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The impacts of polydatin treatments on <t>JAK2</t> and STAT3 expression levels. (A) STAT3 and JAK2 mRNA expressions in breast cancer tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. (B) STAT3, JAK2, phospho-STAT3, and phospho-JAK2 protein expressions in BC tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. All blots were subjected to scanning densitometry in triplicate, and the integrated optical density of each band was standardized to that of GAPDH in the same blot. *P<0.05, **P<0.01 was considered statistically significant. mRNA, messenger RNA; BC, breast cancer.
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The impacts of polydatin treatments on <t>JAK2</t> and STAT3 expression levels. (A) STAT3 and JAK2 mRNA expressions in breast cancer tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. (B) STAT3, JAK2, phospho-STAT3, and phospho-JAK2 protein expressions in BC tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. All blots were subjected to scanning densitometry in triplicate, and the integrated optical density of each band was standardized to that of GAPDH in the same blot. *P<0.05, **P<0.01 was considered statistically significant. mRNA, messenger RNA; BC, breast cancer.
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The impacts of polydatin treatments on <t>JAK2</t> and STAT3 expression levels. (A) STAT3 and JAK2 mRNA expressions in breast cancer tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. (B) STAT3, JAK2, phospho-STAT3, and phospho-JAK2 protein expressions in BC tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. All blots were subjected to scanning densitometry in triplicate, and the integrated optical density of each band was standardized to that of GAPDH in the same blot. *P<0.05, **P<0.01 was considered statistically significant. mRNA, messenger RNA; BC, breast cancer.
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The impacts of polydatin treatments on <t>JAK2</t> and STAT3 expression levels. (A) STAT3 and JAK2 mRNA expressions in breast cancer tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. (B) STAT3, JAK2, phospho-STAT3, and phospho-JAK2 protein expressions in BC tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. All blots were subjected to scanning densitometry in triplicate, and the integrated optical density of each band was standardized to that of GAPDH in the same blot. *P<0.05, **P<0.01 was considered statistically significant. mRNA, messenger RNA; BC, breast cancer.
Anti P Jak2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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The impacts of polydatin treatments on <t>JAK2</t> and STAT3 expression levels. (A) STAT3 and JAK2 mRNA expressions in breast cancer tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. (B) STAT3, JAK2, phospho-STAT3, and phospho-JAK2 protein expressions in BC tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. All blots were subjected to scanning densitometry in triplicate, and the integrated optical density of each band was standardized to that of GAPDH in the same blot. *P<0.05, **P<0.01 was considered statistically significant. mRNA, messenger RNA; BC, breast cancer.
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Santa Cruz Biotechnology p jak2
Neogenin (Neo1) deficiency promoted macrophage transformation to the proinflammatory phenotype through the janus kinase 1 (JAK1)-signal transduction and activator of transcription 1 (STAT1) signal pathway, not STAT6 and P65 pathways, a The protein bands of p/T-JAK1, <t>p/T-JAK2,</t> p/T-STAT1, p/T-P65, p/T-STAT6 and GAPDH 3 days after myocardial infarction (MI), n = 5 in each group; b-f Quantitative analysis of p-JAK1, p-JAK2, p-STAT1, p-P65 and p-STAT6 in each group 3 days after MI, n = 5, two way ANOVA followed by Tukey’s test; g The double-labelling immunofluorescence of p-STAT1 and F4/80 3 days after MI, n = 4 in each group; h The protein bands of p/T-JAK1 and p/T-STAT1 3 days after MI in Neo1F/F and Neo1F/F;Cx3cr1cre mice; i, j Quantitative analysis of p-JAK1 and p-STAT1 in each group 3 days after MI in Neo1F/F and Neo1F/F;Cx3cr1cre mice, n = 5, two way ANOVA followed by Tukey’s test; k The protein bands and quantitative analysis of p/T-JAK1 and p/T-STAT1 in bone marrow derived-macrophages (BMDMs) 12 h after stimulation with LPS + IFN-γ, n = 3 in each group, two way ANOVA followed by Tukey’s test; l The immunofluorescence of p-STAT1 in BMDMs was analyzed by a confocal laser scanning microscope, n = 3 in each group. Data are expressed as the mean ± SEM. In b-f, *p < 0.05 vs. Sham + IgG group, #p < 0.05 vs. MI + IgG group, n.s. indicating no significance; in i and j *p < 0.05 vs. Sham + Neo1F/F group, #p < 0.05 vs. MI + Neo1F/F group; in k, *p < 0.05 vs. Sham + IgG group, #p < 0.05 vs. LPS + IFN-γ + IgG group
P Jak2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


The impacts of polydatin treatments on JAK2 and STAT3 expression levels. (A) STAT3 and JAK2 mRNA expressions in breast cancer tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. (B) STAT3, JAK2, phospho-STAT3, and phospho-JAK2 protein expressions in BC tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. All blots were subjected to scanning densitometry in triplicate, and the integrated optical density of each band was standardized to that of GAPDH in the same blot. *P<0.05, **P<0.01 was considered statistically significant. mRNA, messenger RNA; BC, breast cancer.

Journal: Annals of Translational Medicine

Article Title: Polydatin down-regulates the phosphorylation level of STAT3 and induces pyroptosis in triple-negative breast cancer mice with a high-fat diet

doi: 10.21037/atm-22-73

Figure Lengend Snippet: The impacts of polydatin treatments on JAK2 and STAT3 expression levels. (A) STAT3 and JAK2 mRNA expressions in breast cancer tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. (B) STAT3, JAK2, phospho-STAT3, and phospho-JAK2 protein expressions in BC tissues treated with 4T1, 4T1 + polydatin, 4T1 + polydatin + fat diet, and 4T1 + fat diet. All blots were subjected to scanning densitometry in triplicate, and the integrated optical density of each band was standardized to that of GAPDH in the same blot. *P<0.05, **P<0.01 was considered statistically significant. mRNA, messenger RNA; BC, breast cancer.

Article Snippet: The following primary antibodies were used: Rabbit anti-STAT3 antibody (1:1,000, Abcam, Cambridge, USA), Rabbit anti-JAK2 antibody [1:1,000, Cell Signaling Technology (CST), Danvers, MA, USA], rabbit anti-Phospho-STAT3 antibody (1:500, CST, USA), rabbit anti-IL1β antibody (1:500, Abcam, USA), rabbit anti-Phospho-JAK2 antibody (1:500, CST, USA), rabbit anti-pro Caspase-1 + p10 + p12 antibody (1:500, Abcam, USA), rabbit anti-Cleaved Caspase-3 antibody (1:1,000, CST, USA), rabbit anti-NLRP3 antibody (1:800, Abcam, USA), rabbit anti-IL18 antibody (1:500, Abcam, USA), rabbit anti-Caspase-3 antibody (1:1,000, CST, USA), rabbit anti-Caspase-1 antibody (1:500, Abcam, USA), rabbit anti-GSDMD antibody (1:500, Abcam, USA), rabbit anti-GAPDH antibody (1:3,000, Abcam, USA), and mouse β-actin monoclonal antibody (1:3,000, Abcam, USA).

Techniques: Expressing

Neogenin (Neo1) deficiency promoted macrophage transformation to the proinflammatory phenotype through the janus kinase 1 (JAK1)-signal transduction and activator of transcription 1 (STAT1) signal pathway, not STAT6 and P65 pathways, a The protein bands of p/T-JAK1, p/T-JAK2, p/T-STAT1, p/T-P65, p/T-STAT6 and GAPDH 3 days after myocardial infarction (MI), n = 5 in each group; b-f Quantitative analysis of p-JAK1, p-JAK2, p-STAT1, p-P65 and p-STAT6 in each group 3 days after MI, n = 5, two way ANOVA followed by Tukey’s test; g The double-labelling immunofluorescence of p-STAT1 and F4/80 3 days after MI, n = 4 in each group; h The protein bands of p/T-JAK1 and p/T-STAT1 3 days after MI in Neo1F/F and Neo1F/F;Cx3cr1cre mice; i, j Quantitative analysis of p-JAK1 and p-STAT1 in each group 3 days after MI in Neo1F/F and Neo1F/F;Cx3cr1cre mice, n = 5, two way ANOVA followed by Tukey’s test; k The protein bands and quantitative analysis of p/T-JAK1 and p/T-STAT1 in bone marrow derived-macrophages (BMDMs) 12 h after stimulation with LPS + IFN-γ, n = 3 in each group, two way ANOVA followed by Tukey’s test; l The immunofluorescence of p-STAT1 in BMDMs was analyzed by a confocal laser scanning microscope, n = 3 in each group. Data are expressed as the mean ± SEM. In b-f, *p < 0.05 vs. Sham + IgG group, #p < 0.05 vs. MI + IgG group, n.s. indicating no significance; in i and j *p < 0.05 vs. Sham + Neo1F/F group, #p < 0.05 vs. MI + Neo1F/F group; in k, *p < 0.05 vs. Sham + IgG group, #p < 0.05 vs. LPS + IFN-γ + IgG group

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Macrophage neogenin deficiency exacerbates myocardial remodeling and inflammation after acute myocardial infarction through JAK1-STAT1 signaling

doi: 10.1007/s00018-023-04974-7

Figure Lengend Snippet: Neogenin (Neo1) deficiency promoted macrophage transformation to the proinflammatory phenotype through the janus kinase 1 (JAK1)-signal transduction and activator of transcription 1 (STAT1) signal pathway, not STAT6 and P65 pathways, a The protein bands of p/T-JAK1, p/T-JAK2, p/T-STAT1, p/T-P65, p/T-STAT6 and GAPDH 3 days after myocardial infarction (MI), n = 5 in each group; b-f Quantitative analysis of p-JAK1, p-JAK2, p-STAT1, p-P65 and p-STAT6 in each group 3 days after MI, n = 5, two way ANOVA followed by Tukey’s test; g The double-labelling immunofluorescence of p-STAT1 and F4/80 3 days after MI, n = 4 in each group; h The protein bands of p/T-JAK1 and p/T-STAT1 3 days after MI in Neo1F/F and Neo1F/F;Cx3cr1cre mice; i, j Quantitative analysis of p-JAK1 and p-STAT1 in each group 3 days after MI in Neo1F/F and Neo1F/F;Cx3cr1cre mice, n = 5, two way ANOVA followed by Tukey’s test; k The protein bands and quantitative analysis of p/T-JAK1 and p/T-STAT1 in bone marrow derived-macrophages (BMDMs) 12 h after stimulation with LPS + IFN-γ, n = 3 in each group, two way ANOVA followed by Tukey’s test; l The immunofluorescence of p-STAT1 in BMDMs was analyzed by a confocal laser scanning microscope, n = 3 in each group. Data are expressed as the mean ± SEM. In b-f, *p < 0.05 vs. Sham + IgG group, #p < 0.05 vs. MI + IgG group, n.s. indicating no significance; in i and j *p < 0.05 vs. Sham + Neo1F/F group, #p < 0.05 vs. MI + Neo1F/F group; in k, *p < 0.05 vs. Sham + IgG group, #p < 0.05 vs. LPS + IFN-γ + IgG group

Article Snippet: Primary antibodies included: Neo1 (R&D system), collagen I (Servicebio), Bax (Abcam), Bcl-2 (Abcam), cleaved-caspase3 (GeneTex), phospho (p)/total (T)-P38 (CST), p/T-ERK (CST), p/T-JNK (CST), p-janus kinase 1 (JAK1) (CST), T-JAK1 (Abcam), p-JAK2 (CST), T-JAK2 (Abcam), p-signal transduction and activator of transcription 1 (STAT1) (Abcam), T-STAT1 (CST), p/T-P65 (Abcam), p/T-STAT6 (CST), GAPDH (GeneTex), Chemerin receptor 23 (ChemR23) (Santa Cruz), formyl-peptide receptor-2 (FPR2) (Santa Cruz), and G protein-coupled receptor 37 (GPR37) (Santa Cruz).

Techniques: Transformation Assay, Transduction, Immunofluorescence, Derivative Assay, Laser-Scanning Microscopy