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runx1t1 overexpression plasmid  (Addgene inc)


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    Addgene inc runx1t1 overexpression plasmid
    Identification of <t>RUNX1T1</t> as a novel early driver of early NE transdifferentiation. A. Inverted funnel summarizing stepwise identification of candidate early epigenetic regulators driving NEPC development; B. C. Volcano plot of NEPC (clusters 10,13) vs Adeno (clusters 1–12) and intermediate cluster 14 vs Adeno clusters, fold change >2 and p <0.001 are highlighted; D. Feature UMAP (left) and violin plot (right) of RUNX1T1 expression across all clusters, showing upregulation in clusters 10, 13 and 14; E. RUNX1T1 expression by western-blot in prostate cancer cell lines; F. RNA (left) and protein (right) expression of RUNX1T1 in LTL PDX samples; G. RUNX1T1 expression in bulk RNA-seq from three clinical cohorts; H. Spearman correlation of RUNX1T1 with SYP, NCAM1, CHGA and AR expression across NEPC samples.
    Runx1t1 Overexpression Plasmid, 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
    https://www.bioz.com/result/runx1t1 overexpression plasmid/product/Addgene inc
    Average 93 stars, based on 1 article reviews
    runx1t1 overexpression plasmid - by Bioz Stars, 2026-02
    93/100 stars

    Images

    1) Product Images from "Longitudinal single-cell analysis reveals RUNX1T1 as an early driver in treatment-induced neuroendocrine transdifferentiation"

    Article Title: Longitudinal single-cell analysis reveals RUNX1T1 as an early driver in treatment-induced neuroendocrine transdifferentiation

    Journal: bioRxiv

    doi: 10.1101/2025.05.14.653660

    Identification of RUNX1T1 as a novel early driver of early NE transdifferentiation. A. Inverted funnel summarizing stepwise identification of candidate early epigenetic regulators driving NEPC development; B. C. Volcano plot of NEPC (clusters 10,13) vs Adeno (clusters 1–12) and intermediate cluster 14 vs Adeno clusters, fold change >2 and p <0.001 are highlighted; D. Feature UMAP (left) and violin plot (right) of RUNX1T1 expression across all clusters, showing upregulation in clusters 10, 13 and 14; E. RUNX1T1 expression by western-blot in prostate cancer cell lines; F. RNA (left) and protein (right) expression of RUNX1T1 in LTL PDX samples; G. RUNX1T1 expression in bulk RNA-seq from three clinical cohorts; H. Spearman correlation of RUNX1T1 with SYP, NCAM1, CHGA and AR expression across NEPC samples.
    Figure Legend Snippet: Identification of RUNX1T1 as a novel early driver of early NE transdifferentiation. A. Inverted funnel summarizing stepwise identification of candidate early epigenetic regulators driving NEPC development; B. C. Volcano plot of NEPC (clusters 10,13) vs Adeno (clusters 1–12) and intermediate cluster 14 vs Adeno clusters, fold change >2 and p <0.001 are highlighted; D. Feature UMAP (left) and violin plot (right) of RUNX1T1 expression across all clusters, showing upregulation in clusters 10, 13 and 14; E. RUNX1T1 expression by western-blot in prostate cancer cell lines; F. RNA (left) and protein (right) expression of RUNX1T1 in LTL PDX samples; G. RUNX1T1 expression in bulk RNA-seq from three clinical cohorts; H. Spearman correlation of RUNX1T1 with SYP, NCAM1, CHGA and AR expression across NEPC samples.

    Techniques Used: Expressing, Western Blot, RNA Sequencing

    RUNX1T1 drives ARPI-induced NE transdifferentiation and resistance in prostate adenocarcinoma. A. qRT–PCR (top) and western blot (bottom) confirming RUNX1T1 overexpression in V16D cells, Vinculin serves as loading control; B. Flow cytometry histograms of NCAM1 in WT (green/orange) and RUNX1T1-OE (red/blue) V16D cells after 2 weeks in FBS (left) or 10 µM enzalutamide (Enza; right). Mean fluorescence intensity (MFI) is indicated; C. Bar plot of normalized NCAM1 MFI in WT and RUNX1T1-OE cells under FBS and Enza; D. qRT–PCR of RNA expression of NE markers (CHGA, SYP, NSE, NCAM1), AR and AR target KLK3 in WT and RUNX1T1-OE cells after 2 weeks cultured with FBS or Enza; E. Western blot of RUNX1T1, NCAM1, NSE, SYP and CHGA in WT and RUNX1T1-OE V16D cells cultured in FBS or Enza; vinculin as loading control; F. RUNX1T1 - OE markedly enhances the proliferation rate of V16D cells cultured in 10 µM enzalutamide, as shown by real - time growth curves (left; WT in blue, OE in red) and by endpoint phase-area confluence and absorbance at day 15 (right; *** p < 0.001, **** p < 0.0001).
    Figure Legend Snippet: RUNX1T1 drives ARPI-induced NE transdifferentiation and resistance in prostate adenocarcinoma. A. qRT–PCR (top) and western blot (bottom) confirming RUNX1T1 overexpression in V16D cells, Vinculin serves as loading control; B. Flow cytometry histograms of NCAM1 in WT (green/orange) and RUNX1T1-OE (red/blue) V16D cells after 2 weeks in FBS (left) or 10 µM enzalutamide (Enza; right). Mean fluorescence intensity (MFI) is indicated; C. Bar plot of normalized NCAM1 MFI in WT and RUNX1T1-OE cells under FBS and Enza; D. qRT–PCR of RNA expression of NE markers (CHGA, SYP, NSE, NCAM1), AR and AR target KLK3 in WT and RUNX1T1-OE cells after 2 weeks cultured with FBS or Enza; E. Western blot of RUNX1T1, NCAM1, NSE, SYP and CHGA in WT and RUNX1T1-OE V16D cells cultured in FBS or Enza; vinculin as loading control; F. RUNX1T1 - OE markedly enhances the proliferation rate of V16D cells cultured in 10 µM enzalutamide, as shown by real - time growth curves (left; WT in blue, OE in red) and by endpoint phase-area confluence and absorbance at day 15 (right; *** p < 0.001, **** p < 0.0001).

    Techniques Used: Quantitative RT-PCR, Western Blot, Over Expression, Control, Flow Cytometry, Fluorescence, RNA Expression, Cell Culture

    RUNX1T1 knockdown reverses NE phenotype and impairs NEPC cell survival. A. NA expression of RUNX1T1, NCAM1, NSE, ASCL1 and AR by qRT-PCR in H660-ShNC and two independent H660-ShRUNX1T1 lines (Sh1, Sh2) with (Dox+) or without (Dox-) doxycycline (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001); B. Protein expression of RUNX1T1, NCAM1, ASCL1, NSE, CHGA and SYP by western blot in H660-ShNC and H660-ShRUNX1T1 cells ± doxycycline, Vinculin serves as loading control; C. Cell viability of H660-ShNC and H660-ShRUNX1T1 over 21 days with or without Dox, showing impaired proliferation upon RUNX1T1 knockdown; D. EdU assay by flow cytometry showed H660-ShRUNX1T1 cells incorporate fewer EdU+ cells (Q3) than H660-ShNC, indicating RUNX1T1 knockdown impairs H660 proliferation; E. Annexin V/PI apoptosis assay revealing increased apoptotic fraction (Q3) in H660-ShRUNX1T1 cells; F. GSEA bar chart of the top 25 downregulated GO pathways in H660-ShRUNX1T1 vs ShNC (NES values), highlighting loss of neuronal development programs (red); G. Hallmark pathway dot plot of upregulated features in H660-ShRUNX1T1 cells (dot size represents gene counts and color indicates –log₁₀ p); H. I. J. GSEA enrichment plots showing significant enrichment in H660-ShRUNX1T1 cells of the published NEPC-down signature (G), the EMT hallmark pathway (H), and the cluster 14 signature (top 50 upregulated genes; J), with NES and FDR values indicated.
    Figure Legend Snippet: RUNX1T1 knockdown reverses NE phenotype and impairs NEPC cell survival. A. NA expression of RUNX1T1, NCAM1, NSE, ASCL1 and AR by qRT-PCR in H660-ShNC and two independent H660-ShRUNX1T1 lines (Sh1, Sh2) with (Dox+) or without (Dox-) doxycycline (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001); B. Protein expression of RUNX1T1, NCAM1, ASCL1, NSE, CHGA and SYP by western blot in H660-ShNC and H660-ShRUNX1T1 cells ± doxycycline, Vinculin serves as loading control; C. Cell viability of H660-ShNC and H660-ShRUNX1T1 over 21 days with or without Dox, showing impaired proliferation upon RUNX1T1 knockdown; D. EdU assay by flow cytometry showed H660-ShRUNX1T1 cells incorporate fewer EdU+ cells (Q3) than H660-ShNC, indicating RUNX1T1 knockdown impairs H660 proliferation; E. Annexin V/PI apoptosis assay revealing increased apoptotic fraction (Q3) in H660-ShRUNX1T1 cells; F. GSEA bar chart of the top 25 downregulated GO pathways in H660-ShRUNX1T1 vs ShNC (NES values), highlighting loss of neuronal development programs (red); G. Hallmark pathway dot plot of upregulated features in H660-ShRUNX1T1 cells (dot size represents gene counts and color indicates –log₁₀ p); H. I. J. GSEA enrichment plots showing significant enrichment in H660-ShRUNX1T1 cells of the published NEPC-down signature (G), the EMT hallmark pathway (H), and the cluster 14 signature (top 50 upregulated genes; J), with NES and FDR values indicated.

    Techniques Used: Knockdown, Expressing, Quantitative RT-PCR, Western Blot, Control, EdU Assay, Flow Cytometry, Apoptosis Assay



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    Identification of <t>RUNX1T1</t> as a novel early driver of early NE transdifferentiation. A. Inverted funnel summarizing stepwise identification of candidate early epigenetic regulators driving NEPC development; B. C. Volcano plot of NEPC (clusters 10,13) vs Adeno (clusters 1–12) and intermediate cluster 14 vs Adeno clusters, fold change >2 and p <0.001 are highlighted; D. Feature UMAP (left) and violin plot (right) of RUNX1T1 expression across all clusters, showing upregulation in clusters 10, 13 and 14; E. RUNX1T1 expression by western-blot in prostate cancer cell lines; F. RNA (left) and protein (right) expression of RUNX1T1 in LTL PDX samples; G. RUNX1T1 expression in bulk RNA-seq from three clinical cohorts; H. Spearman correlation of RUNX1T1 with SYP, NCAM1, CHGA and AR expression across NEPC samples.
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    Image Search Results


    Identification of RUNX1T1 as a novel early driver of early NE transdifferentiation. A. Inverted funnel summarizing stepwise identification of candidate early epigenetic regulators driving NEPC development; B. C. Volcano plot of NEPC (clusters 10,13) vs Adeno (clusters 1–12) and intermediate cluster 14 vs Adeno clusters, fold change >2 and p <0.001 are highlighted; D. Feature UMAP (left) and violin plot (right) of RUNX1T1 expression across all clusters, showing upregulation in clusters 10, 13 and 14; E. RUNX1T1 expression by western-blot in prostate cancer cell lines; F. RNA (left) and protein (right) expression of RUNX1T1 in LTL PDX samples; G. RUNX1T1 expression in bulk RNA-seq from three clinical cohorts; H. Spearman correlation of RUNX1T1 with SYP, NCAM1, CHGA and AR expression across NEPC samples.

    Journal: bioRxiv

    Article Title: Longitudinal single-cell analysis reveals RUNX1T1 as an early driver in treatment-induced neuroendocrine transdifferentiation

    doi: 10.1101/2025.05.14.653660

    Figure Lengend Snippet: Identification of RUNX1T1 as a novel early driver of early NE transdifferentiation. A. Inverted funnel summarizing stepwise identification of candidate early epigenetic regulators driving NEPC development; B. C. Volcano plot of NEPC (clusters 10,13) vs Adeno (clusters 1–12) and intermediate cluster 14 vs Adeno clusters, fold change >2 and p <0.001 are highlighted; D. Feature UMAP (left) and violin plot (right) of RUNX1T1 expression across all clusters, showing upregulation in clusters 10, 13 and 14; E. RUNX1T1 expression by western-blot in prostate cancer cell lines; F. RNA (left) and protein (right) expression of RUNX1T1 in LTL PDX samples; G. RUNX1T1 expression in bulk RNA-seq from three clinical cohorts; H. Spearman correlation of RUNX1T1 with SYP, NCAM1, CHGA and AR expression across NEPC samples.

    Article Snippet: The RUNX1T1 overexpression plasmid (TFORF1679, Addgene#143835) and the corresponding GFP vector control (TFORF3549, Addgene#145025) were used in these experiments.

    Techniques: Expressing, Western Blot, RNA Sequencing

    RUNX1T1 drives ARPI-induced NE transdifferentiation and resistance in prostate adenocarcinoma. A. qRT–PCR (top) and western blot (bottom) confirming RUNX1T1 overexpression in V16D cells, Vinculin serves as loading control; B. Flow cytometry histograms of NCAM1 in WT (green/orange) and RUNX1T1-OE (red/blue) V16D cells after 2 weeks in FBS (left) or 10 µM enzalutamide (Enza; right). Mean fluorescence intensity (MFI) is indicated; C. Bar plot of normalized NCAM1 MFI in WT and RUNX1T1-OE cells under FBS and Enza; D. qRT–PCR of RNA expression of NE markers (CHGA, SYP, NSE, NCAM1), AR and AR target KLK3 in WT and RUNX1T1-OE cells after 2 weeks cultured with FBS or Enza; E. Western blot of RUNX1T1, NCAM1, NSE, SYP and CHGA in WT and RUNX1T1-OE V16D cells cultured in FBS or Enza; vinculin as loading control; F. RUNX1T1 - OE markedly enhances the proliferation rate of V16D cells cultured in 10 µM enzalutamide, as shown by real - time growth curves (left; WT in blue, OE in red) and by endpoint phase-area confluence and absorbance at day 15 (right; *** p < 0.001, **** p < 0.0001).

    Journal: bioRxiv

    Article Title: Longitudinal single-cell analysis reveals RUNX1T1 as an early driver in treatment-induced neuroendocrine transdifferentiation

    doi: 10.1101/2025.05.14.653660

    Figure Lengend Snippet: RUNX1T1 drives ARPI-induced NE transdifferentiation and resistance in prostate adenocarcinoma. A. qRT–PCR (top) and western blot (bottom) confirming RUNX1T1 overexpression in V16D cells, Vinculin serves as loading control; B. Flow cytometry histograms of NCAM1 in WT (green/orange) and RUNX1T1-OE (red/blue) V16D cells after 2 weeks in FBS (left) or 10 µM enzalutamide (Enza; right). Mean fluorescence intensity (MFI) is indicated; C. Bar plot of normalized NCAM1 MFI in WT and RUNX1T1-OE cells under FBS and Enza; D. qRT–PCR of RNA expression of NE markers (CHGA, SYP, NSE, NCAM1), AR and AR target KLK3 in WT and RUNX1T1-OE cells after 2 weeks cultured with FBS or Enza; E. Western blot of RUNX1T1, NCAM1, NSE, SYP and CHGA in WT and RUNX1T1-OE V16D cells cultured in FBS or Enza; vinculin as loading control; F. RUNX1T1 - OE markedly enhances the proliferation rate of V16D cells cultured in 10 µM enzalutamide, as shown by real - time growth curves (left; WT in blue, OE in red) and by endpoint phase-area confluence and absorbance at day 15 (right; *** p < 0.001, **** p < 0.0001).

    Article Snippet: The RUNX1T1 overexpression plasmid (TFORF1679, Addgene#143835) and the corresponding GFP vector control (TFORF3549, Addgene#145025) were used in these experiments.

    Techniques: Quantitative RT-PCR, Western Blot, Over Expression, Control, Flow Cytometry, Fluorescence, RNA Expression, Cell Culture

    RUNX1T1 knockdown reverses NE phenotype and impairs NEPC cell survival. A. NA expression of RUNX1T1, NCAM1, NSE, ASCL1 and AR by qRT-PCR in H660-ShNC and two independent H660-ShRUNX1T1 lines (Sh1, Sh2) with (Dox+) or without (Dox-) doxycycline (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001); B. Protein expression of RUNX1T1, NCAM1, ASCL1, NSE, CHGA and SYP by western blot in H660-ShNC and H660-ShRUNX1T1 cells ± doxycycline, Vinculin serves as loading control; C. Cell viability of H660-ShNC and H660-ShRUNX1T1 over 21 days with or without Dox, showing impaired proliferation upon RUNX1T1 knockdown; D. EdU assay by flow cytometry showed H660-ShRUNX1T1 cells incorporate fewer EdU+ cells (Q3) than H660-ShNC, indicating RUNX1T1 knockdown impairs H660 proliferation; E. Annexin V/PI apoptosis assay revealing increased apoptotic fraction (Q3) in H660-ShRUNX1T1 cells; F. GSEA bar chart of the top 25 downregulated GO pathways in H660-ShRUNX1T1 vs ShNC (NES values), highlighting loss of neuronal development programs (red); G. Hallmark pathway dot plot of upregulated features in H660-ShRUNX1T1 cells (dot size represents gene counts and color indicates –log₁₀ p); H. I. J. GSEA enrichment plots showing significant enrichment in H660-ShRUNX1T1 cells of the published NEPC-down signature (G), the EMT hallmark pathway (H), and the cluster 14 signature (top 50 upregulated genes; J), with NES and FDR values indicated.

    Journal: bioRxiv

    Article Title: Longitudinal single-cell analysis reveals RUNX1T1 as an early driver in treatment-induced neuroendocrine transdifferentiation

    doi: 10.1101/2025.05.14.653660

    Figure Lengend Snippet: RUNX1T1 knockdown reverses NE phenotype and impairs NEPC cell survival. A. NA expression of RUNX1T1, NCAM1, NSE, ASCL1 and AR by qRT-PCR in H660-ShNC and two independent H660-ShRUNX1T1 lines (Sh1, Sh2) with (Dox+) or without (Dox-) doxycycline (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001); B. Protein expression of RUNX1T1, NCAM1, ASCL1, NSE, CHGA and SYP by western blot in H660-ShNC and H660-ShRUNX1T1 cells ± doxycycline, Vinculin serves as loading control; C. Cell viability of H660-ShNC and H660-ShRUNX1T1 over 21 days with or without Dox, showing impaired proliferation upon RUNX1T1 knockdown; D. EdU assay by flow cytometry showed H660-ShRUNX1T1 cells incorporate fewer EdU+ cells (Q3) than H660-ShNC, indicating RUNX1T1 knockdown impairs H660 proliferation; E. Annexin V/PI apoptosis assay revealing increased apoptotic fraction (Q3) in H660-ShRUNX1T1 cells; F. GSEA bar chart of the top 25 downregulated GO pathways in H660-ShRUNX1T1 vs ShNC (NES values), highlighting loss of neuronal development programs (red); G. Hallmark pathway dot plot of upregulated features in H660-ShRUNX1T1 cells (dot size represents gene counts and color indicates –log₁₀ p); H. I. J. GSEA enrichment plots showing significant enrichment in H660-ShRUNX1T1 cells of the published NEPC-down signature (G), the EMT hallmark pathway (H), and the cluster 14 signature (top 50 upregulated genes; J), with NES and FDR values indicated.

    Article Snippet: The RUNX1T1 overexpression plasmid (TFORF1679, Addgene#143835) and the corresponding GFP vector control (TFORF3549, Addgene#145025) were used in these experiments.

    Techniques: Knockdown, Expressing, Quantitative RT-PCR, Western Blot, Control, EdU Assay, Flow Cytometry, Apoptosis Assay