p50 and c-Rel in LD-R infected MФs 4hrs pi with Histone (H3) as loading control. (D.ii.) Confocal images representing the localization of p50 and c-Rel, in MФs, with DAPI representing the nucleus. The right-most panel shows the RGB-profile plot with grey regions demarcating the region where p50 and cRel are colocalized with DAPI. p50 and c-Rel were found to be localized in the nucleus of LD-R-infected MФs. One representative small nucleus of LD has been marked in ( * ) to show the infected MФs. (E.) Fold luciferase activity of RAW264.7 cell lysate transfected either with HO1+PGL3 promoter, or Site A ( −/− ), Site B( −/− ) deleted constructs followed by infection with LD-S and LD-R for 4hrs. PGL3 enhancer empty vector is used for normalization for each transfected set. Each experiment was performed in 3 biological replicates and graphical data are represented as Mean with SEM. P ≤ 0.05 is marked as *, P ≤ 0.01 is marked as **, P ≤ 0.001 is marked as ***, and P ≤ 0.0001 is marked as ****.

Article Snippet: Murine HO-1 promoters (−1385/+137), 1522bp using primers 5’-AAGGTACCTGAGGCTGGAGAGATGGCC-3’ and 3’-TAAAAGCTTCACCGGACTGGGCTAGTTCAG-5’ were PCR amplified and cloned in promoterless PGL3 enhancer empty vector (Promega, E1771) at the upstream of luciferase gene.

Techniques: Staining, Infection, Western Blot, Expressing, Positive Control, Binding Assay, Luciferase, Activity Assay, Transfection, Construct, Plasmid Preparation

(a) Schematic diagram for constructing wild-type or mutant promoter at the ABCG1 rs57137919G>A polymorphism site. Two constructs were subcloned into pGL3-basic plasmid vectors with firefly luciferase reporter gene. pG, -367G (open bar); pA, -367A (grey bar). Luciferase activity assays for two ABCG1 promoter constructs in HEK293T cells (b), THP-1 cells (c), and HepG2 cells (d) are shown. Luciferase activities were measured with the dual-luciferase reporter assay system and normalized to Renilla luciferase activity 24 hours after transfection in the presence or absence of TO901317. The luciferase activity was a corrected relative value. Data are shown as mean ± SD of four independent experiments in triplicate. P <0.01 vs. pG in HEK293 cells, THP-1 cells, and HepG2 cells under both basal state and LXR agonist stimulation.

Journal: PLoS ONE

Article Title: ABCG1 rs57137919G>A Polymorphism Is Functionally Associated with Varying Gene Expression and Apoptosis of Macrophages

doi: 10.1371/journal.pone.0097044

Figure Lengend Snippet: (a) Schematic diagram for constructing wild-type or mutant promoter at the ABCG1 rs57137919G>A polymorphism site. Two constructs were subcloned into pGL3-basic plasmid vectors with firefly luciferase reporter gene. pG, -367G (open bar); pA, -367A (grey bar). Luciferase activity assays for two ABCG1 promoter constructs in HEK293T cells (b), THP-1 cells (c), and HepG2 cells (d) are shown. Luciferase activities were measured with the dual-luciferase reporter assay system and normalized to Renilla luciferase activity 24 hours after transfection in the presence or absence of TO901317. The luciferase activity was a corrected relative value. Data are shown as mean ± SD of four independent experiments in triplicate. P <0.01 vs. pG in HEK293 cells, THP-1 cells, and HepG2 cells under both basal state and LXR agonist stimulation.

Article Snippet: The pGL3-basic empty vector was used as a negative control and the pGL3-control vector (Promega) was used as a positive control for the luciferase assay.

Techniques: Mutagenesis, Construct, Plasmid Preparation, Luciferase, Activity Assay, Reporter Assay, Transfection