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ha ms2 gfp overexpression vector  (Addgene inc)


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    Addgene inc ha ms2 gfp overexpression vector
    c-Jun Was Essential for MEG3 Inhibition of c-Myc Transcription in Human Bladder Cancer Cells (A) Diagram of the potential transcription factor binding sites in human c-Myc promoter-driven luciferase reporter. (B) The effect of MEG3 <t>overexpression</t> on the expression of potential transcription factors listed in (A), with GAPDH used as the internal loading control. (C) The effect of MEG3 on AP-1 activity in UMUC3 cells. The AP-1 luciferase reporter was co-transfected into UMUC3(Vector) and UMUC3(MEG3) cells with TK at a ratio of 10:1. After 24 h, the luciferase activity was determined and presented as luciferase activity relative to vector control. (D and E) Ectopic expression of TAM67 on c-Myc expression at the protein (D) and the mRNA (E) levels in UMUC3 cells. GAPDH was used as the internal loading control. (F) Diagram indicating the c-Myc promoter-driven luciferase reporter Del2 and its c-Jun binding site point mutation. (G) WT and mutant (Mut) c-Myc promoter-driven luciferase reporters were stably co-transfected with MEG3 or its scrambled vector into T24T cells, and the stable transfectants were used to evaluate the essential role of the c-Myc binding site in MEG3’s inhibition of c-Myc promoter transcription. Results are presented as relative c-Myc promoter activity. The asterisk indicates a significant inhibition compared with the vector transfectant (p < 0.05). The bars represent the mean ± SD of triplicates.
    Ha Ms2 Gfp Overexpression Vector, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 12 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ha+ms2+gfp+overexpression+vector/pmc06396102-190-5-14?v=Addgene+inc
    Average 93 stars, based on 12 article reviews
    ha ms2 gfp overexpression vector - by Bioz Stars, 2026-07
    93/100 stars

    Images

    1) Product Images from "MEG3, as a Competing Endogenous RNA, Binds with miR-27a to Promote PHLPP2 Protein Translation and Impairs Bladder Cancer Invasion"

    Article Title: MEG3, as a Competing Endogenous RNA, Binds with miR-27a to Promote PHLPP2 Protein Translation and Impairs Bladder Cancer Invasion

    Journal: Molecular Therapy. Nucleic Acids

    doi: 10.1016/j.omtn.2019.01.014

    c-Jun Was Essential for MEG3 Inhibition of c-Myc Transcription in Human Bladder Cancer Cells (A) Diagram of the potential transcription factor binding sites in human c-Myc promoter-driven luciferase reporter. (B) The effect of MEG3 overexpression on the expression of potential transcription factors listed in (A), with GAPDH used as the internal loading control. (C) The effect of MEG3 on AP-1 activity in UMUC3 cells. The AP-1 luciferase reporter was co-transfected into UMUC3(Vector) and UMUC3(MEG3) cells with TK at a ratio of 10:1. After 24 h, the luciferase activity was determined and presented as luciferase activity relative to vector control. (D and E) Ectopic expression of TAM67 on c-Myc expression at the protein (D) and the mRNA (E) levels in UMUC3 cells. GAPDH was used as the internal loading control. (F) Diagram indicating the c-Myc promoter-driven luciferase reporter Del2 and its c-Jun binding site point mutation. (G) WT and mutant (Mut) c-Myc promoter-driven luciferase reporters were stably co-transfected with MEG3 or its scrambled vector into T24T cells, and the stable transfectants were used to evaluate the essential role of the c-Myc binding site in MEG3’s inhibition of c-Myc promoter transcription. Results are presented as relative c-Myc promoter activity. The asterisk indicates a significant inhibition compared with the vector transfectant (p < 0.05). The bars represent the mean ± SD of triplicates.
    Figure Legend Snippet: c-Jun Was Essential for MEG3 Inhibition of c-Myc Transcription in Human Bladder Cancer Cells (A) Diagram of the potential transcription factor binding sites in human c-Myc promoter-driven luciferase reporter. (B) The effect of MEG3 overexpression on the expression of potential transcription factors listed in (A), with GAPDH used as the internal loading control. (C) The effect of MEG3 on AP-1 activity in UMUC3 cells. The AP-1 luciferase reporter was co-transfected into UMUC3(Vector) and UMUC3(MEG3) cells with TK at a ratio of 10:1. After 24 h, the luciferase activity was determined and presented as luciferase activity relative to vector control. (D and E) Ectopic expression of TAM67 on c-Myc expression at the protein (D) and the mRNA (E) levels in UMUC3 cells. GAPDH was used as the internal loading control. (F) Diagram indicating the c-Myc promoter-driven luciferase reporter Del2 and its c-Jun binding site point mutation. (G) WT and mutant (Mut) c-Myc promoter-driven luciferase reporters were stably co-transfected with MEG3 or its scrambled vector into T24T cells, and the stable transfectants were used to evaluate the essential role of the c-Myc binding site in MEG3’s inhibition of c-Myc promoter transcription. Results are presented as relative c-Myc promoter activity. The asterisk indicates a significant inhibition compared with the vector transfectant (p < 0.05). The bars represent the mean ± SD of triplicates.

    Techniques Used: Inhibition, Binding Assay, Luciferase, Over Expression, Expressing, Activity Assay, Transfection, Plasmid Preparation, Mutagenesis, Stable Transfection



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    ha ms2 gfp overexpression vector  (Addgene inc)
    93
    Addgene inc ha ms2 gfp overexpression vector
    c-Jun Was Essential for MEG3 Inhibition of c-Myc Transcription in Human Bladder Cancer Cells (A) Diagram of the potential transcription factor binding sites in human c-Myc promoter-driven luciferase reporter. (B) The effect of MEG3 <t>overexpression</t> on the expression of potential transcription factors listed in (A), with GAPDH used as the internal loading control. (C) The effect of MEG3 on AP-1 activity in UMUC3 cells. The AP-1 luciferase reporter was co-transfected into UMUC3(Vector) and UMUC3(MEG3) cells with TK at a ratio of 10:1. After 24 h, the luciferase activity was determined and presented as luciferase activity relative to vector control. (D and E) Ectopic expression of TAM67 on c-Myc expression at the protein (D) and the mRNA (E) levels in UMUC3 cells. GAPDH was used as the internal loading control. (F) Diagram indicating the c-Myc promoter-driven luciferase reporter Del2 and its c-Jun binding site point mutation. (G) WT and mutant (Mut) c-Myc promoter-driven luciferase reporters were stably co-transfected with MEG3 or its scrambled vector into T24T cells, and the stable transfectants were used to evaluate the essential role of the c-Myc binding site in MEG3’s inhibition of c-Myc promoter transcription. Results are presented as relative c-Myc promoter activity. The asterisk indicates a significant inhibition compared with the vector transfectant (p < 0.05). The bars represent the mean ± SD of triplicates.
    Ha Ms2 Gfp Overexpression Vector, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ha+ms2+gfp+overexpression+vector/pmc06396102-190-5-14?v=Addgene+inc
    Average 93 stars, based on 1 article reviews
    ha ms2 gfp overexpression vector - by Bioz Stars, 2026-07
    93/100 stars
    		  Buy from Supplier

    Image Search Results


    c-Jun Was Essential for MEG3 Inhibition of c-Myc Transcription in Human Bladder Cancer Cells (A) Diagram of the potential transcription factor binding sites in human c-Myc promoter-driven luciferase reporter. (B) The effect of MEG3 overexpression on the expression of potential transcription factors listed in (A), with GAPDH used as the internal loading control. (C) The effect of MEG3 on AP-1 activity in UMUC3 cells. The AP-1 luciferase reporter was co-transfected into UMUC3(Vector) and UMUC3(MEG3) cells with TK at a ratio of 10:1. After 24 h, the luciferase activity was determined and presented as luciferase activity relative to vector control. (D and E) Ectopic expression of TAM67 on c-Myc expression at the protein (D) and the mRNA (E) levels in UMUC3 cells. GAPDH was used as the internal loading control. (F) Diagram indicating the c-Myc promoter-driven luciferase reporter Del2 and its c-Jun binding site point mutation. (G) WT and mutant (Mut) c-Myc promoter-driven luciferase reporters were stably co-transfected with MEG3 or its scrambled vector into T24T cells, and the stable transfectants were used to evaluate the essential role of the c-Myc binding site in MEG3’s inhibition of c-Myc promoter transcription. Results are presented as relative c-Myc promoter activity. The asterisk indicates a significant inhibition compared with the vector transfectant (p < 0.05). The bars represent the mean ± SD of triplicates.

    Journal: Molecular Therapy. Nucleic Acids

    Article Title: MEG3, as a Competing Endogenous RNA, Binds with miR-27a to Promote PHLPP2 Protein Translation and Impairs Bladder Cancer Invasion

    doi: 10.1016/j.omtn.2019.01.014

    Figure Lengend Snippet: c-Jun Was Essential for MEG3 Inhibition of c-Myc Transcription in Human Bladder Cancer Cells (A) Diagram of the potential transcription factor binding sites in human c-Myc promoter-driven luciferase reporter. (B) The effect of MEG3 overexpression on the expression of potential transcription factors listed in (A), with GAPDH used as the internal loading control. (C) The effect of MEG3 on AP-1 activity in UMUC3 cells. The AP-1 luciferase reporter was co-transfected into UMUC3(Vector) and UMUC3(MEG3) cells with TK at a ratio of 10:1. After 24 h, the luciferase activity was determined and presented as luciferase activity relative to vector control. (D and E) Ectopic expression of TAM67 on c-Myc expression at the protein (D) and the mRNA (E) levels in UMUC3 cells. GAPDH was used as the internal loading control. (F) Diagram indicating the c-Myc promoter-driven luciferase reporter Del2 and its c-Jun binding site point mutation. (G) WT and mutant (Mut) c-Myc promoter-driven luciferase reporters were stably co-transfected with MEG3 or its scrambled vector into T24T cells, and the stable transfectants were used to evaluate the essential role of the c-Myc binding site in MEG3’s inhibition of c-Myc promoter transcription. Results are presented as relative c-Myc promoter activity. The asterisk indicates a significant inhibition compared with the vector transfectant (p < 0.05). The bars represent the mean ± SD of triplicates.

    Article Snippet: The c-Myc promoter luciferase reporter, HA-MS2-GFP overexpression vector and pSL-MS2-12X plasmids were obtained from Addgene (Cambridge, MA, USA).

    Techniques: Inhibition, Binding Assay, Luciferase, Over Expression, Expressing, Activity Assay, Transfection, Plasmid Preparation, Mutagenesis, Stable Transfection