TAF10 Antibody - BSA Free

Western Blot: TAF10 Antibody - BSA Free [NBP1-80706] -

Z363 promotes MYC and TAF10 degradation. (A) Identification of small inhibitory molecules for MYC. (B) MCF7 cells were treated with Z363 (0, 2.5, 7.5 and 15 μg/ml) for 24 h. The protein levels of MYC and TAF10 were analysed by Western blotting. (C) MCF7 cells were treated with Z363 (7.5 μg/ml) for 0, 6, 12 and 24 h. Furthermore, the protein levels of MYC and TAF10 were analysed by Western blotting. (D) MCF7 cells were treated with 25 μM MG132 at the indicated time points, followed by treatment with or without Z363 (7.5 μg/ml) for 24 h, and MYC and TAF10 expressions were analysed by Western blotting. (E) Western blots for MYC, phosphorylated MYC T58 and S62 in MCF7 cells treated with Z363 at the times indicated. (F) Ratios of pT58 or pS62 to total MYC protein levels from the experiment (E). (G) IF staining for Ki67 and pT58 in Z363‐treated MCF7 cells, scale bar, 10 μm. (H) MCF7 cells were treated with 25 μM MG132 for 2 h, followed by Z363 treatment (7.5 μg/ml) for 24 h. Expressions of MYC and TAF10 were assessed using Western blot analysis. Data shown in F were analysed by two‐way ANOVA. Fluorescence images and blots were representative of three independent experiments. All data are presented as the mean +/- SEM of n = 3. ***p <.001, ns, no significance Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36639831), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: TAF10 Antibody - BSA Free [NBP1-80706] -

TAF10 promotes cancer cell proliferation and migration. (A and B) MCF7 cells were transfected with Flag‐labelled MYC and HA‐labelled TAF10, and the interaction between MYC and TAF10 was detected by Co‐IP. (C) Endogenous interaction of MYC and TAF10 was tested in MCF7 cells. (D) Schematic representation of MYC mutants. (E) Schematic representation of TAF10 mutants. Co‐IP was used to detect the interaction between the TAF10 mutants and MYC in MCF7 cells. Co‐IP was used to detect the interaction. (G) Interaction between the MYC mutants and TAF10 in MCF7 cells was detected using Co‐IP. (H) MCF7 cells were co‐transfected with empty vector (Vec) and HA‐labelled TAF10 wild‐type (HA‐TAF10 WT) or mutants (HA‐TAF10 delta 1‐116, HA‐TAF10 delta 116‐206, HA‐TAF10 delta 206‐218). The MYC promoter activity was analysed using the dual luciferase reporter assay 24 h later. (I) Overexpression of TAF10 assessed the capacity for colony formation. MCF7 cells were transfected with either Control‐vec or HA‐TAF10. The ability of cells to form colonies was measured using crystal violet staining. (J) Overexpression of TAF10 measured the migration capacity of cells. MCF7 cells were transfected with either Control‐vec or HA‐TAF10. Transwell assays were used to assess the migration capacity of cells. Scale bar, 20 μm. Data shown in H were analysed by one‐way ANOVA. Data shown in I and J were analysed by t‐test. The blots represented three independent experiments. All data are presented as the mean +/- SEM of n = 3. ***p <.001, **p <.01, ns, no significance Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36639831), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: TAF10 Antibody - BSA Free [NBP1-80706] -

Z363 promotes MYC and TAF10 degradation. (A) Identification of small inhibitory molecules for MYC. (B) MCF7 cells were treated with Z363 (0, 2.5, 7.5 and 15 μg/ml) for 24 h. The protein levels of MYC and TAF10 were analysed by Western blotting. (C) MCF7 cells were treated with Z363 (7.5 μg/ml) for 0, 6, 12 and 24 h. Furthermore, the protein levels of MYC and TAF10 were analysed by Western blotting. (D) MCF7 cells were treated with 25 μM MG132 at the indicated time points, followed by treatment with or without Z363 (7.5 μg/ml) for 24 h, and MYC and TAF10 expressions were analysed by Western blotting. (E) Western blots for MYC, phosphorylated MYC T58 and S62 in MCF7 cells treated with Z363 at the times indicated. (F) Ratios of pT58 or pS62 to total MYC protein levels from the experiment (E). (G) IF staining for Ki67 and pT58 in Z363‐treated MCF7 cells, scale bar, 10 μm. (H) MCF7 cells were treated with 25 μM MG132 for 2 h, followed by Z363 treatment (7.5 μg/ml) for 24 h. Expressions of MYC and TAF10 were assessed using Western blot analysis. Data shown in F were analysed by two‐way ANOVA. Fluorescence images and blots were representative of three independent experiments. All data are presented as the mean +/- SEM of n = 3. ***p <.001, ns, no significance Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36639831), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: TAF10 Antibody - BSA Free [NBP1-80706] -

TAF10 plays oncogenic role in LUAD. A mRNA expression levels of the corresponding gene in human normal bronchial epithelial cells (16HBE) and LUAD cell lines. B TAF10 mRNA expression levels in various tumors and matched normal tissues from the TCGA and GTEx databases, analyzed using SangerBox platform. C The stemness features (RNA expression-based stemness scores) analyses of TAF10 across different types of tumors in the TCGA database, analyzed by SangerBox platform. (D-E) Disease-free survival (D) and overall survival (E) analyses of TAF10 in LUAD samples from the TCGA database, performed using the GEPIA2 platform. (F) Protein expression levels of TAF10 in 16HBE and LUAD cell lines. G Representative IHC analysis of TAF10 expression in paired adjacent and tumorous tissues from LUAD patients (n = 5 pairs, 10 tissues in total). Black scale bar: 50 μm; red scale bar: 20 μm. H TAF10 knockdown in LUAD cells was confirmed by Western blot analysis. I LUAD cell lines were stably transfected with either shCtl or shTAF10 for 24, 48, and 72 h, and cell viability was measured using a CCK-8 assay. (J) The effect of TAF10 knockdown on colony formation in LUAD cells was assessed using a colony formation assay. (K) Representative micrographs and quantification of tumor sphere formation by TAF10-silenced cells (shTAF10) or vector control cells (shCtl). Scale bar, 100 μm. L–N GSEA plot of KEGG (L), GOBP (M), and Hallmark pathways (N), grouped by TAF10 expression into TAF10-high and TAF10-low subgroups. NES represents the normalized enrichment score, and FDR represents the adjusted p-value Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/39987127), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: TAF10 Antibody - BSA Free [NBP1-80706] -

TAF10 promotes cancer cell proliferation and migration. (A and B) MCF7 cells were transfected with Flag‐labelled MYC and HA‐labelled TAF10, and the interaction between MYC and TAF10 was detected by Co‐IP. (C) Endogenous interaction of MYC and TAF10 was tested in MCF7 cells. (D) Schematic representation of MYC mutants. (E) Schematic representation of TAF10 mutants. Co‐IP was used to detect the interaction between the TAF10 mutants and MYC in MCF7 cells. Co‐IP was used to detect the interaction. (G) Interaction between the MYC mutants and TAF10 in MCF7 cells was detected using Co‐IP. (H) MCF7 cells were co‐transfected with empty vector (Vec) and HA‐labelled TAF10 wild‐type (HA‐TAF10 WT) or mutants (HA‐TAF10 delta 1‐116, HA‐TAF10 delta 116‐206, HA‐TAF10 delta 206‐218). The MYC promoter activity was analysed using the dual luciferase reporter assay 24 h later. (I) Overexpression of TAF10 assessed the capacity for colony formation. MCF7 cells were transfected with either Control‐vec or HA‐TAF10. The ability of cells to form colonies was measured using crystal violet staining. (J) Overexpression of TAF10 measured the migration capacity of cells. MCF7 cells were transfected with either Control‐vec or HA‐TAF10. Transwell assays were used to assess the migration capacity of cells. Scale bar, 20 μm. Data shown in H were analysed by one‐way ANOVA. Data shown in I and J were analysed by t‐test. The blots represented three independent experiments. All data are presented as the mean +/- SEM of n = 3. ***p <.001, **p <.01, ns, no significance Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36639831), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: TAF10 Antibody - BSA Free [NBP1-80706] -

Z363 promotes MYC and TAF10 degradation. (A) Identification of small inhibitory molecules for MYC. (B) MCF7 cells were treated with Z363 (0, 2.5, 7.5 and 15 μg/ml) for 24 h. The protein levels of MYC and TAF10 were analysed by Western blotting. (C) MCF7 cells were treated with Z363 (7.5 μg/ml) for 0, 6, 12 and 24 h. Furthermore, the protein levels of MYC and TAF10 were analysed by Western blotting. (D) MCF7 cells were treated with 25 μM MG132 at the indicated time points, followed by treatment with or without Z363 (7.5 μg/ml) for 24 h, and MYC and TAF10 expressions were analysed by Western blotting. (E) Western blots for MYC, phosphorylated MYC T58 and S62 in MCF7 cells treated with Z363 at the times indicated. (F) Ratios of pT58 or pS62 to total MYC protein levels from the experiment (E). (G) IF staining for Ki67 and pT58 in Z363‐treated MCF7 cells, scale bar, 10 μm. (H) MCF7 cells were treated with 25 μM MG132 for 2 h, followed by Z363 treatment (7.5 μg/ml) for 24 h. Expressions of MYC and TAF10 were assessed using Western blot analysis. Data shown in F were analysed by two‐way ANOVA. Fluorescence images and blots were representative of three independent experiments. All data are presented as the mean +/- SEM of n = 3. ***p <.001, ns, no significance Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36639831), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: TAF10 Antibody - BSA Free [NBP1-80706] -

TAF10 plays oncogenic role in LUAD. A mRNA expression levels of the corresponding gene in human normal bronchial epithelial cells (16HBE) and LUAD cell lines. B TAF10 mRNA expression levels in various tumors and matched normal tissues from the TCGA and GTEx databases, analyzed using SangerBox platform. C The stemness features (RNA expression-based stemness scores) analyses of TAF10 across different types of tumors in the TCGA database, analyzed by SangerBox platform. (D-E) Disease-free survival (D) and overall survival (E) analyses of TAF10 in LUAD samples from the TCGA database, performed using the GEPIA2 platform. (F) Protein expression levels of TAF10 in 16HBE and LUAD cell lines. G Representative IHC analysis of TAF10 expression in paired adjacent and tumorous tissues from LUAD patients (n = 5 pairs, 10 tissues in total). Black scale bar: 50 μm; red scale bar: 20 μm. H TAF10 knockdown in LUAD cells was confirmed by Western blot analysis. I LUAD cell lines were stably transfected with either shCtl or shTAF10 for 24, 48, and 72 h, and cell viability was measured using a CCK-8 assay. (J) The effect of TAF10 knockdown on colony formation in LUAD cells was assessed using a colony formation assay. (K) Representative micrographs and quantification of tumor sphere formation by TAF10-silenced cells (shTAF10) or vector control cells (shCtl). Scale bar, 100 μm. L–N GSEA plot of KEGG (L), GOBP (M), and Hallmark pathways (N), grouped by TAF10 expression into TAF10-high and TAF10-low subgroups. NES represents the normalized enrichment score, and FDR represents the adjusted p-value Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/39987127), licensed under a CC-BY license. Not internally tested by Novus Biologicals.

Western Blot: TAF10 Antibody - BSA Free [NBP1-80706] -

Co‐inhibition of MYC and TAF10 causes synergistic reduction of cell proliferation and tumour growth. (A) Cells (WT, TAF10 KO) were treated with different doses of Z363 for 24 h. Cell proliferation was determined by the CCK‐8 assay. (B) Knockout reliability was detected by Western blotting. (C) The proliferation of wild‐type cells (WT), single and double KO cells (MYC KO, TAF10 KO, DKO) and Z363‐treated cells were detected by Ki67 ELISA kit. (D) The apoptosis of wild‐type cells (WT), single and double KO cells (MYC KO, TAF10 KO, DKO) and Z363‐treated cells were detected by flow cytometry. (E) Cell apoptosis‐related proteins levels were detected by Western blotting. (F) The migration of wild‐type cells (WT), single and double KO cells (MYC KO, TAF10 KO, DKO), and Z363‐treated cells were detected by a Transwell migration assay. Scale bar, 20 μm. (G) Representative images showing xenograft tumours at day 28 post‐subcutaneous injection (n = 5). (H and I) Tumours were measured and depicted as tumour volume (H) or tumour weight (I). Data shown in A were analysed by two‐way ANOVA. Data shown in C, D, F, H and I were analysed by one‐way ANOVA. Flow cytometry, transwell and blots were representative of three independent experiments. All data are presented as the mean +/- SEM of n = 3. ***p <.001, **p <.01, *p <.05 Image collected and cropped by CiteAb from the following open publication (https://pubmed.ncbi.nlm.nih.gov/36639831), licensed under a CC-BY license. Not internally tested by Novus Biologicals.