Journal: PloS one

Article Title: Brg1 is required for Cdx2-mediated repression of Oct4 expression in mouse blastocysts.

doi: 10.1371/journal.pone.0010622

Figure Lengend Snippet: Figure 1. Brg1 is required for repression of Oct4 expression at the blastocyst stage. (A) qRT-PCR analysis of Brg1, Cdx2, and Oct4 transcripts in Brg1 KD 8-cell embryos, morulae, and blastocysts. Data were normalized to Ubtf (house keeping gene) and are relative to control embryos at each stage; black line = 1. Asterisk denotes significant difference between Brg1 KD and control blastocysts (p,0.05). (B) ICC analysis of Oct4 and Cdx2 expression in Brg1 KD 8-cell embryos, morulae, and blastocysts. Nuclei were counter stained with DAPI (blue). (C) Brg1 represses Oct4 expression in a dose dependent manner. One-cell embryos were injected with 0 mM (control), 0.1 mM, 1 mM, or 100 mM Brg1 siRNA and cultured to the blastocyst stage. Real-time qPCR was used to analyze the levels of Brg1 and Oct4 transcripts. Data were normalized to Ubtf and are relative to control blastocysts; dashed line = 1. doi:10.1371/journal.pone.0010622.g001

Article Snippet: CDX2 was detected by Western blot analysis using an affinity purified rabbit anti-CDX2 antibody (A300-692A, Bethyl Laboratories, Inc).

Techniques: Expressing, Quantitative RT-PCR, Control, Staining, Injection, Cell Culture

Journal: PloS one

Article Title: Brg1 is required for Cdx2-mediated repression of Oct4 expression in mouse blastocysts.

doi: 10.1371/journal.pone.0010622

Figure Lengend Snippet: Figure 2. Expression and localization of Cdx2 and Oct4 in Brg1 KD blastocysts. (A) ICC analysis of Oct4 and Cdx2 in Brg1 KD and control blastocysts. In control blastocysts (a–d) Oct4 expression (green) is restricted to the ICM and is largely absent in the Cdx2-positive (red) trophectoderm. In contrast, in Brg1 KD blastocysts (e–h) Oct4 is widely expressed in both the ICM and cdx2-positive (yellow) trophectoderm. Arrowheads denote co- expression of Oct4 and Cdx2. Nuclei were counter stained with DAPI (blue). (B) Quantification of the average number of cells in Brg1 KD and control blastocysts expressing Oct4, Cdx2, and Oct4 & Cdx2 (double expression). Asterisks denote statistical significance (p,0.05) between Brg1 KD and control blastocysts. A total of 25 Brg1 KD blastocysts and 15 control blastocysts were analyzed. doi:10.1371/journal.pone.0010622.g002

Article Snippet: CDX2 was detected by Western blot analysis using an affinity purified rabbit anti-CDX2 antibody (A300-692A, Bethyl Laboratories, Inc).

Techniques: Expressing, Control, Staining

Journal: PloS one

Article Title: Brg1 is required for Cdx2-mediated repression of Oct4 expression in mouse blastocysts.

doi: 10.1371/journal.pone.0010622

Figure Lengend Snippet: Figure 5. Model for Brg1/Cdx2-mediated repression of Oct4 expression in trophectoderm. Schematic diagram of Oct4 regulation in blastocysts. In the trophectoderm Brg1 is recruited to the ARE of the Oct4 promoter via Cdx2. Once at the Oct4 promoter Brg1 and Cdx2 facilitate recruitment of additional co-repressors to repress transcription. doi:10.1371/journal.pone.0010622.g005

Article Snippet: CDX2 was detected by Western blot analysis using an affinity purified rabbit anti-CDX2 antibody (A300-692A, Bethyl Laboratories, Inc).

Techniques: Expressing

Journal: Molecular reproduction and development

Article Title: Loss of KANSL3 leads to defective inner cell mass and early embryonic lethality

doi: 10.1002/mrd.23760

Figure Lengend Snippet: Assisted hatching partially rescues the mutant phenotype. (a) Outgrowth assays performed on blastocysts from heterozygous intercrosses after zona pellucida removal. Representative images of wildtype (WT), Heterozygous (HET), and mutant (MUT) embryos and their corresponding outgrowths are shown. Three mutant embryos are shown to reveal consistently abnormal ICM morphology. Scale bars, 100 μm. (b) Immunofluorescence against OCT4 (ICM) in green and CDX2 (TE) in red with DAPI as nuclear stain in blue on embryo outgrowths. Representative IF images of control (top row) and mutant (bottom row) are shown.

Article Snippet: The primary antibodies used are as follows: Rabbit anti-OCT4 (Abcam Cat# ab200834, RRID:AB_2924374, 1:200); mouse anti-CDX2 (BioGenex Cat# MU392A, RRID:AB_2923402, 1:100); rabbit anti-CDX2 (Abcam Cat# ab76541, RRID:AB_1523334, 1/500); goat-anti SOX2 (R and D Systems Cat# AF2018, RRID:AB_355110, 1:200); rabbit anti-NANOG (ReproCELL Incorporated Cat# RCAB0002P-F, RRID:AB_2616320, 1:500); goat anti-SOX17 (R and D Systems Cat# AF1924, RRID:AB_355060, 1:200); rabbit anti-Histone H3 (phospho S10) (Abcam Cat# ab5176, RRID:AB_304763, 1:200); mouse anti-H4K16ac (Thermo Fisher Scientific Cat# MA5-27794, RRID:AB_2735098, 1:150); Rabbit anti-H4K5ac (Thermo Fisher Scientific Cat# MA5-32009-25UG, RRID:AB_2866507, 1:200), Mouse anti-H4K8ac (Thermo Fisher Scientific Cat# MA5-31553, RRID:AB_2787181, 1:200), Rabbit anti-H4K12 (Active Motif Cat# 39927, RRID:AB_2793396, 1:250).

Techniques: Mutagenesis, Immunofluorescence, Staining, Control

Journal: Molecular reproduction and development

Article Title: Loss of KANSL3 leads to defective inner cell mass and early embryonic lethality

doi: 10.1002/mrd.23760

Figure Lengend Snippet: Kansl3 null mutants display ICM-specific defects. (a) Immunofluorescence of SOX2 (ICM) in red and CDX2 (TE) in white with DAPI as nuclear stain in blue on E3.5 blastocysts. Representative image of control (top row) and mutant (bottom row) embryo. (b) Scatter plot comparing absolute numbers of SOX2 positive cells (13 mutant embryos and 18 control embryos). (c) Scatter plot comparing the percentage of SOX2 positive cells (7 control and 7 mutant embryos). There is a significant reduction in SOX2-positive cells in mutant embryos compared to control littermates. (d) Scatter plot comparing absolute number of CDX2 positive cells (13 mutant and 18 control embryos). (e) Scatter plot comparing the percentage of CDX2 positive cells (7 control and 7 mutant embryos). (f) Scatter plot comparing the total number of cells (DAPI nuclei) in 7 control and 7 mutant embryos. (g) Scatter plot comparing intensity of SOX2 normalized against DAPI intensity in individual nuclei in 8 control and 5 mutant embryos. There is a significant reduction in SOX2 intensity in mutant ICM cells. (h) Representative image of TUNEL staining (green) and nuclei (blue). No obvious TUNEL + cells were observed, regardless of genotype. Statistical significance was calculated by a two-tailed Student’s t-test. Error bars represent standard deviation. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. ICM, inner cell mass. TUNEL, terminal deoxynucleotidyl transferase dUTP nick end labeling.

Article Snippet: The primary antibodies used are as follows: Rabbit anti-OCT4 (Abcam Cat# ab200834, RRID:AB_2924374, 1:200); mouse anti-CDX2 (BioGenex Cat# MU392A, RRID:AB_2923402, 1:100); rabbit anti-CDX2 (Abcam Cat# ab76541, RRID:AB_1523334, 1/500); goat-anti SOX2 (R and D Systems Cat# AF2018, RRID:AB_355110, 1:200); rabbit anti-NANOG (ReproCELL Incorporated Cat# RCAB0002P-F, RRID:AB_2616320, 1:500); goat anti-SOX17 (R and D Systems Cat# AF1924, RRID:AB_355060, 1:200); rabbit anti-Histone H3 (phospho S10) (Abcam Cat# ab5176, RRID:AB_304763, 1:200); mouse anti-H4K16ac (Thermo Fisher Scientific Cat# MA5-27794, RRID:AB_2735098, 1:150); Rabbit anti-H4K5ac (Thermo Fisher Scientific Cat# MA5-32009-25UG, RRID:AB_2866507, 1:200), Mouse anti-H4K8ac (Thermo Fisher Scientific Cat# MA5-31553, RRID:AB_2787181, 1:200), Rabbit anti-H4K12 (Active Motif Cat# 39927, RRID:AB_2793396, 1:250).

Techniques: Immunofluorescence, Staining, Control, Mutagenesis, TUNEL Assay, Two Tailed Test, Standard Deviation

Journal: Molecular reproduction and development

Article Title: Loss of KANSL3 leads to defective inner cell mass and early embryonic lethality

doi: 10.1002/mrd.23760

Figure Lengend Snippet: Kansl3 null mutants have fewer epiblast and primitive endoderm cells. (a) Immunofluorescence of Phospho-H3 (green), SOX2 (ICM, red), and CDX2 (TE white) with DAPI (blue). Representative control and a mutant are shown. (b) Scatter plot comparing the percentage of Phospho-H3 positive cells (5 control and 5 mutant embryos). No significant difference is observed. (c) Immunofluorescence of NANOG (EPI, green), SOX17 (PrE) in white and CDX2 (TE, red) with DAPI as nuclear stain. Representative control mutant shown. (d) Scatter plot comparing the percentage of SOX17 positive cells (6 control and 6 mutant embryos). There is a significant reduction in SOX17 cells in mutant embryos. (e) Scatter plot comparing the percentage of NANOG-positive cells (6 control and 6 mutant embryos). There is a significant reduction in NANOG-positive cells in mutant embryos. Statistical significance was calculated by a two-tailed Student’s t-test. Error bars represent standard deviation. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001. ICM, inner cell mass.

Article Snippet: The primary antibodies used are as follows: Rabbit anti-OCT4 (Abcam Cat# ab200834, RRID:AB_2924374, 1:200); mouse anti-CDX2 (BioGenex Cat# MU392A, RRID:AB_2923402, 1:100); rabbit anti-CDX2 (Abcam Cat# ab76541, RRID:AB_1523334, 1/500); goat-anti SOX2 (R and D Systems Cat# AF2018, RRID:AB_355110, 1:200); rabbit anti-NANOG (ReproCELL Incorporated Cat# RCAB0002P-F, RRID:AB_2616320, 1:500); goat anti-SOX17 (R and D Systems Cat# AF1924, RRID:AB_355060, 1:200); rabbit anti-Histone H3 (phospho S10) (Abcam Cat# ab5176, RRID:AB_304763, 1:200); mouse anti-H4K16ac (Thermo Fisher Scientific Cat# MA5-27794, RRID:AB_2735098, 1:150); Rabbit anti-H4K5ac (Thermo Fisher Scientific Cat# MA5-32009-25UG, RRID:AB_2866507, 1:200), Mouse anti-H4K8ac (Thermo Fisher Scientific Cat# MA5-31553, RRID:AB_2787181, 1:200), Rabbit anti-H4K12 (Active Motif Cat# 39927, RRID:AB_2793396, 1:250).

Techniques: Immunofluorescence, Control, Mutagenesis, Staining, Two Tailed Test, Standard Deviation

Journal: Molecular reproduction and development

Article Title: Loss of KANSL3 leads to defective inner cell mass and early embryonic lethality

doi: 10.1002/mrd.23760

Figure Lengend Snippet: Kansl3 mutants display lower levels of H4k5ac. (a) Immunofluorescence of H4k5ac (green), SOX2 (ICM, red), and CDX2 (white) with DAPI as a nuclear stain (blue). Representative control (top row) and mutant (bottom row) embryo. (b) Scatter plot comparing the intensity of H4k5ac normalized against DAPI in individual nuclei (3 control and 4 mutant embryos). (c) Immunofluorescence of H4k8ac (white), SOX2 (ICM, red), and CDX2 (green) with DAPI as a nuclear stain (blue). Representative control (top row) and mutant (bottom row) embryo. (d) Scatter plot comparing the intensity of H4k8ac normalized against DAPI in individual nuclei (3 control and 3 mutant embryos). (e) Immunofluorescence of H4k12ac (green) and CDX2 (white) with DAPI as nuclear stain (blue). Representative control (top row) and mutant (bottom row) embryo. (f) Scatter plot comparing the intensity of H4k12ac normalized against DAPI in individual nuclei (3 control and 3 mutant embryos). (g) Immunofluorescence of SOX2 (ICM, red) and H4k16ac (white) with DAPI as a nuclear stain (blue). Representative control (top row) and mutant (bottom row) embryo. (h) Scatter plot comparing the intensity of H4k16ac normalized against DAPI in individual nuclei (4 control and 2 mutant embryos). No significant difference is observed. Statistical significance was calculated by a two-tailed Student’s t-test. Error bars represent standard deviation. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Article Snippet: The primary antibodies used are as follows: Rabbit anti-OCT4 (Abcam Cat# ab200834, RRID:AB_2924374, 1:200); mouse anti-CDX2 (BioGenex Cat# MU392A, RRID:AB_2923402, 1:100); rabbit anti-CDX2 (Abcam Cat# ab76541, RRID:AB_1523334, 1/500); goat-anti SOX2 (R and D Systems Cat# AF2018, RRID:AB_355110, 1:200); rabbit anti-NANOG (ReproCELL Incorporated Cat# RCAB0002P-F, RRID:AB_2616320, 1:500); goat anti-SOX17 (R and D Systems Cat# AF1924, RRID:AB_355060, 1:200); rabbit anti-Histone H3 (phospho S10) (Abcam Cat# ab5176, RRID:AB_304763, 1:200); mouse anti-H4K16ac (Thermo Fisher Scientific Cat# MA5-27794, RRID:AB_2735098, 1:150); Rabbit anti-H4K5ac (Thermo Fisher Scientific Cat# MA5-32009-25UG, RRID:AB_2866507, 1:200), Mouse anti-H4K8ac (Thermo Fisher Scientific Cat# MA5-31553, RRID:AB_2787181, 1:200), Rabbit anti-H4K12 (Active Motif Cat# 39927, RRID:AB_2793396, 1:250).

Techniques: Immunofluorescence, Staining, Control, Mutagenesis, Two Tailed Test, Standard Deviation

Journal: Advanced Science

Article Title: Prediction of Clinical Precision Chemotherapy by Patient‐Derived 3D Bioprinting Models of Colorectal Cancer and Its Liver Metastases

doi: 10.1002/advs.202304460

Figure Lengend Snippet: Study process and histopathological characterization of CRC 3DP models. A) The study process in primary colorectal cancer. A total of 40 patients undergoing surgery for CRC were enrolled, and 3DP models were successfully established and stably cultured for 37 patients. B) Bright‐field images of CRC 3DP models and CRC PDTOs on day 6 after production. Scale bar = 100 µm. C) HE staining comparing CRC 3DP models with corresponding organoids and parental tumors. Scale bar of tumor, 100 µm. Organoid and 3DP scale bars, 20 µm. D) CRC 3DP models and corresponding organoids and parent tumors were co‐stained with CK20 (green), CK7 (red), CDX2 (green), CK‐pan (red), β‐catenin (red), Ki‐67 (green) to examine the profiles of CRC biomarkers. DAPI was used to visualize nuclei (blue). Scale bar of tumor staining = 50 µm. Scale bars of 3DP and organoids staining = 20 µm.

Article Snippet: Rabbit anti‐CK20 (1:200, Abcam, Cambridge, MA, USA), mouse anti‐CK7 (1:200, Abcam), rabbit anti‐CDX2 (1:200, Abcam), rabbit anti‐β‐catenin (1:200, Abcam), mouse anti‐Ki‐67 (1:200, Abcam), and mouse anti‐CK‐pan (1:200, Abcam) were used as primary antibodies for immunohistochemical staining.

Techniques: Stable Transfection, Cell Culture, Staining

Journal: Advanced Science

Article Title: Prediction of Clinical Precision Chemotherapy by Patient‐Derived 3D Bioprinting Models of Colorectal Cancer and Its Liver Metastases

doi: 10.1002/advs.202304460

Figure Lengend Snippet: Histological and genetic mutational characterization of CRLM 3DP models. A) CRLM 3DP models and corresponding organoids and parent tumors were co‐stained with CK20 (green), CK7 (red), CDX2 (green), CK‐pan (red), β‐catenin (red), Ki‐67(green) to examine the profiles of CRC biomarkers. DAPI was used to visualize nuclei (blue). Scale bar of tumor staining = 50 µm. Scale bars of 3DP and organoids staining = 20 µm. B) Proportions of exonic variants for all tested samples (T, tumor; P, 3DP; O, PDTO). C) Spectrum of SNVs in the most frequently mutated genes of CRLM. Each row represents a driver gene, and each column represents the mutational profile of CRLM 3DP models, PDTOs, and parental tumors (T, tumor; P, 3DP; O, PDTO). D) Bar plots present the concordance among the SNVs of the most frequently mutated genes identified in CRLM 3DP models, PDTOs, and corresponding primary tumors.

Article Snippet: Rabbit anti‐CK20 (1:200, Abcam, Cambridge, MA, USA), mouse anti‐CK7 (1:200, Abcam), rabbit anti‐CDX2 (1:200, Abcam), rabbit anti‐β‐catenin (1:200, Abcam), mouse anti‐Ki‐67 (1:200, Abcam), and mouse anti‐CK‐pan (1:200, Abcam) were used as primary antibodies for immunohistochemical staining.

Techniques: Staining

Journal: Molecular Therapy. Methods & Clinical Development

Article Title: iPSC-Derived Intestinal Organoids from Cystic Fibrosis Patients Acquire CFTR Activity upon TALEN-Mediated Repair of the p.F508del Mutation

doi: 10.1016/j.omtm.2020.04.005

Figure Lengend Snippet: Directed Differentiation of CFTR-Corrected L2-64.12 iPSCs toward Human Intestinal Organoids (A) Following 3 days of ACTIVIN-A/WNT3A treatment, CFTR-repaired iPSCs show expression of DE markers FOXA2 (green), GATA4 (red), and SOX17 (green). Scale bar, 50 μm. (B) Definitive endodermal cells were further differentiated into HGE (8 days) by additional exposure to the WNT3A agonist CHIR99021 for 5 days. At that point the cells expressed the hindgut marker CDX2 (green) and were completely negative for the anterior foregut markers FOXA2 (green) and SOX2 (red). Scale bar, 50 μm. (C) Generation of iPSC-derived intestinal organoids from the p.F508del mutant (L2) and corrected iPSCs (L2-64.12) in the absence of mesenchymal cells. Scale bars, 100 μm. (D) Immunostaining of CFTR-repaired HIO for the intestinal markers CDX2 (red), SOX9 (green), E-CAD (red), and VILLIN (green). Scale bars, 50 μm. Nuclei were counterstained with DAPI (blue) (A, B, and D).

Article Snippet: Immunocytochemistry was performed for Nanog (1:150, rabbit immunoglobulin [Ig]G polyclonal; Abcam, Spain), Oct4 (1:100, rabbit IgG polyclonal; Santa Cruz Biotechnology, USA), Tra-1-60 (1:100, mouse IgM; Millipore, USA), AFP (1:100, rabbit IgG; Dako, Denmark), Nestin (1:500, rabbit IgG; Sigma, Spain), Tuj1 (1:500, rabbit IgG; Covance, UK), Sox17 (1:100, goat IgG; R&D Systems, UK), α-actinin (1:200, mouse IgM; Sigma, Spain), SMA (1:200, mouse; Sigma), CFTR (clone MM13-4 or M3A7, 1:100; Merck Millipore, Spain), E-CAD (1:200, rabbit; Cell Signaling Technology), SOX9 (1:100, goat; R&D Systems, UK), Villin (1:100, goat; Santa Cruz Biotechnology, USA), FOXA2 (1:100, goat IgG; Santa Cruz Biotechnology, USA), CDX2 (1:100, mouse IgG; DCS ImmunoLine, Germany), and GATA4 (1:300, mouse IgG; Santa Cruz Biotechnology, USA).

Techniques: Expressing, Marker, Derivative Assay, Mutagenesis, Immunostaining

Journal: Frontiers in Pharmacology

Article Title: Rabeprazole suppressed gastric intestinal metaplasia through activation of GPX4-mediated ferroptosis

doi: 10.3389/fphar.2024.1409001

Figure Lengend Snippet: Rabeprazole suppressed gastric intestinal metaplasia. (A) HEK293 cells were transfected with reporter gene containing CDX2 promoter and renilla plasmid for 12 h, following by treatment with or without rabeprazole for another48 h, the CDX2 transactivation was determined and analyzed using two sample t-test. Data was exhibited as mean ± s.d of three independent experiments, *** p < 0.001. (B) After treatment with or without rabeprazole for 48 h in BGC823 and AGS cells, the whole RNA was extracted to detect CDX2 ( left panel ) and MUC2 ( right panel ) mRNA level, data was displayed as mean ± s.d of three independent experiments, one sample t-test was employed to determine the significance. **** p < 0.0001; (C) After cell adhesion overnight, BGC823 and AGS cells were starved with serum-free medium for 16 h and treated with or without rabeprazole (100uM) for another 48 h. The whole cell lysate was collected and detected indicated protein expression by immunoblotting, band intensity was analyzed and quantified using two sample t-test, Data was exhibited as mean ± s.d of three independent experiments, **** p < 0.0001.

Article Snippet: Antibody against CDX2 monoclonal antibody (60243-1-Ig, Proteintech), SLC7A11/xCT polyclonal antibody (26864-1-AP, Proteintech), GPX4 monoclonal antibody (67763-1-Ig, Proteintech), Lamin A/C recombinant antibody (81042-1-RR, Proteintech), CREB1 Monoclonal antibody (67927-1-Ig, Proteintech) and phospho-CREB1 (Ser133) Polyclonal antibody (28792-1-AP, Proteintech) were from Proteintech (Wuhan, China).

Techniques: Transfection, Plasmid Preparation, Expressing, Western Blot

Journal: Frontiers in Pharmacology

Article Title: Rabeprazole suppressed gastric intestinal metaplasia through activation of GPX4-mediated ferroptosis

doi: 10.3389/fphar.2024.1409001

Figure Lengend Snippet: Rabeprazole modulated gastric intestinal metaplasia in dependent of ferroptosis. (A) BGC823 cells were digested and re-seeded into a 24-well plate and grown to 80% confluence, after serum-sstarvation overnight, BGC823 cells were treated with or without rabeprazole (100uM) for 48 h, the ROS level was detected according to the manufacter’s instruction and captured under fluorescent microscope (upper panel) as well as FCM analysis (bottom panel), bar: 250 um. (B) BGC823 and AGS cells were cultured without FBS overnight and incubated with or without rabeprazole (100uM) for another 48 h, real-time PCR was utilized to test indicated genes expression, control group was normalized as 1, data was exhibited as mean ± s.d of three independent experiments, one sample t-test was used to determine the significance. ** p < 0.01, **** p < 0.0001. (C) BGC823 and AGS cells was treated as described in B, immunoblotting was utilized to analyze GPX4 and SLC7A11 protein expression. Control group was normalized as 1, data was exhibited as mean ± s.d of three independent experiments, one sample t-test was used to determine the significance. * p < 0.05, ** p < 0.01, **** p < 0.0001. (D) After serum-starved culture overnight, BGC823 cells were treated with Ferrostatin-1 (Fer-1, 10 uM) for 1 h, subsequently followed by treatment with rabeprazole for another 48 h. The total protein was harvested to test MUC2 and CDX2 expression by immunoblotting. the band intensity was measured and quantified by one-ANOVA with multiple comparisons, followed by Bonferroni post hoc test for significance, control group was normalized as 1, data was exhibited as mean ± s.d of three independent experiments, **** p < 0.0001. (E) CCK8 analysis of cell viability in BGC823 cells treated as indicated for 48 h, data was exhibited as mean ± s.d of five independent experiments, one-ANOVA with multiple comparisons, followed by Bonferroni post hoc test for significance, **** p < 0.0001.

Article Snippet: Antibody against CDX2 monoclonal antibody (60243-1-Ig, Proteintech), SLC7A11/xCT polyclonal antibody (26864-1-AP, Proteintech), GPX4 monoclonal antibody (67763-1-Ig, Proteintech), Lamin A/C recombinant antibody (81042-1-RR, Proteintech), CREB1 Monoclonal antibody (67927-1-Ig, Proteintech) and phospho-CREB1 (Ser133) Polyclonal antibody (28792-1-AP, Proteintech) were from Proteintech (Wuhan, China).

Techniques: Microscopy, Cell Culture, Incubation, Real-time Polymerase Chain Reaction, Expressing, Control, Western Blot

Journal: Frontiers in Pharmacology

Article Title: Rabeprazole suppressed gastric intestinal metaplasia through activation of GPX4-mediated ferroptosis

doi: 10.3389/fphar.2024.1409001

Figure Lengend Snippet: Ferroptosis was decreased in patients with IM. (A) IHC was performed to detect GPX4 and SLC7A11 expression as well as CDX2 expression in a set of healthy control and patients with IM, the quantitation of GPX4 and SLC7A11 expression were performed upon IHC score, ** p < 0.01, **** p < 0.0001. (B) IF experiment was employed to determine GPX4 and SLC7A11 expression in a set of healthy control and patients with IM, the quantitation of GPX4 and SLC7A11 expression were performed upon mean fluorescence intensity (MFI) analysis, ** p < 0.01, **** p < 0.0001.

Article Snippet: Antibody against CDX2 monoclonal antibody (60243-1-Ig, Proteintech), SLC7A11/xCT polyclonal antibody (26864-1-AP, Proteintech), GPX4 monoclonal antibody (67763-1-Ig, Proteintech), Lamin A/C recombinant antibody (81042-1-RR, Proteintech), CREB1 Monoclonal antibody (67927-1-Ig, Proteintech) and phospho-CREB1 (Ser133) Polyclonal antibody (28792-1-AP, Proteintech) were from Proteintech (Wuhan, China).

Techniques: Expressing, Control, Quantitation Assay, Fluorescence