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Intrathoracic ABE treatment corrects Tnni3 R193H mutation in cardiac tissue (A and B) Schematic illustration of the dual <t>AAV9</t> vector construction strategy and ABE treatment, administered via intrathoracic injections in 6-week-old Tnni3 R193H/R193H mice. (C and D) Efficient correction of Tnni3 mutation in the heart. Assessment of gene editing efficiency in the hearts of Tnni3 R193H/R193H mice 12 weeks after the AAV treatment. A>G editing efficiencies were measured in genomic DNA and mRNA using high-throughput sequencing. Each point represents an individual mouse. ∗∗∗∗ p < 0.0001 based on Student’s unpaired t test analysis. Data are presented as mean ± SEM. (E and F) Lack of liver editing following <t>the</t> <t>AAV9-ABE</t> treatment. As in (C), gene editing efficiency in the livers of Tnni3 R193H/R193H mice after 12 weeks of dual AAV treatment. A>G editing efficiency was also assessed in the genomic DNA and mRNA extracted from liver tissue, demonstrating diminished delivery and expression of the ABE system in the hepatic tissue. Each point represents an individual mouse. ns, not statistically significant (Student’s unpaired t test analysis). Data are presented as mean ± SEM.
Cbh V5 Aav9 Abe C Terminus, 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
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Intrathoracic ABE treatment corrects Tnni3 R193H mutation in cardiac tissue (A and B) Schematic illustration of the dual <t>AAV9</t> vector construction strategy and ABE treatment, administered via intrathoracic injections in 6-week-old Tnni3 R193H/R193H mice. (C and D) Efficient correction of Tnni3 mutation in the heart. Assessment of gene editing efficiency in the hearts of Tnni3 R193H/R193H mice 12 weeks after the AAV treatment. A>G editing efficiencies were measured in genomic DNA and mRNA using high-throughput sequencing. Each point represents an individual mouse. ∗∗∗∗ p < 0.0001 based on Student’s unpaired t test analysis. Data are presented as mean ± SEM. (E and F) Lack of liver editing following <t>the</t> <t>AAV9-ABE</t> treatment. As in (C), gene editing efficiency in the livers of Tnni3 R193H/R193H mice after 12 weeks of dual AAV treatment. A>G editing efficiency was also assessed in the genomic DNA and mRNA extracted from liver tissue, demonstrating diminished delivery and expression of the ABE system in the hepatic tissue. Each point represents an individual mouse. ns, not statistically significant (Student’s unpaired t test analysis). Data are presented as mean ± SEM.
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Intrathoracic ABE treatment corrects Tnni3 R193H mutation in cardiac tissue (A and B) Schematic illustration of the dual <t>AAV9</t> vector construction strategy and ABE treatment, administered via intrathoracic injections in 6-week-old Tnni3 R193H/R193H mice. (C and D) Efficient correction of Tnni3 mutation in the heart. Assessment of gene editing efficiency in the hearts of Tnni3 R193H/R193H mice 12 weeks after the AAV treatment. A>G editing efficiencies were measured in genomic DNA and mRNA using high-throughput sequencing. Each point represents an individual mouse. ∗∗∗∗ p < 0.0001 based on Student’s unpaired t test analysis. Data are presented as mean ± SEM. (E and F) Lack of liver editing following <t>the</t> <t>AAV9-ABE</t> treatment. As in (C), gene editing efficiency in the livers of Tnni3 R193H/R193H mice after 12 weeks of dual AAV treatment. A>G editing efficiency was also assessed in the genomic DNA and mRNA extracted from liver tissue, demonstrating diminished delivery and expression of the ABE system in the hepatic tissue. Each point represents an individual mouse. ns, not statistically significant (Student’s unpaired t test analysis). Data are presented as mean ± SEM.
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Intrathoracic ABE treatment corrects Tnni3 R193H mutation in cardiac tissue (A and B) Schematic illustration of the dual <t>AAV9</t> vector construction strategy and ABE treatment, administered via intrathoracic injections in 6-week-old Tnni3 R193H/R193H mice. (C and D) Efficient correction of Tnni3 mutation in the heart. Assessment of gene editing efficiency in the hearts of Tnni3 R193H/R193H mice 12 weeks after the AAV treatment. A>G editing efficiencies were measured in genomic DNA and mRNA using high-throughput sequencing. Each point represents an individual mouse. ∗∗∗∗ p < 0.0001 based on Student’s unpaired t test analysis. Data are presented as mean ± SEM. (E and F) Lack of liver editing following <t>the</t> <t>AAV9-ABE</t> treatment. As in (C), gene editing efficiency in the livers of Tnni3 R193H/R193H mice after 12 weeks of dual AAV treatment. A>G editing efficiency was also assessed in the genomic DNA and mRNA extracted from liver tissue, demonstrating diminished delivery and expression of the ABE system in the hepatic tissue. Each point represents an individual mouse. ns, not statistically significant (Student’s unpaired t test analysis). Data are presented as mean ± SEM.
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Novus Biologicals periostin
(A) <t>Periostin</t> ( Postn ) expression assessed by qPCR in primary cardiac fibroblasts treated for 72 h. (B-C) Representative Western blot (B) and densitometry normalized to GAPDH and Ctrl (C) of Periostin across 6 biological replicates. (D-E) Representative Western blots for α-SMA (D) and densitometric quantification (E) following treatment with p38 MAPK inhibitor SB203580 (10 μM). (F-G) Representative Western blots for periosotin (F) and densitometric quantification (G) following treatment with p38 MAPK inhibitor SB203580 (10 μM). (H) Total soluble collagen secretion measured by Picrosirius Red. Data are mean ± SEM. Statistical significance was determined by one-way ANOVA or two-way ANOVA as appropriate.
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Bethyl anti rad21 c terminus
(A) <t>Periostin</t> ( Postn ) expression assessed by qPCR in primary cardiac fibroblasts treated for 72 h. (B-C) Representative Western blot (B) and densitometry normalized to GAPDH and Ctrl (C) of Periostin across 6 biological replicates. (D-E) Representative Western blots for α-SMA (D) and densitometric quantification (E) following treatment with p38 MAPK inhibitor SB203580 (10 μM). (F-G) Representative Western blots for periosotin (F) and densitometric quantification (G) following treatment with p38 MAPK inhibitor SB203580 (10 μM). (H) Total soluble collagen secretion measured by Picrosirius Red. Data are mean ± SEM. Statistical significance was determined by one-way ANOVA or two-way ANOVA as appropriate.
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Santa Cruz Biotechnology anti stag2 c terminus
(A) <t>Periostin</t> ( Postn ) expression assessed by qPCR in primary cardiac fibroblasts treated for 72 h. (B-C) Representative Western blot (B) and densitometry normalized to GAPDH and Ctrl (C) of Periostin across 6 biological replicates. (D-E) Representative Western blots for α-SMA (D) and densitometric quantification (E) following treatment with p38 MAPK inhibitor SB203580 (10 μM). (F-G) Representative Western blots for periosotin (F) and densitometric quantification (G) following treatment with p38 MAPK inhibitor SB203580 (10 μM). (H) Total soluble collagen secretion measured by Picrosirius Red. Data are mean ± SEM. Statistical significance was determined by one-way ANOVA or two-way ANOVA as appropriate.
Anti Stag2 C Terminus, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Intrathoracic ABE treatment corrects Tnni3 R193H mutation in cardiac tissue (A and B) Schematic illustration of the dual AAV9 vector construction strategy and ABE treatment, administered via intrathoracic injections in 6-week-old Tnni3 R193H/R193H mice. (C and D) Efficient correction of Tnni3 mutation in the heart. Assessment of gene editing efficiency in the hearts of Tnni3 R193H/R193H mice 12 weeks after the AAV treatment. A>G editing efficiencies were measured in genomic DNA and mRNA using high-throughput sequencing. Each point represents an individual mouse. ∗∗∗∗ p < 0.0001 based on Student’s unpaired t test analysis. Data are presented as mean ± SEM. (E and F) Lack of liver editing following the AAV9-ABE treatment. As in (C), gene editing efficiency in the livers of Tnni3 R193H/R193H mice after 12 weeks of dual AAV treatment. A>G editing efficiency was also assessed in the genomic DNA and mRNA extracted from liver tissue, demonstrating diminished delivery and expression of the ABE system in the hepatic tissue. Each point represents an individual mouse. ns, not statistically significant (Student’s unpaired t test analysis). Data are presented as mean ± SEM.

Journal: Cell Reports Medicine

Article Title: Therapeutic base editing alleviates restrictive cardiomyopathy

doi: 10.1016/j.xcrm.2026.102639

Figure Lengend Snippet: Intrathoracic ABE treatment corrects Tnni3 R193H mutation in cardiac tissue (A and B) Schematic illustration of the dual AAV9 vector construction strategy and ABE treatment, administered via intrathoracic injections in 6-week-old Tnni3 R193H/R193H mice. (C and D) Efficient correction of Tnni3 mutation in the heart. Assessment of gene editing efficiency in the hearts of Tnni3 R193H/R193H mice 12 weeks after the AAV treatment. A>G editing efficiencies were measured in genomic DNA and mRNA using high-throughput sequencing. Each point represents an individual mouse. ∗∗∗∗ p < 0.0001 based on Student’s unpaired t test analysis. Data are presented as mean ± SEM. (E and F) Lack of liver editing following the AAV9-ABE treatment. As in (C), gene editing efficiency in the livers of Tnni3 R193H/R193H mice after 12 weeks of dual AAV treatment. A>G editing efficiency was also assessed in the genomic DNA and mRNA extracted from liver tissue, demonstrating diminished delivery and expression of the ABE system in the hepatic tissue. Each point represents an individual mouse. ns, not statistically significant (Student’s unpaired t test analysis). Data are presented as mean ± SEM.

Article Snippet: The plasmids Cbh_v5 AAV9-ABE N-terminus (Addgene plasmid no. 137177) and Cbh_v5 AAV9-ABE C-terminus (Addgene plasmid no. 137178) were employed for AAV plasmid construction.

Techniques: Mutagenesis, Plasmid Preparation, Next-Generation Sequencing, Expressing

(A) Periostin ( Postn ) expression assessed by qPCR in primary cardiac fibroblasts treated for 72 h. (B-C) Representative Western blot (B) and densitometry normalized to GAPDH and Ctrl (C) of Periostin across 6 biological replicates. (D-E) Representative Western blots for α-SMA (D) and densitometric quantification (E) following treatment with p38 MAPK inhibitor SB203580 (10 μM). (F-G) Representative Western blots for periosotin (F) and densitometric quantification (G) following treatment with p38 MAPK inhibitor SB203580 (10 μM). (H) Total soluble collagen secretion measured by Picrosirius Red. Data are mean ± SEM. Statistical significance was determined by one-way ANOVA or two-way ANOVA as appropriate.

Journal: bioRxiv

Article Title: WISP1 drives a mechanically active immune modulatory and proliferative cardiac myofibroblast state

doi: 10.64898/2026.02.17.706476

Figure Lengend Snippet: (A) Periostin ( Postn ) expression assessed by qPCR in primary cardiac fibroblasts treated for 72 h. (B-C) Representative Western blot (B) and densitometry normalized to GAPDH and Ctrl (C) of Periostin across 6 biological replicates. (D-E) Representative Western blots for α-SMA (D) and densitometric quantification (E) following treatment with p38 MAPK inhibitor SB203580 (10 μM). (F-G) Representative Western blots for periosotin (F) and densitometric quantification (G) following treatment with p38 MAPK inhibitor SB203580 (10 μM). (H) Total soluble collagen secretion measured by Picrosirius Red. Data are mean ± SEM. Statistical significance was determined by one-way ANOVA or two-way ANOVA as appropriate.

Article Snippet: Membranes were incubated overnight at 4 °C with primary antibodies (1:1,000 in 5% BSA): Periostin (Novus Biologicals, NBP1-30042), α-SMA (Cell Signaling, D4K9N), Col1a1 (Cell Signaling, E8F47), Fibronectin (Cell Signaling, E7F5X), and GAPDH (Cell Signaling, 14C10).

Techniques: Expressing, Western Blot