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cmv promoter  (Addgene inc)


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    Addgene inc cmv promoter
    Evaluation of dCas13e to modulate splicing defects of ABCA4 c.5461-10T>C <t>in</t> <t>ARPE19</t> (A) A schematic illustration of the pSPL3– ABCA4 c.5461-10T>C minigene and the all-in-one construct of a U6 promoter-driven sgRNA sequence followed by the <t>CMV</t> promoter-driven RBFOX1N-dCas13e-C factor. The sgRNA targeted the same region downstream of E39 (green) as a previously reported antisense oligonucleotide (AON) target site. Positions of SD6 and SA2 primers for splicing product amplification are displayed. (B) RT-PCR results of ABCA4 splice variants in ARPE19 cells transfected with the ABCA4 minigene system (MT), RBFOX1N-dCas13e-C, sgRNAs targeting mCherry (control), or ABCA4 . ACTB was used as a housekeeping gene. Mock control represents ARPE19 without transfection of the ABCA4 minigene system. (C) Gel quantification of relative transcript expression of ABCA4 splice variants compared to MT control without treatment. Data are represented as mean ± SEM ( n = 5). (D) Gel quantification of the ratio of disease transcript to FL transcript. Data are represented as mean ± SEM ( n = 3).
    Cmv Promoter, supplied by Addgene inc, used in various techniques. Bioz Stars score: 94/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cmv promoter/product/Addgene inc
    Average 94 stars, based on 15 article reviews
    cmv promoter - by Bioz Stars, 2026-04
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    1) Product Images from "Using RNA-targeting CRISPR-Cas13 and engineered U1 systems to target ABCA4 splice variants in Stargardt disease"

    Article Title: Using RNA-targeting CRISPR-Cas13 and engineered U1 systems to target ABCA4 splice variants in Stargardt disease

    Journal: Molecular Therapy. Nucleic Acids

    doi: 10.1016/j.omtn.2025.102789

    Evaluation of dCas13e to modulate splicing defects of ABCA4 c.5461-10T>C in ARPE19 (A) A schematic illustration of the pSPL3– ABCA4 c.5461-10T>C minigene and the all-in-one construct of a U6 promoter-driven sgRNA sequence followed by the CMV promoter-driven RBFOX1N-dCas13e-C factor. The sgRNA targeted the same region downstream of E39 (green) as a previously reported antisense oligonucleotide (AON) target site. Positions of SD6 and SA2 primers for splicing product amplification are displayed. (B) RT-PCR results of ABCA4 splice variants in ARPE19 cells transfected with the ABCA4 minigene system (MT), RBFOX1N-dCas13e-C, sgRNAs targeting mCherry (control), or ABCA4 . ACTB was used as a housekeeping gene. Mock control represents ARPE19 without transfection of the ABCA4 minigene system. (C) Gel quantification of relative transcript expression of ABCA4 splice variants compared to MT control without treatment. Data are represented as mean ± SEM ( n = 5). (D) Gel quantification of the ratio of disease transcript to FL transcript. Data are represented as mean ± SEM ( n = 3).
    Figure Legend Snippet: Evaluation of dCas13e to modulate splicing defects of ABCA4 c.5461-10T>C in ARPE19 (A) A schematic illustration of the pSPL3– ABCA4 c.5461-10T>C minigene and the all-in-one construct of a U6 promoter-driven sgRNA sequence followed by the CMV promoter-driven RBFOX1N-dCas13e-C factor. The sgRNA targeted the same region downstream of E39 (green) as a previously reported antisense oligonucleotide (AON) target site. Positions of SD6 and SA2 primers for splicing product amplification are displayed. (B) RT-PCR results of ABCA4 splice variants in ARPE19 cells transfected with the ABCA4 minigene system (MT), RBFOX1N-dCas13e-C, sgRNAs targeting mCherry (control), or ABCA4 . ACTB was used as a housekeeping gene. Mock control represents ARPE19 without transfection of the ABCA4 minigene system. (C) Gel quantification of relative transcript expression of ABCA4 splice variants compared to MT control without treatment. Data are represented as mean ± SEM ( n = 5). (D) Gel quantification of the ratio of disease transcript to FL transcript. Data are represented as mean ± SEM ( n = 3).

    Techniques Used: Construct, Sequencing, Amplification, Reverse Transcription Polymerase Chain Reaction, Transfection, Control, Expressing



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    Evaluation of dCas13e to modulate splicing defects of ABCA4 c.5461-10T>C <t>in</t> <t>ARPE19</t> (A) A schematic illustration of the pSPL3– ABCA4 c.5461-10T>C minigene and the all-in-one construct of a U6 promoter-driven sgRNA sequence followed by the <t>CMV</t> promoter-driven RBFOX1N-dCas13e-C factor. The sgRNA targeted the same region downstream of E39 (green) as a previously reported antisense oligonucleotide (AON) target site. Positions of SD6 and SA2 primers for splicing product amplification are displayed. (B) RT-PCR results of ABCA4 splice variants in ARPE19 cells transfected with the ABCA4 minigene system (MT), RBFOX1N-dCas13e-C, sgRNAs targeting mCherry (control), or ABCA4 . ACTB was used as a housekeeping gene. Mock control represents ARPE19 without transfection of the ABCA4 minigene system. (C) Gel quantification of relative transcript expression of ABCA4 splice variants compared to MT control without treatment. Data are represented as mean ± SEM ( n = 5). (D) Gel quantification of the ratio of disease transcript to FL transcript. Data are represented as mean ± SEM ( n = 3).
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    Image Search Results


    Evaluation of dCas13e to modulate splicing defects of ABCA4 c.5461-10T>C in ARPE19 (A) A schematic illustration of the pSPL3– ABCA4 c.5461-10T>C minigene and the all-in-one construct of a U6 promoter-driven sgRNA sequence followed by the CMV promoter-driven RBFOX1N-dCas13e-C factor. The sgRNA targeted the same region downstream of E39 (green) as a previously reported antisense oligonucleotide (AON) target site. Positions of SD6 and SA2 primers for splicing product amplification are displayed. (B) RT-PCR results of ABCA4 splice variants in ARPE19 cells transfected with the ABCA4 minigene system (MT), RBFOX1N-dCas13e-C, sgRNAs targeting mCherry (control), or ABCA4 . ACTB was used as a housekeeping gene. Mock control represents ARPE19 without transfection of the ABCA4 minigene system. (C) Gel quantification of relative transcript expression of ABCA4 splice variants compared to MT control without treatment. Data are represented as mean ± SEM ( n = 5). (D) Gel quantification of the ratio of disease transcript to FL transcript. Data are represented as mean ± SEM ( n = 3).

    Journal: Molecular Therapy. Nucleic Acids

    Article Title: Using RNA-targeting CRISPR-Cas13 and engineered U1 systems to target ABCA4 splice variants in Stargardt disease

    doi: 10.1016/j.omtn.2025.102789

    Figure Lengend Snippet: Evaluation of dCas13e to modulate splicing defects of ABCA4 c.5461-10T>C in ARPE19 (A) A schematic illustration of the pSPL3– ABCA4 c.5461-10T>C minigene and the all-in-one construct of a U6 promoter-driven sgRNA sequence followed by the CMV promoter-driven RBFOX1N-dCas13e-C factor. The sgRNA targeted the same region downstream of E39 (green) as a previously reported antisense oligonucleotide (AON) target site. Positions of SD6 and SA2 primers for splicing product amplification are displayed. (B) RT-PCR results of ABCA4 splice variants in ARPE19 cells transfected with the ABCA4 minigene system (MT), RBFOX1N-dCas13e-C, sgRNAs targeting mCherry (control), or ABCA4 . ACTB was used as a housekeeping gene. Mock control represents ARPE19 without transfection of the ABCA4 minigene system. (C) Gel quantification of relative transcript expression of ABCA4 splice variants compared to MT control without treatment. Data are represented as mean ± SEM ( n = 5). (D) Gel quantification of the ratio of disease transcript to FL transcript. Data are represented as mean ± SEM ( n = 3).

    Article Snippet: For lentiviral transduction efficiency testing, ARPE19 was transduced using with lentiviruses with dsRed reporter driven by CMV promoter (Addgene #141148) and the fluorescence signal was analyzed after 4 days using MOI of 30.

    Techniques: Construct, Sequencing, Amplification, Reverse Transcription Polymerase Chain Reaction, Transfection, Control, Expressing