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jak2 p phospho jak  (Cell Signaling Technology Inc)


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    Cell Signaling Technology Inc jak2 p phospho jak
    Jak2 P Phospho Jak, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1268 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell-Signaling:

    Article Title: OZ-001 Suppresses the Growth of Triple-Negative Breast Cancer and Pancreatic Cancer by Targeting STAT3 Phosphorylation and the Calcium Signaling Pathway
    Article Snippet: .. 4E)XP Cell signaling #4370 ERK p44/42 MAPK(Erk1/2) antibody Cell signaling #9102 JAK2 Jak2(D2E12) XP Rabbit mAb cell signaling #3230 JAK2-p phospho-Jak(Tyr 1007/1008) antibody cell signaling #3771 Supplementary figure & legends 1 Supplementary Figure 1. ..



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    IL‐6 induced VSMC phenotypic switch <t>through</t> <t>JAK/STAT</t> signal pathway. A) UMAP plot of single‐cell clustering, showing the spatial distribution of different cell types (B cells, endothelial cells, fibroblasts, macrophages, smooth muscle cells, neutrophils, natural killer cells, and proliferating cells). B,C) UMAP plots of subpopulations of macrophages (MAC) and smooth muscle cells (SMC), with macrophages divided into MAC1 to MAC8 subpopulations and smooth muscle cells divided into SMC1 to SMC6 subpopulations. D) Proportional changes in macrophage and smooth muscle cell subpopulations across different groups, illustrating the relative differences in subpopulation proportions between the Control group and the TAD group. E) Differences in cell–cell communication between MAC1, MAC3 clusters and SMC1, SMC3, SMC4 clusters in the Control and TAD groups. Green and red arrows represent communication interactions between different cell clusters, with arrow thickness indicating communication strength. F) Differential expression of IL‐6 in macrophage and smooth muscle cell subpopulations, showing IL‐6 expression levels and statistical significance across different subpopulations in the Control and TAD groups. G) Representative confocal images of αSMA (green) in vascular smooth muscle cells and primary smooth muscle cells. (scale bar, 20 µm). H,I) Quantification of αSMA levels from confocal images ( n = 6 per group). J) Representative Western blot images of <t>p‐JAK,</t> JAK, p‐STAT, STAT, αSMA, and SM22α in primary VSMCs. K) Graphical abstract. IL‐6 induced VSMC phenotypic switch though JAK/STAT. L–O) Western blot analysis and quantification of p‐JAK/JAK, p‐STAT/STAT, SM22α, and α‐SMA expressed in VSMCs ( n = 3 per group). * p < 0.05, ** p < 0.01 and *** p < 0.001. Data were presented as the mean ± SD and analyzed by using one‐way ANOVA, Tukey's multiple comparisons test.
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    IL‐6 induced VSMC phenotypic switch <t>through</t> <t>JAK/STAT</t> signal pathway. A) UMAP plot of single‐cell clustering, showing the spatial distribution of different cell types (B cells, endothelial cells, fibroblasts, macrophages, smooth muscle cells, neutrophils, natural killer cells, and proliferating cells). B,C) UMAP plots of subpopulations of macrophages (MAC) and smooth muscle cells (SMC), with macrophages divided into MAC1 to MAC8 subpopulations and smooth muscle cells divided into SMC1 to SMC6 subpopulations. D) Proportional changes in macrophage and smooth muscle cell subpopulations across different groups, illustrating the relative differences in subpopulation proportions between the Control group and the TAD group. E) Differences in cell–cell communication between MAC1, MAC3 clusters and SMC1, SMC3, SMC4 clusters in the Control and TAD groups. Green and red arrows represent communication interactions between different cell clusters, with arrow thickness indicating communication strength. F) Differential expression of IL‐6 in macrophage and smooth muscle cell subpopulations, showing IL‐6 expression levels and statistical significance across different subpopulations in the Control and TAD groups. G) Representative confocal images of αSMA (green) in vascular smooth muscle cells and primary smooth muscle cells. (scale bar, 20 µm). H,I) Quantification of αSMA levels from confocal images ( n = 6 per group). J) Representative Western blot images of <t>p‐JAK,</t> JAK, p‐STAT, STAT, αSMA, and SM22α in primary VSMCs. K) Graphical abstract. IL‐6 induced VSMC phenotypic switch though JAK/STAT. L–O) Western blot analysis and quantification of p‐JAK/JAK, p‐STAT/STAT, SM22α, and α‐SMA expressed in VSMCs ( n = 3 per group). * p < 0.05, ** p < 0.01 and *** p < 0.001. Data were presented as the mean ± SD and analyzed by using one‐way ANOVA, Tukey's multiple comparisons test.
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    IL‐6 induced VSMC phenotypic switch <t>through</t> <t>JAK/STAT</t> signal pathway. A) UMAP plot of single‐cell clustering, showing the spatial distribution of different cell types (B cells, endothelial cells, fibroblasts, macrophages, smooth muscle cells, neutrophils, natural killer cells, and proliferating cells). B,C) UMAP plots of subpopulations of macrophages (MAC) and smooth muscle cells (SMC), with macrophages divided into MAC1 to MAC8 subpopulations and smooth muscle cells divided into SMC1 to SMC6 subpopulations. D) Proportional changes in macrophage and smooth muscle cell subpopulations across different groups, illustrating the relative differences in subpopulation proportions between the Control group and the TAD group. E) Differences in cell–cell communication between MAC1, MAC3 clusters and SMC1, SMC3, SMC4 clusters in the Control and TAD groups. Green and red arrows represent communication interactions between different cell clusters, with arrow thickness indicating communication strength. F) Differential expression of IL‐6 in macrophage and smooth muscle cell subpopulations, showing IL‐6 expression levels and statistical significance across different subpopulations in the Control and TAD groups. G) Representative confocal images of αSMA (green) in vascular smooth muscle cells and primary smooth muscle cells. (scale bar, 20 µm). H,I) Quantification of αSMA levels from confocal images ( n = 6 per group). J) Representative Western blot images of <t>p‐JAK,</t> JAK, p‐STAT, STAT, αSMA, and SM22α in primary VSMCs. K) Graphical abstract. IL‐6 induced VSMC phenotypic switch though JAK/STAT. L–O) Western blot analysis and quantification of p‐JAK/JAK, p‐STAT/STAT, SM22α, and α‐SMA expressed in VSMCs ( n = 3 per group). * p < 0.05, ** p < 0.01 and *** p < 0.001. Data were presented as the mean ± SD and analyzed by using one‐way ANOVA, Tukey's multiple comparisons test.
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    IL‐6 induced VSMC phenotypic switch <t>through</t> <t>JAK/STAT</t> signal pathway. A) UMAP plot of single‐cell clustering, showing the spatial distribution of different cell types (B cells, endothelial cells, fibroblasts, macrophages, smooth muscle cells, neutrophils, natural killer cells, and proliferating cells). B,C) UMAP plots of subpopulations of macrophages (MAC) and smooth muscle cells (SMC), with macrophages divided into MAC1 to MAC8 subpopulations and smooth muscle cells divided into SMC1 to SMC6 subpopulations. D) Proportional changes in macrophage and smooth muscle cell subpopulations across different groups, illustrating the relative differences in subpopulation proportions between the Control group and the TAD group. E) Differences in cell–cell communication between MAC1, MAC3 clusters and SMC1, SMC3, SMC4 clusters in the Control and TAD groups. Green and red arrows represent communication interactions between different cell clusters, with arrow thickness indicating communication strength. F) Differential expression of IL‐6 in macrophage and smooth muscle cell subpopulations, showing IL‐6 expression levels and statistical significance across different subpopulations in the Control and TAD groups. G) Representative confocal images of αSMA (green) in vascular smooth muscle cells and primary smooth muscle cells. (scale bar, 20 µm). H,I) Quantification of αSMA levels from confocal images ( n = 6 per group). J) Representative Western blot images of <t>p‐JAK,</t> JAK, p‐STAT, STAT, αSMA, and SM22α in primary VSMCs. K) Graphical abstract. IL‐6 induced VSMC phenotypic switch though JAK/STAT. L–O) Western blot analysis and quantification of p‐JAK/JAK, p‐STAT/STAT, SM22α, and α‐SMA expressed in VSMCs ( n = 3 per group). * p < 0.05, ** p < 0.01 and *** p < 0.001. Data were presented as the mean ± SD and analyzed by using one‐way ANOVA, Tukey's multiple comparisons test.
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    IL‐6 induced VSMC phenotypic switch <t>through</t> <t>JAK/STAT</t> signal pathway. A) UMAP plot of single‐cell clustering, showing the spatial distribution of different cell types (B cells, endothelial cells, fibroblasts, macrophages, smooth muscle cells, neutrophils, natural killer cells, and proliferating cells). B,C) UMAP plots of subpopulations of macrophages (MAC) and smooth muscle cells (SMC), with macrophages divided into MAC1 to MAC8 subpopulations and smooth muscle cells divided into SMC1 to SMC6 subpopulations. D) Proportional changes in macrophage and smooth muscle cell subpopulations across different groups, illustrating the relative differences in subpopulation proportions between the Control group and the TAD group. E) Differences in cell–cell communication between MAC1, MAC3 clusters and SMC1, SMC3, SMC4 clusters in the Control and TAD groups. Green and red arrows represent communication interactions between different cell clusters, with arrow thickness indicating communication strength. F) Differential expression of IL‐6 in macrophage and smooth muscle cell subpopulations, showing IL‐6 expression levels and statistical significance across different subpopulations in the Control and TAD groups. G) Representative confocal images of αSMA (green) in vascular smooth muscle cells and primary smooth muscle cells. (scale bar, 20 µm). H,I) Quantification of αSMA levels from confocal images ( n = 6 per group). J) Representative Western blot images of <t>p‐JAK,</t> JAK, p‐STAT, STAT, αSMA, and SM22α in primary VSMCs. K) Graphical abstract. IL‐6 induced VSMC phenotypic switch though JAK/STAT. L–O) Western blot analysis and quantification of p‐JAK/JAK, p‐STAT/STAT, SM22α, and α‐SMA expressed in VSMCs ( n = 3 per group). * p < 0.05, ** p < 0.01 and *** p < 0.001. Data were presented as the mean ± SD and analyzed by using one‐way ANOVA, Tukey's multiple comparisons test.
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    IL‐6 induced VSMC phenotypic switch <t>through</t> <t>JAK/STAT</t> signal pathway. A) UMAP plot of single‐cell clustering, showing the spatial distribution of different cell types (B cells, endothelial cells, fibroblasts, macrophages, smooth muscle cells, neutrophils, natural killer cells, and proliferating cells). B,C) UMAP plots of subpopulations of macrophages (MAC) and smooth muscle cells (SMC), with macrophages divided into MAC1 to MAC8 subpopulations and smooth muscle cells divided into SMC1 to SMC6 subpopulations. D) Proportional changes in macrophage and smooth muscle cell subpopulations across different groups, illustrating the relative differences in subpopulation proportions between the Control group and the TAD group. E) Differences in cell–cell communication between MAC1, MAC3 clusters and SMC1, SMC3, SMC4 clusters in the Control and TAD groups. Green and red arrows represent communication interactions between different cell clusters, with arrow thickness indicating communication strength. F) Differential expression of IL‐6 in macrophage and smooth muscle cell subpopulations, showing IL‐6 expression levels and statistical significance across different subpopulations in the Control and TAD groups. G) Representative confocal images of αSMA (green) in vascular smooth muscle cells and primary smooth muscle cells. (scale bar, 20 µm). H,I) Quantification of αSMA levels from confocal images ( n = 6 per group). J) Representative Western blot images of <t>p‐JAK,</t> JAK, p‐STAT, STAT, αSMA, and SM22α in primary VSMCs. K) Graphical abstract. IL‐6 induced VSMC phenotypic switch though JAK/STAT. L–O) Western blot analysis and quantification of p‐JAK/JAK, p‐STAT/STAT, SM22α, and α‐SMA expressed in VSMCs ( n = 3 per group). * p < 0.05, ** p < 0.01 and *** p < 0.001. Data were presented as the mean ± SD and analyzed by using one‐way ANOVA, Tukey's multiple comparisons test.
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    Image Search Results


    IL‐6 induced VSMC phenotypic switch through JAK/STAT signal pathway. A) UMAP plot of single‐cell clustering, showing the spatial distribution of different cell types (B cells, endothelial cells, fibroblasts, macrophages, smooth muscle cells, neutrophils, natural killer cells, and proliferating cells). B,C) UMAP plots of subpopulations of macrophages (MAC) and smooth muscle cells (SMC), with macrophages divided into MAC1 to MAC8 subpopulations and smooth muscle cells divided into SMC1 to SMC6 subpopulations. D) Proportional changes in macrophage and smooth muscle cell subpopulations across different groups, illustrating the relative differences in subpopulation proportions between the Control group and the TAD group. E) Differences in cell–cell communication between MAC1, MAC3 clusters and SMC1, SMC3, SMC4 clusters in the Control and TAD groups. Green and red arrows represent communication interactions between different cell clusters, with arrow thickness indicating communication strength. F) Differential expression of IL‐6 in macrophage and smooth muscle cell subpopulations, showing IL‐6 expression levels and statistical significance across different subpopulations in the Control and TAD groups. G) Representative confocal images of αSMA (green) in vascular smooth muscle cells and primary smooth muscle cells. (scale bar, 20 µm). H,I) Quantification of αSMA levels from confocal images ( n = 6 per group). J) Representative Western blot images of p‐JAK, JAK, p‐STAT, STAT, αSMA, and SM22α in primary VSMCs. K) Graphical abstract. IL‐6 induced VSMC phenotypic switch though JAK/STAT. L–O) Western blot analysis and quantification of p‐JAK/JAK, p‐STAT/STAT, SM22α, and α‐SMA expressed in VSMCs ( n = 3 per group). * p < 0.05, ** p < 0.01 and *** p < 0.001. Data were presented as the mean ± SD and analyzed by using one‐way ANOVA, Tukey's multiple comparisons test.

    Journal: Advanced Science

    Article Title: 12‐HETE is an Endogenous Modulator of BLT2 Triggering Vascular Degeneration, Dissection, and Rupture

    doi: 10.1002/advs.202515897

    Figure Lengend Snippet: IL‐6 induced VSMC phenotypic switch through JAK/STAT signal pathway. A) UMAP plot of single‐cell clustering, showing the spatial distribution of different cell types (B cells, endothelial cells, fibroblasts, macrophages, smooth muscle cells, neutrophils, natural killer cells, and proliferating cells). B,C) UMAP plots of subpopulations of macrophages (MAC) and smooth muscle cells (SMC), with macrophages divided into MAC1 to MAC8 subpopulations and smooth muscle cells divided into SMC1 to SMC6 subpopulations. D) Proportional changes in macrophage and smooth muscle cell subpopulations across different groups, illustrating the relative differences in subpopulation proportions between the Control group and the TAD group. E) Differences in cell–cell communication between MAC1, MAC3 clusters and SMC1, SMC3, SMC4 clusters in the Control and TAD groups. Green and red arrows represent communication interactions between different cell clusters, with arrow thickness indicating communication strength. F) Differential expression of IL‐6 in macrophage and smooth muscle cell subpopulations, showing IL‐6 expression levels and statistical significance across different subpopulations in the Control and TAD groups. G) Representative confocal images of αSMA (green) in vascular smooth muscle cells and primary smooth muscle cells. (scale bar, 20 µm). H,I) Quantification of αSMA levels from confocal images ( n = 6 per group). J) Representative Western blot images of p‐JAK, JAK, p‐STAT, STAT, αSMA, and SM22α in primary VSMCs. K) Graphical abstract. IL‐6 induced VSMC phenotypic switch though JAK/STAT. L–O) Western blot analysis and quantification of p‐JAK/JAK, p‐STAT/STAT, SM22α, and α‐SMA expressed in VSMCs ( n = 3 per group). * p < 0.05, ** p < 0.01 and *** p < 0.001. Data were presented as the mean ± SD and analyzed by using one‐way ANOVA, Tukey's multiple comparisons test.

    Article Snippet: The membranes were blocked with 5% non‐fat milk in TBST for 1 h at room‐temperature and then incubated overnight at 4 °C with the following primary antibodies: NOX1 (Proteintech, 17772‐1‐AP, 1:1000), p‐IκBα (Santa Cruz, sc‐8404, 1:1000), IκBα (Santa Cruz, sc‐1643, 1:1000), IL‐6 (Santa Cruz, sc‐35596, 1:1000), p‐JAK (Abclonal, AP0531, 1:1000), JAK (Santa Cruz, sc‐390539, 1:1000), p‐STAT (CST, 9145S, 1:1000), STAT (CST, 9139S, 1:1000), Collagen I (Abclonal, A16891, 1:1000), α‐SMA (CST, 48938S, 1:1000), SM22α (Santa Cruz, sc‐53932, 1:1000), α‐Tubulin (CST, 2144S, 1:1000), and GAPDH (CST, 2118S, 1:1000).

    Techniques: Control, Quantitative Proteomics, Expressing, Western Blot