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marathon cdna  (TaKaRa)


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    Structured Review

    TaKaRa marathon cdna
    Marathon Cdna, supplied by TaKaRa, used in various techniques. Bioz Stars score: 93/100, based on 288 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+brain+cdna/Mouse+Brain+Marathon+-Ready+cDNA/us12371698-1474-2-4
    Average 93 stars, based on 288 article reviews
    marathon cdna - by Bioz Stars, 2026-10
    93/100 stars

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    Related Articles

    Amplification:

    Article Title: Rapid and reversible fluorescent probe enables repeated snapshot imaging of AMPA receptors during synaptic plasticity.
    Article Snippet: .. cDNAs of mouse GluA1flip(Q), 5′UTR- GluA1flip(Q)- 3′UTR, GluA2flip(Q), GluA2flip(Q)- 3′UTR, GluA3flip(Q), GluA4flip(Q), GSG1L, and TARP γ7 were amplified from mouse brain marathon- ready cDNA (Clontech) by polymerase chain reaction (PCR). ..

    Article Title: AID–2×RBD27, an auxin-inducible degron-based Rab27 trapper that reversibly inhibits the function of Rab27A in melanocytes
    Article Snippet: The following plasmids used in this study [pEGFP-C1-2×RBD27-WT (or -mut), pEF-TIR1(F74G)-P2A-AID-2×RBD27, pEF-MST-2×EGFP, pEF-Kif5b-ΔCC-EGFP and pEF-Kif5b-ΔCC-EGFP-SHD] are available from the RIKEN BioResource Research Center in Japan ( https://dnaconda.riken.jp/search/depositor/dep005893.html ; RDB20906–RDB20911 ). .. cDNAs of the N-terminal 87 amino acids of rat Slp2-a and mouse Slp2-a (RBD27-WT) were amplified from cDNAs of rat PC12 cells and the Marathon-Ready mouse brain cDNAs (Takara Bio, Shiga, Japan), respectively, by PCR using the specific pairs of oligonucleotides shown in . .. Rat RBD27 and mouse RBD27 were then arranged in tandem ( ) by standard molecular biology techniques. cDNAs of AID and Oryza sativa TIR1 were prepared as described previously ( ; ).

    Article Title: Oxr1 and Ncoa7 regulate V-ATPase to achieve optimal pH for glycosylation within the Golgi apparatus and trans-Golgi network.
    Article Snippet: .. The cDNAs encoding Mus musculus Oxr1 (NM_001358977.1), Ncoa7 (NM_172495.6), ATP6V1A (BC038392.1), and ATP6V1B2 (BC012497) were amplified by KOD Plus- Ver.2 (TOYOBO) using 17- d embryo Marathon- Ready mouse cDNA (TaKaRa Clontech). .. Homo sapiens Rab GDI- alpha cDNA (D45021.1) was amplified from human fetal Marathon- Ready cDNA (TaKaRa Clontech) using KOD One DNA polymerase (TOYOBO).

    Article Title: A fluorophore–ligand conjugate for the rapid and reversible staining of native AMPA receptors in living neurons
    Article Snippet: .. cDNAs of mouse GluA1 flip (Q), 5’UTR - GluA1 flip (Q) - 3’UTR, GluA2 flip (Q), GluA2 flip (Q) - 3’UTR, GluA3 flip (Q), and GluA4 flip (Q) were amplified from mouse brain marathon-ready cDNA (Clontech) by PCR. ..

    Polymerase Chain Reaction:

    Article Title: Rapid and reversible fluorescent probe enables repeated snapshot imaging of AMPA receptors during synaptic plasticity.
    Article Snippet: .. cDNAs of mouse GluA1flip(Q), 5′UTR- GluA1flip(Q)- 3′UTR, GluA2flip(Q), GluA2flip(Q)- 3′UTR, GluA3flip(Q), GluA4flip(Q), GSG1L, and TARP γ7 were amplified from mouse brain marathon- ready cDNA (Clontech) by polymerase chain reaction (PCR). ..

    Article Title: AID–2×RBD27, an auxin-inducible degron-based Rab27 trapper that reversibly inhibits the function of Rab27A in melanocytes
    Article Snippet: The following plasmids used in this study [pEGFP-C1-2×RBD27-WT (or -mut), pEF-TIR1(F74G)-P2A-AID-2×RBD27, pEF-MST-2×EGFP, pEF-Kif5b-ΔCC-EGFP and pEF-Kif5b-ΔCC-EGFP-SHD] are available from the RIKEN BioResource Research Center in Japan ( https://dnaconda.riken.jp/search/depositor/dep005893.html ; RDB20906–RDB20911 ). .. cDNAs of the N-terminal 87 amino acids of rat Slp2-a and mouse Slp2-a (RBD27-WT) were amplified from cDNAs of rat PC12 cells and the Marathon-Ready mouse brain cDNAs (Takara Bio, Shiga, Japan), respectively, by PCR using the specific pairs of oligonucleotides shown in . .. Rat RBD27 and mouse RBD27 were then arranged in tandem ( ) by standard molecular biology techniques. cDNAs of AID and Oryza sativa TIR1 were prepared as described previously ( ; ).

    Article Title: A fluorophore–ligand conjugate for the rapid and reversible staining of native AMPA receptors in living neurons
    Article Snippet: .. cDNAs of mouse GluA1 flip (Q), 5’UTR - GluA1 flip (Q) - 3’UTR, GluA2 flip (Q), GluA2 flip (Q) - 3’UTR, GluA3 flip (Q), and GluA4 flip (Q) were amplified from mouse brain marathon-ready cDNA (Clontech) by PCR. ..

    Article Title: Rapid and reversible fluorescent probe enables repeated snapshot imaging of AMPA receptors during synaptic plasticity
    Article Snippet: .. cDNAs of mouse GluA1 flip (Q), 5′UTR-GluA1 flip (Q)-3′UTR, GluA2 flip (Q), GluA2 flip (Q)-3′UTR, GluA3 flip (Q), GluA4 flip (Q), GSG1L, and TARP γ7 were amplified from mouse brain marathon-ready cDNA (Clontech) by polymerase chain reaction (PCR). ..

    Article Title: Targeted nuclear RNA cleavage and polyadenylation with CRISPR-Cas
    Article Snippet: Using RACE-ready Marathon cDNA (Clontech) (fetal and adult: skeletal muscle, brain, lung and stomach), 3′RACE is performed using nested primers specific to exon 11 of human DMPK, which represents the most 5′ sequence present within the human mutant DMPK construct and inducible DM1 mouse model. PCR-generated 3′RACE products are separated using agarose gel-electrophoresis, subcloned using TOPO cloning, sequenced and mapped to identify their cleavage site. .. Using RACE-ready Marathon cDNA (Clontech) (fetal and adult: skeletal muscle, brain, lung and stomach), 3′RACE is performed using nested primers specific to exon 11 of human DMPK, which represents the most 5′ sequence present within the human mutant DMPK construct and inducible DM1 mouse model. PCR-generated 3′RACE products are separated using agarose gel-electrophoresis, subcloned using TOPO cloning, sequenced and mapped to identify their cleavage site. ..

    other:

    Article Title: Ultraviolet-A radiation induces changes in cyclin G gene expression in mouse melanoma B16-F1 cells
    Article Snippet: Gene expression of 1176 tumor-related genes was analyzed using AtlasTM mouse cancer 1.2 cDNA array (Clonetech, USA).

    Clone Assay:

    Article Title: Nogo receptor-Fc delivered by haematopoietic cells enhances neurorepair in a multiple sclerosis model
    Article Snippet: We cloned the NgR1(1-310) ectodomain construct fused with an additional myc-tag and Fc-binding ligand into the lentiviral packaging plasmid, pLVX-EF1-IRES-ZsGreen1 (Clontech). .. Briefly, the NgR(310)ecto cDNA was cloned from the adult mouse brain Marathon-Ready cDNA (Clontech) and inserted into pFUSE-mIgG1-Fc plasmid (InvivoGen) to add the Fc component. .. The NgR(310)ecto-Fc portion was amplified and inserted into the pCMV-Tag 5 plasmid (Agilent Technologies) to add a myc-tag for tracking purposes.

    Plasmid Preparation:

    Article Title: Nogo receptor-Fc delivered by haematopoietic cells enhances neurorepair in a multiple sclerosis model
    Article Snippet: We cloned the NgR1(1-310) ectodomain construct fused with an additional myc-tag and Fc-binding ligand into the lentiviral packaging plasmid, pLVX-EF1-IRES-ZsGreen1 (Clontech). .. Briefly, the NgR(310)ecto cDNA was cloned from the adult mouse brain Marathon-Ready cDNA (Clontech) and inserted into pFUSE-mIgG1-Fc plasmid (InvivoGen) to add the Fc component. .. The NgR(310)ecto-Fc portion was amplified and inserted into the pCMV-Tag 5 plasmid (Agilent Technologies) to add a myc-tag for tracking purposes.

    Sequencing:

    Article Title: Targeted nuclear RNA cleavage and polyadenylation with CRISPR-Cas
    Article Snippet: Using RACE-ready Marathon cDNA (Clontech) (fetal and adult: skeletal muscle, brain, lung and stomach), 3′RACE is performed using nested primers specific to exon 11 of human DMPK, which represents the most 5′ sequence present within the human mutant DMPK construct and inducible DM1 mouse model. PCR-generated 3′RACE products are separated using agarose gel-electrophoresis, subcloned using TOPO cloning, sequenced and mapped to identify their cleavage site. .. Using RACE-ready Marathon cDNA (Clontech) (fetal and adult: skeletal muscle, brain, lung and stomach), 3′RACE is performed using nested primers specific to exon 11 of human DMPK, which represents the most 5′ sequence present within the human mutant DMPK construct and inducible DM1 mouse model. PCR-generated 3′RACE products are separated using agarose gel-electrophoresis, subcloned using TOPO cloning, sequenced and mapped to identify their cleavage site. ..

    Mutagenesis:

    Article Title: Targeted nuclear RNA cleavage and polyadenylation with CRISPR-Cas
    Article Snippet: Using RACE-ready Marathon cDNA (Clontech) (fetal and adult: skeletal muscle, brain, lung and stomach), 3′RACE is performed using nested primers specific to exon 11 of human DMPK, which represents the most 5′ sequence present within the human mutant DMPK construct and inducible DM1 mouse model. PCR-generated 3′RACE products are separated using agarose gel-electrophoresis, subcloned using TOPO cloning, sequenced and mapped to identify their cleavage site. .. Using RACE-ready Marathon cDNA (Clontech) (fetal and adult: skeletal muscle, brain, lung and stomach), 3′RACE is performed using nested primers specific to exon 11 of human DMPK, which represents the most 5′ sequence present within the human mutant DMPK construct and inducible DM1 mouse model. PCR-generated 3′RACE products are separated using agarose gel-electrophoresis, subcloned using TOPO cloning, sequenced and mapped to identify their cleavage site. ..

    Construct:

    Article Title: Targeted nuclear RNA cleavage and polyadenylation with CRISPR-Cas
    Article Snippet: Using RACE-ready Marathon cDNA (Clontech) (fetal and adult: skeletal muscle, brain, lung and stomach), 3′RACE is performed using nested primers specific to exon 11 of human DMPK, which represents the most 5′ sequence present within the human mutant DMPK construct and inducible DM1 mouse model. PCR-generated 3′RACE products are separated using agarose gel-electrophoresis, subcloned using TOPO cloning, sequenced and mapped to identify their cleavage site. .. Using RACE-ready Marathon cDNA (Clontech) (fetal and adult: skeletal muscle, brain, lung and stomach), 3′RACE is performed using nested primers specific to exon 11 of human DMPK, which represents the most 5′ sequence present within the human mutant DMPK construct and inducible DM1 mouse model. PCR-generated 3′RACE products are separated using agarose gel-electrophoresis, subcloned using TOPO cloning, sequenced and mapped to identify their cleavage site. ..

    Agarose Gel Electrophoresis:

    Article Title: Targeted nuclear RNA cleavage and polyadenylation with CRISPR-Cas
    Article Snippet: Using RACE-ready Marathon cDNA (Clontech) (fetal and adult: skeletal muscle, brain, lung and stomach), 3′RACE is performed using nested primers specific to exon 11 of human DMPK, which represents the most 5′ sequence present within the human mutant DMPK construct and inducible DM1 mouse model. PCR-generated 3′RACE products are separated using agarose gel-electrophoresis, subcloned using TOPO cloning, sequenced and mapped to identify their cleavage site. .. Using RACE-ready Marathon cDNA (Clontech) (fetal and adult: skeletal muscle, brain, lung and stomach), 3′RACE is performed using nested primers specific to exon 11 of human DMPK, which represents the most 5′ sequence present within the human mutant DMPK construct and inducible DM1 mouse model. PCR-generated 3′RACE products are separated using agarose gel-electrophoresis, subcloned using TOPO cloning, sequenced and mapped to identify their cleavage site. ..

    Cloning:

    Article Title: Targeted nuclear RNA cleavage and polyadenylation with CRISPR-Cas
    Article Snippet: Using RACE-ready Marathon cDNA (Clontech) (fetal and adult: skeletal muscle, brain, lung and stomach), 3′RACE is performed using nested primers specific to exon 11 of human DMPK, which represents the most 5′ sequence present within the human mutant DMPK construct and inducible DM1 mouse model. PCR-generated 3′RACE products are separated using agarose gel-electrophoresis, subcloned using TOPO cloning, sequenced and mapped to identify their cleavage site. .. Using RACE-ready Marathon cDNA (Clontech) (fetal and adult: skeletal muscle, brain, lung and stomach), 3′RACE is performed using nested primers specific to exon 11 of human DMPK, which represents the most 5′ sequence present within the human mutant DMPK construct and inducible DM1 mouse model. PCR-generated 3′RACE products are separated using agarose gel-electrophoresis, subcloned using TOPO cloning, sequenced and mapped to identify their cleavage site. ..



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    (A and B) Top: Correction of Atp1a3 mutations (red) to the wild type nucleotide (green) with co-installation of benign synonymous (silent) edits (blue). Bottom: Correction with RNA electroporation in mouse fibroblasts ( n = 3). Dots show individual replicates. (A) Correction <t>in</t> <t>C57BL/6J</t> Atp1a3 D801N c.2401A mouse primary fibroblasts. (B) Correction in E815K mouse primary fibroblasts. (C) D801N-PE-AAV9 (top) and E815K-PE-AAV9 (bottom) optimized components. (D) PE-AAV9 system encoding split-intein PE6c prime editor halves, epegRNA, ngRNA, and dsgRNA. Npu N or Npu C, Nostoc punctiforme intein N-terminal or C-terminal halves, respectively; P EFS , Promoter, elongation factor 1α short; P hU6 , Promoter, human U6 polymerase III; P mU6, Promoter, mouse U6 polymerase III; W3, minimized gamma portion of the woodchuck hepatitis virus post-transcriptional regulatory element; bGH, bovine growth hormone polyadenylation signal. (E) Mice were characterized by molecular, behavioral, and biometric readouts. (F–I) HTS quantification ( n = 4–7) from gDNA (F and G) and <t>cDNA</t> (H and I) of bulk and GFP + nuclei from D801N mice (F and H) or E815K mice (G and I) injected with PE-AAV9 (PE) or phosphate-buffer saline (PBS, vehicle). (J and K) Specific activity of Atp1a3 in hippocampal homogenates of PE- or vehicle-treated D801N mice (J, n =3–16) or E815K mice (K, n = 5–12). Two-way ANOVA with Tukey’s multiple comparisons. ns = not significant, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. For (F)–(K), dots show values from individual mice with tissue collected at P28. For (A), (B), and (F)–(I), samples start from ~50% wild-type genotype heterozygous baseline (dotted line). See also .
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    (A and B) Top: Correction of Atp1a3 mutations (red) to the wild type nucleotide (green) with co-installation of benign synonymous (silent) edits (blue). Bottom: Correction with RNA electroporation in mouse fibroblasts ( n = 3). Dots show individual replicates. (A) Correction <t>in</t> <t>C57BL/6J</t> Atp1a3 D801N c.2401A mouse primary fibroblasts. (B) Correction in E815K mouse primary fibroblasts. (C) D801N-PE-AAV9 (top) and E815K-PE-AAV9 (bottom) optimized components. (D) PE-AAV9 system encoding split-intein PE6c prime editor halves, epegRNA, ngRNA, and dsgRNA. Npu N or Npu C, Nostoc punctiforme intein N-terminal or C-terminal halves, respectively; P EFS , Promoter, elongation factor 1α short; P hU6 , Promoter, human U6 polymerase III; P mU6, Promoter, mouse U6 polymerase III; W3, minimized gamma portion of the woodchuck hepatitis virus post-transcriptional regulatory element; bGH, bovine growth hormone polyadenylation signal. (E) Mice were characterized by molecular, behavioral, and biometric readouts. (F–I) HTS quantification ( n = 4–7) from gDNA (F and G) and <t>cDNA</t> (H and I) of bulk and GFP + nuclei from D801N mice (F and H) or E815K mice (G and I) injected with PE-AAV9 (PE) or phosphate-buffer saline (PBS, vehicle). (J and K) Specific activity of Atp1a3 in hippocampal homogenates of PE- or vehicle-treated D801N mice (J, n =3–16) or E815K mice (K, n = 5–12). Two-way ANOVA with Tukey’s multiple comparisons. ns = not significant, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. For (F)–(K), dots show values from individual mice with tissue collected at P28. For (A), (B), and (F)–(I), samples start from ~50% wild-type genotype heterozygous baseline (dotted line). See also .
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    (A and B) Top: Correction of Atp1a3 mutations (red) to the wild type nucleotide (green) with co-installation of benign synonymous (silent) edits (blue). Bottom: Correction with RNA electroporation in mouse fibroblasts ( n = 3). Dots show individual replicates. (A) Correction <t>in</t> <t>C57BL/6J</t> Atp1a3 D801N c.2401A mouse primary fibroblasts. (B) Correction in E815K mouse primary fibroblasts. (C) D801N-PE-AAV9 (top) and E815K-PE-AAV9 (bottom) optimized components. (D) PE-AAV9 system encoding split-intein PE6c prime editor halves, epegRNA, ngRNA, and dsgRNA. Npu N or Npu C, Nostoc punctiforme intein N-terminal or C-terminal halves, respectively; P EFS , Promoter, elongation factor 1α short; P hU6 , Promoter, human U6 polymerase III; P mU6, Promoter, mouse U6 polymerase III; W3, minimized gamma portion of the woodchuck hepatitis virus post-transcriptional regulatory element; bGH, bovine growth hormone polyadenylation signal. (E) Mice were characterized by molecular, behavioral, and biometric readouts. (F–I) HTS quantification ( n = 4–7) from gDNA (F and G) and <t>cDNA</t> (H and I) of bulk and GFP + nuclei from D801N mice (F and H) or E815K mice (G and I) injected with PE-AAV9 (PE) or phosphate-buffer saline (PBS, vehicle). (J and K) Specific activity of Atp1a3 in hippocampal homogenates of PE- or vehicle-treated D801N mice (J, n =3–16) or E815K mice (K, n = 5–12). Two-way ANOVA with Tukey’s multiple comparisons. ns = not significant, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. For (F)–(K), dots show values from individual mice with tissue collected at P28. For (A), (B), and (F)–(I), samples start from ~50% wild-type genotype heterozygous baseline (dotted line). See also .
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    93
    TaKaRa mouse brain cdna
    (A and B) Top: Correction of Atp1a3 mutations (red) to the wild type nucleotide (green) with co-installation of benign synonymous (silent) edits (blue). Bottom: Correction with RNA electroporation in mouse fibroblasts ( n = 3). Dots show individual replicates. (A) Correction <t>in</t> <t>C57BL/6J</t> Atp1a3 D801N c.2401A mouse primary fibroblasts. (B) Correction in E815K mouse primary fibroblasts. (C) D801N-PE-AAV9 (top) and E815K-PE-AAV9 (bottom) optimized components. (D) PE-AAV9 system encoding split-intein PE6c prime editor halves, epegRNA, ngRNA, and dsgRNA. Npu N or Npu C, Nostoc punctiforme intein N-terminal or C-terminal halves, respectively; P EFS , Promoter, elongation factor 1α short; P hU6 , Promoter, human U6 polymerase III; P mU6, Promoter, mouse U6 polymerase III; W3, minimized gamma portion of the woodchuck hepatitis virus post-transcriptional regulatory element; bGH, bovine growth hormone polyadenylation signal. (E) Mice were characterized by molecular, behavioral, and biometric readouts. (F–I) HTS quantification ( n = 4–7) from gDNA (F and G) and <t>cDNA</t> (H and I) of bulk and GFP + nuclei from D801N mice (F and H) or E815K mice (G and I) injected with PE-AAV9 (PE) or phosphate-buffer saline (PBS, vehicle). (J and K) Specific activity of Atp1a3 in hippocampal homogenates of PE- or vehicle-treated D801N mice (J, n =3–16) or E815K mice (K, n = 5–12). Two-way ANOVA with Tukey’s multiple comparisons. ns = not significant, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. For (F)–(K), dots show values from individual mice with tissue collected at P28. For (A), (B), and (F)–(I), samples start from ~50% wild-type genotype heterozygous baseline (dotted line). See also .
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    (A and B) Top: Correction of Atp1a3 mutations (red) to the wild type nucleotide (green) with co-installation of benign synonymous (silent) edits (blue). Bottom: Correction with RNA electroporation in mouse fibroblasts ( n = 3). Dots show individual replicates. (A) Correction in C57BL/6J Atp1a3 D801N c.2401A mouse primary fibroblasts. (B) Correction in E815K mouse primary fibroblasts. (C) D801N-PE-AAV9 (top) and E815K-PE-AAV9 (bottom) optimized components. (D) PE-AAV9 system encoding split-intein PE6c prime editor halves, epegRNA, ngRNA, and dsgRNA. Npu N or Npu C, Nostoc punctiforme intein N-terminal or C-terminal halves, respectively; P EFS , Promoter, elongation factor 1α short; P hU6 , Promoter, human U6 polymerase III; P mU6, Promoter, mouse U6 polymerase III; W3, minimized gamma portion of the woodchuck hepatitis virus post-transcriptional regulatory element; bGH, bovine growth hormone polyadenylation signal. (E) Mice were characterized by molecular, behavioral, and biometric readouts. (F–I) HTS quantification ( n = 4–7) from gDNA (F and G) and cDNA (H and I) of bulk and GFP + nuclei from D801N mice (F and H) or E815K mice (G and I) injected with PE-AAV9 (PE) or phosphate-buffer saline (PBS, vehicle). (J and K) Specific activity of Atp1a3 in hippocampal homogenates of PE- or vehicle-treated D801N mice (J, n =3–16) or E815K mice (K, n = 5–12). Two-way ANOVA with Tukey’s multiple comparisons. ns = not significant, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. For (F)–(K), dots show values from individual mice with tissue collected at P28. For (A), (B), and (F)–(I), samples start from ~50% wild-type genotype heterozygous baseline (dotted line). See also .

    Journal: Cell

    Article Title: In vivo prime editing rescues alternating hemiplegia of childhood in mice

    doi: 10.1016/j.cell.2025.06.038

    Figure Lengend Snippet: (A and B) Top: Correction of Atp1a3 mutations (red) to the wild type nucleotide (green) with co-installation of benign synonymous (silent) edits (blue). Bottom: Correction with RNA electroporation in mouse fibroblasts ( n = 3). Dots show individual replicates. (A) Correction in C57BL/6J Atp1a3 D801N c.2401A mouse primary fibroblasts. (B) Correction in E815K mouse primary fibroblasts. (C) D801N-PE-AAV9 (top) and E815K-PE-AAV9 (bottom) optimized components. (D) PE-AAV9 system encoding split-intein PE6c prime editor halves, epegRNA, ngRNA, and dsgRNA. Npu N or Npu C, Nostoc punctiforme intein N-terminal or C-terminal halves, respectively; P EFS , Promoter, elongation factor 1α short; P hU6 , Promoter, human U6 polymerase III; P mU6, Promoter, mouse U6 polymerase III; W3, minimized gamma portion of the woodchuck hepatitis virus post-transcriptional regulatory element; bGH, bovine growth hormone polyadenylation signal. (E) Mice were characterized by molecular, behavioral, and biometric readouts. (F–I) HTS quantification ( n = 4–7) from gDNA (F and G) and cDNA (H and I) of bulk and GFP + nuclei from D801N mice (F and H) or E815K mice (G and I) injected with PE-AAV9 (PE) or phosphate-buffer saline (PBS, vehicle). (J and K) Specific activity of Atp1a3 in hippocampal homogenates of PE- or vehicle-treated D801N mice (J, n =3–16) or E815K mice (K, n = 5–12). Two-way ANOVA with Tukey’s multiple comparisons. ns = not significant, * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. For (F)–(K), dots show values from individual mice with tissue collected at P28. For (A), (B), and (F)–(I), samples start from ~50% wild-type genotype heterozygous baseline (dotted line). See also .

    Article Snippet: For the validation of TaqMan probes (species specificity or species cross-reaction), TaqMan probes were tested on mouse brain cDNA derived from wild type mice (brain tissue from JR #664, C57BL/6J, The Jackson Laboratory) and human cDNA derived from a mixture of human tissues including the CNS (Takara #636693).

    Techniques: Electroporation, Virus, Injection, Saline, Activity Assay