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dnmt3a knockout plasmid  (Addgene inc)


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    Addgene inc dnmt3a knockout plasmid
    Figure 4. SNHG1 bound to <t>DNMT3A</t> protein and promoted the interaction of DNMT3A with the miR-129-2 promoter, thereby hyper-methylating and inhibiting the transcription of miR-129-2. (A) T24T(Vector) and T24T(SNHG1) cells were incubated with Act-D for 0, 10, and 20h. Total RNA
    Dnmt3a Knockout Plasmid, supplied by Addgene inc, used in various techniques. Bioz Stars score: 94/100, based on 31 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/dnmt3a knockout plasmid/product/Addgene inc
    Average 94 stars, based on 31 article reviews
    dnmt3a knockout plasmid - by Bioz Stars, 2026-05
    94/100 stars

    Images

    1) Product Images from "DNMT3A/ miR-129-2-5p /Rac1 Is an Effector Pathway for SNHG1 to Drive Stem-Cell-like and Invasive Behaviors of Advanced Bladder Cancer Cells."

    Article Title: DNMT3A/ miR-129-2-5p /Rac1 Is an Effector Pathway for SNHG1 to Drive Stem-Cell-like and Invasive Behaviors of Advanced Bladder Cancer Cells.

    Journal: Cancers

    doi: 10.3390/cancers14174159

    Figure 4. SNHG1 bound to DNMT3A protein and promoted the interaction of DNMT3A with the miR-129-2 promoter, thereby hyper-methylating and inhibiting the transcription of miR-129-2. (A) T24T(Vector) and T24T(SNHG1) cells were incubated with Act-D for 0, 10, and 20h. Total RNA
    Figure Legend Snippet: Figure 4. SNHG1 bound to DNMT3A protein and promoted the interaction of DNMT3A with the miR-129-2 promoter, thereby hyper-methylating and inhibiting the transcription of miR-129-2. (A) T24T(Vector) and T24T(SNHG1) cells were incubated with Act-D for 0, 10, and 20h. Total RNA

    Techniques Used: Plasmid Preparation, Incubation

    Figure 5. The binding of SNHG1 to DNMT3A protein inhibited miR-129-5p expression and increased Rac1 expression in UMUC3 cells. (A, Left panel) The total protein extracts from indicated cells were subjected to Western blotting to determine the expression of DNMT1, DNMT3A, and DNMT3B. (A, Right panel) Relative protein levels determined by densitometry and expressed as ratios versus β-Actin. (B) An RNA pull-down assay was employed to determine the interaction between SNHG1 and DNMT3A. Antisense RNA sequences of SNHG1 were used as negative controls (NC). (C, Left
    Figure Legend Snippet: Figure 5. The binding of SNHG1 to DNMT3A protein inhibited miR-129-5p expression and increased Rac1 expression in UMUC3 cells. (A, Left panel) The total protein extracts from indicated cells were subjected to Western blotting to determine the expression of DNMT1, DNMT3A, and DNMT3B. (A, Right panel) Relative protein levels determined by densitometry and expressed as ratios versus β-Actin. (B) An RNA pull-down assay was employed to determine the interaction between SNHG1 and DNMT3A. Antisense RNA sequences of SNHG1 were used as negative controls (NC). (C, Left

    Techniques Used: Binding Assay, Expressing, Western Blot, Pull Down Assay

    Figure 6. The sphere-forming T24T cells with high expression of SNHG1 and Rac1 and low expression of miR-129-5p were markedly more invasive than the non-sphere-forming T24T cells. (A,B) The isolated sphered T24T cells were subjected to transwell migration and invasion assays, and the results are presented relative to their parental T24T cells. (C–E) The parental T24T and sphered T24T cells were collected, and the proteins were extracted and subjected to either Western blotting to assess the expression of Rac1 (C) or real-time PCR to determine the expression of SNHG1 (D) and miR-129-5p levels (E). The results are presented as means ± SD from triplicate experiments, and asterisks (*) indicate a significant difference (p < 0.01). (F) A schematic model of the SNHG1/DNMT3A/miR- 129-5p/Rac1 signaling pathway in regulating the stem-cell-like and invasive properties of advanced bladder cancer cells. Bars in (A) are equal to 100 µm.
    Figure Legend Snippet: Figure 6. The sphere-forming T24T cells with high expression of SNHG1 and Rac1 and low expression of miR-129-5p were markedly more invasive than the non-sphere-forming T24T cells. (A,B) The isolated sphered T24T cells were subjected to transwell migration and invasion assays, and the results are presented relative to their parental T24T cells. (C–E) The parental T24T and sphered T24T cells were collected, and the proteins were extracted and subjected to either Western blotting to assess the expression of Rac1 (C) or real-time PCR to determine the expression of SNHG1 (D) and miR-129-5p levels (E). The results are presented as means ± SD from triplicate experiments, and asterisks (*) indicate a significant difference (p < 0.01). (F) A schematic model of the SNHG1/DNMT3A/miR- 129-5p/Rac1 signaling pathway in regulating the stem-cell-like and invasive properties of advanced bladder cancer cells. Bars in (A) are equal to 100 µm.

    Techniques Used: Expressing, Isolation, Migration, Western Blot, Real-time Polymerase Chain Reaction



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    Figure 4. SNHG1 bound to <t>DNMT3A</t> protein and promoted the interaction of DNMT3A with the miR-129-2 promoter, thereby hyper-methylating and inhibiting the transcription of miR-129-2. (A) T24T(Vector) and T24T(SNHG1) cells were incubated with Act-D for 0, 10, and 20h. Total RNA
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    Figure 4. SNHG1 bound to <t>DNMT3A</t> protein and promoted the interaction of DNMT3A with the miR-129-2 promoter, thereby hyper-methylating and inhibiting the transcription of miR-129-2. (A) T24T(Vector) and T24T(SNHG1) cells were incubated with Act-D for 0, 10, and 20h. Total RNA
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    Image Search Results


    Figure 4. SNHG1 bound to DNMT3A protein and promoted the interaction of DNMT3A with the miR-129-2 promoter, thereby hyper-methylating and inhibiting the transcription of miR-129-2. (A) T24T(Vector) and T24T(SNHG1) cells were incubated with Act-D for 0, 10, and 20h. Total RNA

    Journal: Cancers

    Article Title: DNMT3A/ miR-129-2-5p /Rac1 Is an Effector Pathway for SNHG1 to Drive Stem-Cell-like and Invasive Behaviors of Advanced Bladder Cancer Cells.

    doi: 10.3390/cancers14174159

    Figure Lengend Snippet: Figure 4. SNHG1 bound to DNMT3A protein and promoted the interaction of DNMT3A with the miR-129-2 promoter, thereby hyper-methylating and inhibiting the transcription of miR-129-2. (A) T24T(Vector) and T24T(SNHG1) cells were incubated with Act-D for 0, 10, and 20h. Total RNA

    Article Snippet: The DNMT3A knockout plasmid and the miR-129-2 expression plasmid were obtained from Addgene.

    Techniques: Plasmid Preparation, Incubation

    Figure 5. The binding of SNHG1 to DNMT3A protein inhibited miR-129-5p expression and increased Rac1 expression in UMUC3 cells. (A, Left panel) The total protein extracts from indicated cells were subjected to Western blotting to determine the expression of DNMT1, DNMT3A, and DNMT3B. (A, Right panel) Relative protein levels determined by densitometry and expressed as ratios versus β-Actin. (B) An RNA pull-down assay was employed to determine the interaction between SNHG1 and DNMT3A. Antisense RNA sequences of SNHG1 were used as negative controls (NC). (C, Left

    Journal: Cancers

    Article Title: DNMT3A/ miR-129-2-5p /Rac1 Is an Effector Pathway for SNHG1 to Drive Stem-Cell-like and Invasive Behaviors of Advanced Bladder Cancer Cells.

    doi: 10.3390/cancers14174159

    Figure Lengend Snippet: Figure 5. The binding of SNHG1 to DNMT3A protein inhibited miR-129-5p expression and increased Rac1 expression in UMUC3 cells. (A, Left panel) The total protein extracts from indicated cells were subjected to Western blotting to determine the expression of DNMT1, DNMT3A, and DNMT3B. (A, Right panel) Relative protein levels determined by densitometry and expressed as ratios versus β-Actin. (B) An RNA pull-down assay was employed to determine the interaction between SNHG1 and DNMT3A. Antisense RNA sequences of SNHG1 were used as negative controls (NC). (C, Left

    Article Snippet: The DNMT3A knockout plasmid and the miR-129-2 expression plasmid were obtained from Addgene.

    Techniques: Binding Assay, Expressing, Western Blot, Pull Down Assay

    Figure 6. The sphere-forming T24T cells with high expression of SNHG1 and Rac1 and low expression of miR-129-5p were markedly more invasive than the non-sphere-forming T24T cells. (A,B) The isolated sphered T24T cells were subjected to transwell migration and invasion assays, and the results are presented relative to their parental T24T cells. (C–E) The parental T24T and sphered T24T cells were collected, and the proteins were extracted and subjected to either Western blotting to assess the expression of Rac1 (C) or real-time PCR to determine the expression of SNHG1 (D) and miR-129-5p levels (E). The results are presented as means ± SD from triplicate experiments, and asterisks (*) indicate a significant difference (p < 0.01). (F) A schematic model of the SNHG1/DNMT3A/miR- 129-5p/Rac1 signaling pathway in regulating the stem-cell-like and invasive properties of advanced bladder cancer cells. Bars in (A) are equal to 100 µm.

    Journal: Cancers

    Article Title: DNMT3A/ miR-129-2-5p /Rac1 Is an Effector Pathway for SNHG1 to Drive Stem-Cell-like and Invasive Behaviors of Advanced Bladder Cancer Cells.

    doi: 10.3390/cancers14174159

    Figure Lengend Snippet: Figure 6. The sphere-forming T24T cells with high expression of SNHG1 and Rac1 and low expression of miR-129-5p were markedly more invasive than the non-sphere-forming T24T cells. (A,B) The isolated sphered T24T cells were subjected to transwell migration and invasion assays, and the results are presented relative to their parental T24T cells. (C–E) The parental T24T and sphered T24T cells were collected, and the proteins were extracted and subjected to either Western blotting to assess the expression of Rac1 (C) or real-time PCR to determine the expression of SNHG1 (D) and miR-129-5p levels (E). The results are presented as means ± SD from triplicate experiments, and asterisks (*) indicate a significant difference (p < 0.01). (F) A schematic model of the SNHG1/DNMT3A/miR- 129-5p/Rac1 signaling pathway in regulating the stem-cell-like and invasive properties of advanced bladder cancer cells. Bars in (A) are equal to 100 µm.

    Article Snippet: The DNMT3A knockout plasmid and the miR-129-2 expression plasmid were obtained from Addgene.

    Techniques: Expressing, Isolation, Migration, Western Blot, Real-time Polymerase Chain Reaction

    Table 3

    Journal: Toxicology research

    Article Title: Epigenetic Toxicity of Trichloroethylene: A Single-Molecule Perspective

    doi: 10.1039/C5TX00454C

    Figure Lengend Snippet: Table 3

    Article Snippet: Dnmt3a knockout with CRISPR/Cas9 Endogenous Dnmt3a in HeLa cells was knocked out with Dnmt3a CRISPR/Cas9 KO plasmids (sc-400323,) and UltraCruz transfection reagent (sc-395739, Santa Cruz Biotechnology).

    Techniques: Diffusion-based Assay