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Image Search Results
Journal: Cancer Medicine
Article Title: The Biological and Prognostic Implications of the Nicotinic Acetylcholine Receptor α 3, α 5, and α 7 Subunits in Oral Squamous Cell Carcinoma
doi: 10.1002/cam4.71358
Figure Lengend Snippet: Influences of CHRNA3 , CHRNA5 , and CHRNA7 expression in SCC‐4 tongue cancer cells. (A) The effects of nicotine (1 μM) treatment (qRT‐PCR). (B1–B3) The effects of overexpressed CHRNA3 , CHRNA5 , and CHRNA7 , respectively (qRT‐PCR). (C1–C3) The effects of overexpressed DSG2 , TGF β 1 treatment (2.5 ng/mL), and overexpressed TGFBR2 , respectively (qRT‐PCR). (D1–D2) Summary of the qRT‐PCR results. (E) The expression patterns of our SCC‐4 cells at two different time points (SCC‐4‐1 and SCC‐4‐2) and the DepMap SCC‐4 cells (RNA‐seq). (F1–F2) GSEA results comparing SCC‐4‐2 cells to SCC‐4‐1 cells. qRT‐PCR, quantitative reverse transcription polymerase chain reaction. RNA‐seq, RNA sequencing. TPM, transcripts per million. GO, gene ontology. BP, biological process. CC, cellular component. *, p < 0.05. **, p < 0.01. ***, p < 0.001.
Article Snippet: Nicotine (1 μM) (
Techniques: Expressing, Quantitative RT-PCR, RNA Sequencing, Reverse Transcription, Polymerase Chain Reaction
Journal: Nature Communications
Article Title: IL-17A is increased in diabetic wounds and impairs keratinocyte function via histone demethylase JMJD3
doi: 10.1038/s41467-025-67456-3
Figure Lengend Snippet: a ChIP analysis of H3K27me3 or IgG at indicated promoters in keratinocytes with (white) or without (blue) IL-17A stimulation. Itga3: n = 5 (unstimulated), n = 4 (IL-17A-stimulated) technical replicates, p = 0.0034, Timp1 : n = 3 technical replicates, p = 0.0046, Ccl20 : n = 3 technical replicates, p = 0.0059, Cxcl1 : n = 3 technical replicates, p = 0.0020, Cxcl3 : n = 3 technical replicates, p = 0.0258, Cxcl5 : n = 3 technical replicates, p = 0.0174. n = 3 independent experiments. b qPCR analysis of keratinocytes treated with DMSO only (white), with IL-17A alone (blue), or with IL-17A and GSK-J4 (1 µM) (red). Itga3 : n = 4 biological replicates, p < 0.0001 (DMSO vs. IL-17A), p = 0.0017 (IL-17A vs. IL-17A and inhibitor), Timp1: n = 6 biological replicates, p < 0.0312 (DMSO vs. IL-17A), p = 0.0029 (IL-17A vs. IL-17A and inhibitor), Ccl20: n = 3 biological replicates, p = 0.0008 (DMSO vs. IL-17A), p = 0.0428 (IL-17A vs. IL-17A and inhibitor), Cxcl1 : n = 3 biological replicates, p = 0.0003 (DMSO vs. IL-17A), p = 0.0294 (IL-17A vs. IL-17A and inhibitor), Cxcl3 : n = 3 biological replicates, p < 0.0001 (DMSO vs. IL-17A), p = 0.0003 (IL-17A vs. IL-17A and inhibitor), Cxcl5 : n = 3 biological replicates, p < 0.0001 (DMSO vs. IL-17A), p = 0.0007 (IL-17A vs. IL-17A and inhibitor), n = 3 independent experiments. c Western blot of ITGA-3 expression in keratinocytes treated with DMSO only (white), with IL-17A alone (blue), or with IL-17A and GSK-J4 (red). Representative densitometry plot is shown. n = 3 independent experiments. d Protein quantification of lysates from keratinocytes treated with DMSO only (white), with IL-17A alone (blue), or with IL-17A and GSK-J4 (red). TIMP-1: n = 6 biological replicates, p = 0.0012 (DMSO vs. IL-17A), p = 0.0068 (IL-17A vs. IL-17A and inhibitor), CCL-20: n = 3 biological replicates, p < 0.0001 (DMSO vs. IL-17A), p = 0.0199 (IL-17A vs. IL-17A and inhibitor), CXCL-1: n = 3 biological replicates, p < 0.0001 (DMSO vs. IL-17A), p = 0.0158 (IL-17A vs. IL-17A and inhibitor), CXCL-3: n = 3 biological replicates, p < 0.0001 (DMSO vs. IL-17A), p = 0.0167 (IL-17A vs. IL-17A and inhibitor), CXCL-5: n = 3 biological replicates, p < 0.0001 (DMSO vs. IL-17A), p = 0.0005 (IL-17A vs. IL-17A and inhibitor), n = 3 independent experiments. e qPCR analysis of keratinocytes treated with a non-targeting control (siNTC) (white) or si Jmjd3 (gray). Jmjd3 : n = 6 (siNTC), n = 4 biological replicates (si Jmjd3 ), p = 0.0192, Itga3: n = 6 (siNTC), n = 4 biological replicates (si Jmjd3 ), p = 0.0019, Timp1: n = 3 (siNTC), n = 4 biological replicates (si Jmjd3 ), p = 0.0205, Ccl20: n = 6 (siNTC), n = 4 biological replicates (si Jmjd3 ), p = 0.0015, Cxcl1: n = 6 (siNTC), n = 4 biological replicates (si Jmjd3 ), p = 0.0019, Cxcl3: n = 6 (siNTC), n = 4 biological replicates (si Jmjd3 ), p = 0.0011, Cxcl5: n = 6 (siNTC), n = 4 biological replicates (si Jmjd3 ), p = 0.0011, n = 3 independent experiments. f qPCR analysis of Jmjd3 fl/fl K14 cre+ (red) and Jmjd3 fl/fl K14 cre- (yellow) keratinocytes. n = 3 biological replicates, Itga3 : p = 0.0184, Timp1 : p = 0.0044, Ccl20 : p = 0.0160, Cxcl1 : p = 0.0371, Cxcl3 : p = 0.0042. n = 3 independent experiments. g , h Scratch assays of primary murine ( n = 3 biological replicates, p < 0.0001 (48 h)) and N/TERT ( n = 3 biological replicates, p = 0.0340 (12 h)) keratinocytes treated with IL-17A alone (blue) or IL-17A and GSK-J4 (red). n = 3 independent experiments. i , j Scratch assays of primary murine ( n = 3 biological replicates, p = 0.0016 (48 h)) and N/TERT ( n = 6 biological replicates (IL-17A alone), n = 4 biological replicates (IL-17A and GSK-J1), p = 0.0223 (8 h), p < 0.0001 (12 h)) keratinocytes treated with IL-17A alone (blue) or IL-17A and GSK-J1 (red). n = 3 independent experiments. k Scratch assay of Jmjd3 fl/fl K14 cre+ (red) and Jmjd3 fl/fl K14 cre- (blue) keratinocytes. n = 3 biological replicates, p = 0.0198 (48 h). n = 3 independent experiments. Data were analyzed for variances, and 2-tailed Student’s t tests for ( a ), ( e ), ( f ) and 1-way ANOVA tests for ( b ), ( d ), ( g – k ) were performed. Data are presented as the mean ± SEM.
Article Snippet: After stimulation, cell free supernatant was collected and analyzed by the University of Michigan Immune Monitoring Shared Resource Core for CCL-20, CXCL-1, CXCL-5 or specific enzyme immunoassay kits for
Techniques: Western Blot, Expressing, Control, Wound Healing Assay
Journal: Journal of pharmaceutical analysis
Article Title: Unveiling the role of Pafah1b3 in liver fibrosis: A novel mechanism revealed.
doi: 10.1016/j.jpha.2024.101158
Figure Lengend Snippet: Fig. 4. Platelet-activating factor acetylhydrolase 1B3 (Pafah1b3) enhances transforming growth factor-b (TGF-b) signaling through interaction with mothers against decapentaplegic homolog 7 (SMAD7). (A) Protein expression of phosphorylation-SMAD3 (p-SMAD3), SMAD3, p-SMAD2, SMAD2, and PAFAH1B3 in 293T cells. (B, C) Co-immunoprecipitation (Co-IP) analysis: immunoprecipitation with anti-HA (B) and anti-Flag (C) antibody in 293T cells. (D) Co-IP analysis: immunoprecipitation with anti-HA antibody in TGF-b1 treated-293T cells. (E) Pull-down assay. (F) 293T cells were transfected with hemagglutinin (HA)-Pafah1b3 and Flag-SMAD7 and stained with antibodies against HA and Flag. Co-location between PAFAH1B3 (green) and SMAD7 (red) in 293T cells. The nucleus appears blue after 40,6-diamidino-2-phenylindole (DAPI) staining. The yellow indicates co-location of SMAD7 and PAFAH1B3. (G) Human SMAD7 domains. (H) Co-IP analysis in 293T cells transfected with HA-Pafah1b3 and different domains of SMAD7. (I) Molecular docking analysis. (J) Co-IP analysis of 293T cells transfected with Flag-SMAD7 and HA-Pafah1b3 mutants. (K) Protein expression of p-SMAD3, SMAD3, p-SMAD2, SMAD2, and PAFAH1B3 in 293T cells transfected with HA-Pafah1b3 mutants. ***P < 0.001. NC: negative control; shRNA: short hairpin RNA; GAPDH: glyceraldehyde 3-phosphate dehydrogenase; ND: N-terminal domain; MH2: mad homologous 2 domain; WT: wild type.
Article Snippet: Cells received specific treatments, including
Techniques: Expressing, Phospho-proteomics, Immunoprecipitation, Co-Immunoprecipitation Assay, Pull Down Assay, Transfection, Staining, Negative Control, shRNA