gata6 expression vector (Addgene inc)
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Addgene inc
gata6 expression vector
Gata6 Expression Vector, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/barcoding/pmc12499388-223-0-3?v=Addgene+inc
Average 93 stars, based on 2 article reviews
Gata6 Expression Vector, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/barcoding/pmc12499388-223-0-3?v=Addgene+inc
Average 93 stars, based on 2 article reviews
gata6 expression vector - by Bioz Stars,
2026-07
93/100 stars
Images
1) Product Images from "The TET3/GATA6 Axis Drives Lipid Metabolism and Therapeutic Vulnerabilities in Pancreatic Ductal Adenocarcinoma"
Article Title: The TET3/GATA6 Axis Drives Lipid Metabolism and Therapeutic Vulnerabilities in Pancreatic Ductal Adenocarcinoma
Journal: Advanced Science
doi: 10.1002/advs.202501774
Figure Legend Snippet: TET3 transcriptionally represses GATA6 through histone deacetylation. A) Western blot analysis of GATA6 protein levels in wild‐type (WT) and TET3 knockout (KO) PANC‐1 cells. B) UMAP visualization showing the expression distribution of TET3 and GATA6 in epithelial cells from scRNA‐seq of 25 PDAC patients ( GSE242230 ). C) Violin plots showing the expression levels of GATA6 in type 1 and type 2 ductal cells previously identified in PDAC patients (CRA001160; n = 24). D) RT‐qPCR analysis of GATA6 mRNA in TET3 knockout PANC‐1 cells transduced with doxycycline‐inducible wild‐type TET3 (TET3 wt , unfilled bars) or catalytically inactive mutant TET3 (TET3 mut , striped bars), treated with (purple) or without (gray) doxycycline (1 µg mL −1 ) (n = 3). E) ChIP‐qPCR assay of H3K27ac levels in WT and KO PANC‐1 cells (n = 3). Primers targeted regions upstream or downstream of the GATA6 transcription start site, as indicated in Figure , Supporting Information. F) RT‐qPCR measuring GATA6 mRNA expression in wild‐type PANC‐1 cells treated with SAHA at 0, 5, or 10 µM for 24 or 48 h (n = 3). G) Western blot analysis of GATA6 protein levels in PANC‐1 cells treated with SAHA (0, 5, 10 µM) for 24 h. H) ChIP‐qPCR assay of V5 in PANC‐1 cells ectopically expressing V5‐tagged TET3 (n = 3). qPCR primers are the same as those used in (E). I) Immunoprecipitation of V5‐tagged TET3 in PANC‐1 cells, followed by immunoblotting for HDAC1 and HDAC2 using an anti‐V5 antibody. Data represent mean ± SD. Statistical significance was determined by two‐tailed Wilcoxon test (C), one‐way ANOVA (D, F) or two‐tailed unpaired t ‐test (E, H). * p < 0.05, ** p < 0.01, *** p < 0.001.
Techniques Used: Western Blot, Knock-Out, Expressing, Quantitative RT-PCR, Transduction, Mutagenesis, ChIP-qPCR, Immunoprecipitation, Two Tailed Test
Figure Legend Snippet: GATA6 suppresses lipogenic gene expression and limits tumor growth. A) Western blot showing knockout efficiency of GATA6 in TET3 knockout (KO) PANC‐1 cells. B) RT‐qPCR analysis of lipid metabolic gene expression in PANC‐1 cells with wild‐type (WT), KO, and TET3 / GATA6 double knockout (KO‐sgGATA6) (n = 3). C) Western blot showing overexpression efficiency of GATA6 (GATA6 OE ) in wild‐type PANC‐1 cells. D) RT‐qPCR analysis of lipid metabolic gene expression in PANC‐1 cells with constitutive GATA6 overexpression (GATA6 OE ) (n = 3). E) Representative images of subcutaneous xenograft tumors (left) and tumor weight at 8 weeks post‐implantation (right) for the indicated cell lines. Nude mice were transplanted with WT (n = 5), KO (n = 5), or KO‐sgGATA6 PANC‐1 cells (n = 5). F) Cell viability of wild‐type PANC‐1 cells treated for 24 or 48 h with gemcitabine (1 µM), gemcitabine + SAHA (5 µM), gemcitabine + Erastin (1 µM), or a triple combination of gemcitabine, SAHA, and Erastin (n = 3). G) Representative images of xenografts (left) and tumor weight at 7 weeks post‐implantation (right) following treatment beginning at week 4 with the indicated agents. Nude mice were transplanted with wild‐type PANC‐1 cells. Data represent mean ± SD. Statistical significance was determined by one‐way ANOVA (B, E, F, G) or two‐tailed unpaired t ‐test (D). * p < 0.05, ** p < 0.01, *** p < 0.001.
Techniques Used: Gene Expression, Western Blot, Knock-Out, Quantitative RT-PCR, Double Knockout, Over Expression, Two Tailed Test
Figure Legend Snippet: TET3 promotes invasive PDAC through activation of TGF‐β signaling pathway. A) mRNA expression levels of TET3 in normal pancreatic tissues (n = 7), IPMA tissues (n = 6), and invasive PDAC tissues (n = 3) from GSE19650 (n = 16). B) Representative images and quantification of transwell invasion and migration assays in wild‐type (WT) and TET3 knockout (KO) PANC‐1 cells (n = 3). Scale bars = 200 µm. C) Western blot analysis of epithelial‐mesenchymal transition (EMT) markers E‐cadherin, N‐cadherin, and vimentin in WT and KO PANC‐1 cells. D) Western blot analysis of TGF‐β pathway proteins in WT, KO, and TET3 / GATA6 double knockout (KO‐sgGATA6) PANC‐1 cells. E) Western blot analysis of TGF‐β signaling proteins in wild‐type PANC‐1 cells constitutively overexpressing GATA6 (GATA6 OE ). F) Representative images and quantification of transwell invasion and migration assays in WT and KO in CFPAC‐1 cells (n = 3). G) Survival analysis of TCGA‐PAAD patients stratified by SMAD4 expression (high: top 50%, n = 89; low: bottom 50%, n = 89) and further subdivided by TET3 expression (high: top 25%, n = 22; low: bottom 25%, n = 22). Data are shown as mean ± SD. Statistical significance was assessed by one‐way ANOVA (A), two‐tailed unpaired t ‐test (B, F), or log‐rank Mantel‐Cox test (G). * p < 0.05, ** p < 0.01, *** p < 0.001.
Techniques Used: Activation Assay, Expressing, Migration, Knock-Out, Western Blot, Double Knockout, Two Tailed Test
Figure Legend Snippet: Schematic representation of the TET3/GATA6 axis in regulating lipogenic metabolism and promoting tumor growth and invasion in pancreatic cancer.
Techniques Used: