plasmids cbh v5 aav9 abe n terminus (Addgene inc)
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plasmids cbh v5 aav9 abe n terminus
Plasmids Cbh V5 Aav9 Abe N Terminus, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 28 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/n+terminus/Cbh_v5+AAV-ABE+N-terminal+(Plasmid+%23137177)/pmc13006422-251-1-5
Average 93 stars, based on 28 article reviews
Plasmids Cbh V5 Aav9 Abe N Terminus, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 28 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/n+terminus/Cbh_v5+AAV-ABE+N-terminal+(Plasmid+%23137177)/pmc13006422-251-1-5
Average 93 stars, based on 28 article reviews
plasmids cbh v5 aav9 abe n terminus - by Bioz Stars,
2026-11
93/100 stars
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1) Product Images from "Therapeutic base editing alleviates restrictive cardiomyopathy"
Article Title: Therapeutic base editing alleviates restrictive cardiomyopathy
Journal: Cell Reports Medicine
doi: 10.1016/j.xcrm.2026.102639
Figure Legend 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.
Techniques Used: Mutagenesis, Plasmid Preparation, Next-Generation Sequencing, Expressing
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Gene editors plasmids. plasmid name resource PX549 Addgene #62988 Left-BH-REC12 Derived from PX459, insert BH-REC1-REC2 at N-terminus of REC Left-BH-REC1 Derived from PX459, insert BH-REC1 at N-terminus of REC Right-REC1 Derived from PX459, insert REC1 at c-terminus of REC Right-REC12 Derived from PX459, insert REC1-REC2 at c-terminus of REC Left-Rec12 (=GS-Cas9) Derived from PX459, insert REC1-REC2 at Article Title: Broadly reactive monoclonal antibodies against beta-lactamases for immunodetection of bacterial resistance to antibiotics Article Snippet: Synthetic genes (Invitrogen) of DHA-1 (GenBank no. JN638038.1 ), ACT-14 (GenBank no. JX440354.1 ), PDC-195 (GenBank no. CP007147.1 ) and CMY-34 (GenBank no. EF394370.1 ), each with a BamHI restriction site at the 5’-end and XhoI site at the 3’-end, were cloned into the correspondingly hydrolysed pET28a(+) vector (Sigma-Aldrich, 69864) for the expression of N-terminally His-tagged proteins. .. Similarly, a synthetic gene of ADC-144 (GenBank no. NCXX01000069.1 ) was cloned into the pET28-MBP-TEV vector, fusing the protein with MBP at the Article Title: Epithelial tubule interconnection driven by HGF-Met signaling in the kidney. Article Snippet: .. To generate stable cell lines producing GFP- podocalyxin or RFP- podocalyxin, we cloned canine Podxl1 into the pQCXIZ retroviral plasmid with a GFP or RFP fused to the Article Title: The c-Src inhibitor eCF506 diminishes opioid tolerance creating bias against β-arrestin2 recruitment Article Snippet: .. 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One such often mutated methyltransferase, SETD2, associates with transcribing RNA polymerase II and catalyses H3K36me3—a modification that contributes to gene transcription, splicing and DNA repair.. Although its catalytic function is well-characterized, its non-catalytic roles remain unclear. Article Title: The c-Src inhibitor eCF506 diminishes opioid tolerance creating bias against β-arrestin2 recruitment Article Snippet: .. All constructs are based on human c-Src WT (1-536) c-Src (plasmid #42202; RRID: Addgene_42202), c-terminus truncated (1-249) c-Src (plasmid #42204; RRID: Addgene_42204), Generated:Article Title: Optogenetic construction of de novo integrin-adhesion complexes reveals role for biocondensation in adhesion nucleation Article Snippet: .. The constructs C2-TLN 3LDPXN and C2-TLN 5LDPXN were generated by replacing the FUS-IDR in C2D-TLN with the Article Title: A SETD2-CDK1-lamin axis maintains nuclear morphology and genome stability. 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To generate stable cell lines producing GFP- podocalyxin or RFP- podocalyxin, we cloned canine Podxl1 into the pQCXIZ retroviral plasmid with a GFP or RFP fused to the |
![Aggregated <t>phospho-S670-GRK2</t> on dysfunctional mitochondria of aged AD mice (A) Immunoblot of GRK2 in hippocampal lysates of 18-month-old Tg2576 (AD) and B6 mice. GNAO served as loading control. The lower panel shows quantitative data. (B and C) Immunofluorescence of GRK2 (green) and mitochondrial TOMM40 (red) in the CA1 hippocampal area of 18-month-old Tg2576 (left) and B6 (right) mice. Upper panels show the area marked with a white square frame in a 5-fold higher magnification (scale bars: 20 μm). Nuclei are stained with DAPI (blue). Data are from n = 4 mice per group. Replicates are shown in A and S1B. Quantitative data are shown in (C) and E–S1H. (D–G) Immunoblot of hippocampal cytosolic (D and F) and mitochondrial (E and G) GRK2 and phospho-S670-GRK2 (p-S670) in 18-month-old Tg2576 (AD-18mo), 18-month-old B6 (B6-18mo), and 12-month-old Tg2576 (AD-12mo) mice. Cytosolic PPP2CA was determined (D and F). ADSL and TOMM40 are loading controls. (H) Immunoblot of hippocampal mitochondrial Aβ (IB: Aβ) in 18-month-old Tg2576 (AD-18mo), B6 (B6-18mo), and 12-month-old Tg2576 (AD-12mo) mice. Arrowheads mark monomeric Aβ peptides and APP. TOMM40 is the loading control. (I and J) Hippocampal mitochondrial ACO2 and reactivated ACO2 activity (I) and mitochondrial ATP (J) of 12- and 18-month-old Tg2576 and B6 mice. Data are mean ± SD; n = 4 mice per group (A, C, D, F, I, and J) or n = 4 biological replicates (E, G, and H; hippocampi from three mice were pooled for one isolation, which is defined as a biological replicate); unpaired, two-tailed t test [df = 6; t = 9.179 (A); 3.613, 1.357, 0.3557, 5.674 (C); 3.833, 22.22, 10.66 (D); 6.815, 2.083, 9.466, 2.817 (E); 2.806, 11.00, 4.495 (F); 11.47, 18.28, 11.65, 23.38 (G)]; one-way ANOVA and Tukey’s test [F(2,9) = 55.77 (H); F(3,12) = 113.9, 12.37 (I); 21.54 (J)]. See also A, S1B, S1E–S1H, and .](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_0637/pmc13130637/pmc13130637__gr1.jpg)
![TOMM6 is an interaction partner of phospho-S670-GRK2 (A) Immunoblot of GRK2 in brain lysates of 18- and 12-month-old Tg2576 AD mice. Data are mean ± SD; n = 4 mice; (unpaired, two-tailed t test; df = 6, t = 20.02). (B and C) Immunoaffinity enrichment of phospho-S670-GRK2 (AP: p-S670, lanes 1–4) from 18-month-old (B; lanes 1 and 2) and 12-month-old (C; lanes 3 and 4) Tg2576 mouse brain mitochondria followed by immunoblot detection (IB) of enriched phospho-S670-GRK2 (left) and co-enriched TOMM6 (right). Lane 5 (C) shows a control immuno-affinity matrix (con). Two biological replicates are from 18-month-old mice, and three biological replicates are from 12-month-old Tg2576 mice. (D) Immunoaffinity enrichment of phospho-S670-GRK2 (AP: p-S670-GRK2) from brain mitochondria of 12-month-old Tg2576 mice and nano-LC-ESI-MS/MS identification of co-enriched TOMM6. (E) Immunoblot (IB) of TOMM6 (upper) and TOMM40 (lower) on brain mitochondria from 18-month-old Tg2576 and B6 mice. The right panel shows quantitative data. (F) Immunoaffinity enrichment of TOMM6 (AP: TOMM6) from brain mitochondria of 18-month-old Tg2576 (AD) and B6 (B6) mice, followed by immunoblot detection (IB) of enriched TOMM6 (left) and co-enriched TOMM40 (middle). The right panel shows quantitative data. (E and F) Data are mean ± SD; n = 4 biological replicates; unpaired, two-tailed t test [df = 6; t = 0.06099 (E), 12.59 (F)]. (G and H) In vitro phosphorylation of TOMM6 by GRK2 or p-S670-GRK2 (pS670). TOMM6-ST-AA was not phosphorylated by GRK2. (H) shows quantitative data; mean ± SD; n = 4 biological replicates; one-way ANOVA and Tukey’s test; F(2,9) = 83.12, 206.5. (I) MDS data of TOMM6 showing the frequency distribution of the unfolded molecular weight (MW) of TOMM6 ( n = 40 measurements; left) and the linear regression analysis of the relationship between unfolded MW and TOMM6 (right). (J) Binding energies (E_RDOCK) of monomer-monomer docking, yielding dimers, and tetramer-tetramer docking yielding octamers, of wild-type TOMM6 (WT) and phosphomimetic TOMM6-ST-DD. Data represent means with range; one-way ANOVA and Tukey’s test [F(3,20) = 7.127]. (K) Immunoblot (IB) of TOMM6 in primary neurons expressing wild-type TOMM6 (WT) or TOMM6-ST-DD. Neurons were treated without and with aggregated Aβ and the GRK2 inhibitor, CMPD101 [+Aβ (immunoblot), +Aβ+101 (bar graph)]. Data represent mean ± SD; n = 4 biological replicates; one-way ANOVA and Tukey’s test [F(3,12) = 2141]. See also .](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_0637/pmc13130637/pmc13130637__gr2.jpg)
![Inactive GRK2 enhances TOMM6 aggregation, Aβ plaques, and mortality, whereas wild-type GRK2 is beneficial (A) Immunoblot of hippocampal cytosolic GRK2 in 16-month-old Tg2576- GRK2S670D (S670D) and Tg2576 (AD16mo) mice (upper blot). The control blot detects ADSL (second blot). The third blot shows GRK2 in hippocampal lysates from 16-month-old Tg2576- GRK2S670D (S670D) and 16-month-old Tg2576- GRK2 (GRK2) mice. The lower control blot detects GNAO. (B) Immunoblot of hippocampal cytosolic GRK2 (upper) and p-S670-GRK2 (middle) in 16-month-old Tg2576- GRK2K220R (K220R), Tg2576- GRK2 (GRK2), and Tg2576- GRKInh (Inh) mice. ADSL is the cytosolic loading control. (A and B) Data represent mean ± SD; n = 4 mice per group; unpaired, two-tailed t test (A; df = 6, t = 5.640, 9.369, 4.242); one-way ANOVA and Tukey’s test [B; F(2,9) = 7.991, 31.84]. (C) Immunoblot of hippocampal mitochondrial GRK2 (upper) and mitochondrial TOMM6 (lower) in 16-month-old Tg2576- GRK2S670D (S670D) and Tg2576 (16 mo) mice. TOMM40 is a loading control (middle panel). (D–F) Immunoblot of hippocampal mitochondrial GRK2 (D and E) and TOMM6 (F) in 16-month-old Tg2576- GRK2K220R (K220R), Tg2576- GRK2 (GRK2), and Tg2576- GRKInh (Inh) mice. TOMM40 is the loading control (E, lower panel). (D and F) present quantitative data. (C, D, and F) Data are mean ± SD; n = 4 biological replicates; unpaired, two-tailed t test (C; df = 6, t = 7.403, t = 10.67, t = 4.247); one-way ANOVA and Tukey’s test [D,F; F(2,9) = 38.19, 137.0]. (G) Hippocampal mitochondrial ACO2 activity without (left) and with reactivation (right) in 16-month-old Tg2576- GRK2S670D (S670D), Tg2576- GRK2K220R (K220R), Tg2576- GRKInh (GRKInh), and Tg2576- GRK2 (GRK2) mice in comparison to 16-month-old Tg2576 (AD16mo) mice. Data are mean ± SD; n = 4 mice per group; one-way ANOVA and Tukey’s test; F(4,15) = 63.00 (left), 4.111 (right). (H) Probability of survival of the indicated transgenic mouse lines with Kaplan-Meier survival analysis and log rank (Mantel-Cox) test; n = 103 male and female mice ( n = 136 for Tg- GRK2K220R ); df = 1; chi-square 4.940 and p = 0.0264 for Tg2576- GRK2 vs. Tg2576; chi-square 16.83 and p < 0.0001 for Tg2576- GRK2S670D vs. Tg2576; df = 1; chi-square 20.70 and p < 0.0001 for Tg- GRK2K220R vs. Tg2576; chi-square 7.459 and p = 0.0063 for Tg2576- GRKInh vs. Tg2576; chi-square 28.51 and p < 0.0001 for Tg2576- GRK2K220R vs. Tg2576. (I–K) Hippocampal γ-secretase (I), β-secretase (J), and α-secretase (K) of 16-month-old Tg2576- GRK2S670D (S670D), Tg2576- GRK2K220R (K220R), Tg2576- GRKInh (GRKInh), and Tg2576- GRK2 (GRK2) mice compared to Tg2576 (AD16mo) mice. Data represent mean ± SD; n = 6 mice per group; one-way ANOVA and Tukey’s test; F(4,25) = 55.73 (I), 44.06 (J), 41.47 (K). (L) Aβ plaque load of histological sections shown in (M); E and C. Data are mean ± SD; n = 6 mice per group; one-way ANOVA and Tukey’s test [left panel; F(3,20) = 12.13]; unpaired, two-tailed t test (right panel; df = 10, t = 4.537). (M) Hippocampal Aβ plaques (brown) of 16-month-old Tg2576- GRK2S670D , Tg2576- GRK2K220R , Tg2576- GRKIn h, and Tg2576 (Tg2576 16mo) mice and 18-month-old Tg2576- GRK2 and Tg2576 (Tg2576 18mo) female (f) and male (m) mice. Counterstaining was performed with hematoxylin (HE). Immunohistology is representative of six mice per group; scale bars: 200 μm. Replicates are shown in E and C. See also and .](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_0637/pmc13130637/pmc13130637__gr3.jpg)
