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Proteintech 1 ig
1 Ig, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 41 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/jagged1/Jagged1+Antibody/pm41806839-545-67-65
Average 93 stars, based on 41 article reviews

1 ig - by Bioz Stars, 2026-09

93/100 stars

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Incubation:

Article Title: LIFUS-driven engineered bacteria reprogram immunosuppressive niches via mechano-NOTCH signaling.
Article Snippet: .. Samples were incubated with primary antibodies against Notch1 (Proteintech, KHC1061) and Jagged1 (Proteintech, 66890-1-lg) overnight at 4◦C, followed by fluorochrome-conjugated secondary antibodies. ..

Article Title: Notch signaling pathway regulates the progression of fetal growth restriction through mediating immune dysfunction
Article Snippet: .. After antigen retrieval, the samples were incubated overnight at 4 ̊C with primary antibodies against Notch1 (1:200), Jagged1 (1:200), CD3 (1:200; cat. no. 17617-1-AP), CD86 (1:200; cat. no. 26903-1-AP), CD206 (1:200; cat. no. 18704-1-AP; last 3 obtained from Proteintech Group, Inc.) and Forkhead Box protein 3 (Foxp3; 1:200; cat. no. ab36607; Abcam). .. Subsequently, secondary antibodies conjugated with HRP (1:3,000; cat. no. ab205719; Abcam) were applied for 1 h at 37 ̊C.

Article Title: Notch signaling pathway regulates the progression of fetal growth restriction through mediating immune dysfunction.
Article Snippet: .. After antigen retrieval, the samples were incubated overnight at 4 ̊C with primary antibodies against Notch1 (1:200), Jagged1 (1:200), CD3 (1:200; cat. no. 17617‐1‐AP), CD86 (1:200; cat. no. 26903‐1‐AP), CD206 (1:200; cat. no. 18704‐1‐AP; last 3 obtained from Proteintech Group, Inc.) and Forkhead Box protein 3 (Foxp3; 1:200; cat. no. ab36607; Abcam). .. Subsequently, secondary antibodies conjugated with HRP (1:3,000; cat. no. ab205719; Abcam) were applied for 1 h at 37 ̊C.

Article Title: Notch signaling pathway regulates the progression of fetal growth restriction through mediating immune dysfunction
Article Snippet: .. Following this step, primary antibodies including Notch1 (1:750; cat. no. 20687-1-AP), Jagged1 (1:20,000; cat. no. 66890-1-Ig), β-actin (1:20,000; cat. no. 66009-1-Ig), TNF-α (1:2,000; cat. no. 60291-1-Ig), vascular endothelial growth factor (VEGF; (1:8,000; cat. no. 19003-1-AP), GAPDH (1:50,000; cat. no. 60004-1-Ig; all from Proteintech Group, Inc.), IL-6 (1:1,000; cat. no. bs-0782R), placental growth factor (PLGF; 1:1,000; cat. no. bsm-54066R; both from BIOSS), C-X-C motif chemokine ligand 1 (CXCL1; 1:100; cat. no. ab206411), soluble fms-like tyrosine kinase-1 (sFlt-1; 1:1,000; cat. no. ab32152) and placental protein 13 (PP13; 1:1,000; cat. no. ab218411; all from Abcam) were introduced to the membranes for overnight incubation at 4 ̊C. ..

Article Title: Notch signaling pathway regulates the progression of fetal growth restriction through mediating immune dysfunction.
Article Snippet: .. Following this step, primary antibodies including Notch1 (1:750; cat. no. 20687‐1‐AP), Jagged1 (1:20,000; cat. no. 66890‐1‐Ig), β‐actin (1:20,000; cat. no. 66009‐1‐Ig), TNF‐α (1:2,000; cat. no. 60291‐1‐Ig), vascular endothelial growth factor (VEGF; (1:8,000; cat. no. 19003‐1‐AP), GAPDH (1:50,000; cat. no. 60004‐1‐Ig; all from Proteintech Group, Inc.), IL‐6 (1:1,000; cat. no. bs‐0782R), placental growth factor (PLGF; 1:1,000; cat. no. bsm‐54066R; both from BIOSS), C‐X‐C motif chemokine ligand 1 (CXCL1; 1:100; cat. no. ab206411), soluble fms‐like tyrosine kinase‐1 (sFlt‐1; 1:1,000; cat. no. ab32152) and placental protein 13 (PP13; 1:1,000; cat. no. ab218411; all from Abcam) were introduced to the membranes for overnight incubation at 4 ̊C. ..

Article Title: LIFUS-driven engineered bacteria reprogram immunosuppressive niches via mechano-NOTCH signaling
Article Snippet: .. Samples were incubated with primary antibodies against Notch1 (Proteintech, KHC1061) and Jagged1 (Proteintech, 66890-1-lg) overnight at 4°C, followed by fluorochrome-conjugated secondary antibodies. ..

Image Search Results

NOTCH pathway modulation affects HG‐induced PANoptosis. hRMECs were treated with a NOTCH agonist (Jagged1 peptide) or inhibitor (DAPT) under HG conditions. (A) Cell viability measured by CCK‐8 assay. (B) Caspase‐3/7 activity measured by colorimetric assay. (C) IL‐1 β and IL‐18 levels were quantified by ELISA. (D) Apoptosis rate measured by flow cytometry with quantification. (E) Quantification of Western blot analysis for PANoptosis‐related proteins, including cleaved Caspase‐3, GSDMD‐N, RIPK1, Bax, RIPK3, p‐MLKL, and Bcl‐2. (F) Co‐IP analysis of PANoptosome components (ASC, Caspase‐1, NLRP3, and RIPK3). (G) qPCR analysis of Bax and Bcl-2 mRNA levels. (H, I) IF staining of p‐MLKL (green) with DAPI (blue) and quantification. Scale bar = 150 μ m. Data are presented as mean ± SD ( n = 3). Statistical analysis was performed using one‐way ANOVA followed by Tukey′s post hoc test. ∗ p < 0.01, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ns = not significant.

Journal: Journal of Diabetes Research

Article Title: CD36 Regulates PANoptosis in Diabetic Retinopathy via the NOTCH/MAML Pathway

doi: 10.1155/jdr/9324498

Figure Lengend Snippet: NOTCH pathway modulation affects HG‐induced PANoptosis. hRMECs were treated with a NOTCH agonist (Jagged1 peptide) or inhibitor (DAPT) under HG conditions. (A) Cell viability measured by CCK‐8 assay. (B) Caspase‐3/7 activity measured by colorimetric assay. (C) IL‐1 β and IL‐18 levels were quantified by ELISA. (D) Apoptosis rate measured by flow cytometry with quantification. (E) Quantification of Western blot analysis for PANoptosis‐related proteins, including cleaved Caspase‐3, GSDMD‐N, RIPK1, Bax, RIPK3, p‐MLKL, and Bcl‐2. (F) Co‐IP analysis of PANoptosome components (ASC, Caspase‐1, NLRP3, and RIPK3). (G) qPCR analysis of Bax and Bcl-2 mRNA levels. (H, I) IF staining of p‐MLKL (green) with DAPI (blue) and quantification. Scale bar = 150 μ m. Data are presented as mean ± SD ( n = 3). Statistical analysis was performed using one‐way ANOVA followed by Tukey′s post hoc test. ∗ p < 0.01, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ns = not significant.

Article Snippet: To modulate NOTCH signaling under HG conditions, cells were cultured in 25.0 mmol/L D‐glucose for 72 h. During the final 24 h, the HG group was supplemented with either 5 μ g/mL Jagged1 peptide (MedChemExpress, United States) to activate the pathway or 10 μ M DAPT (MedChemExpress, United States) to inhibit it.

Techniques: CCK-8 Assay, Activity Assay, Colorimetric Assay, Enzyme-linked Immunosorbent Assay, Flow Cytometry, Western Blot, Co-Immunoprecipitation Assay, Staining

( A ) GSEA between the secretory (SEC) and window of implantation (WOI) groups for proliferative epithelium. ( B ) The single-cell pseudotime trajectory of proliferative epithelium, stromal cell, EMT-derived cell and stem-derived epithelium. Cells start at proliferative epithelium and progress to EMT-derived cell. There are seven major states over pseudotime. The black spot indicates the differentiation node between states 4, 5 and 6, indicating the direction from proliferative epithelium to EMT-derived cell. Arrows indicate the direction of the pseudotime trajectory. ( C ) The horizontal axis is the pseudotime point, and the vertical axis is the gene expression level. The solid line represents states 1, 2, 4, and 5 corresponding to Fig. S4B. Different colors represent samples in the CTRL, SEC, and WOI groups. ( D ) Heatmap of genes at the branch node regulating differentiation into EMT-derived cell and stem-derived epithelium. The horizontal axis is the pseudo-time point (the pseudo-time point gradually increases from the middle to both sides). The vertical axis is the gene expression level, representing two differential directions on the left and right sides. Clusters represent the gene sets with a similar branch gene expression trend. Different colors represent the level of gene expression. ( E–F ) Dot plots demonstrating the Cellphone DB analysis of relevant receptors and ligands of EMT-derived cell ( E ) or stromal cell ( F ) with other cell types. The size of the dot represents the level of significance. The color of the dot indicates the mean of the average expression level of interacting molecule 1 in EMT-derived cells ( E ) or stromal cells ( F ) and molecule 2 in other cell types. ( G ) Proximity ligation assay (PLA) validating the interactions of SEMA3A-NRP1 and CD46-JAG1 in the CTRL, SEC and WOI assembloids. Red signals the interaction of two proteins. Nuclei were counterstained with DAPI. Scale bar = 20 μm.

Journal: eLife

Article Title: Human receptive endometrial assembloid for deciphering the implantation window

doi: 10.7554/eLife.90729

Figure Lengend Snippet: ( A ) GSEA between the secretory (SEC) and window of implantation (WOI) groups for proliferative epithelium. ( B ) The single-cell pseudotime trajectory of proliferative epithelium, stromal cell, EMT-derived cell and stem-derived epithelium. Cells start at proliferative epithelium and progress to EMT-derived cell. There are seven major states over pseudotime. The black spot indicates the differentiation node between states 4, 5 and 6, indicating the direction from proliferative epithelium to EMT-derived cell. Arrows indicate the direction of the pseudotime trajectory. ( C ) The horizontal axis is the pseudotime point, and the vertical axis is the gene expression level. The solid line represents states 1, 2, 4, and 5 corresponding to Fig. S4B. Different colors represent samples in the CTRL, SEC, and WOI groups. ( D ) Heatmap of genes at the branch node regulating differentiation into EMT-derived cell and stem-derived epithelium. The horizontal axis is the pseudo-time point (the pseudo-time point gradually increases from the middle to both sides). The vertical axis is the gene expression level, representing two differential directions on the left and right sides. Clusters represent the gene sets with a similar branch gene expression trend. Different colors represent the level of gene expression. ( E–F ) Dot plots demonstrating the Cellphone DB analysis of relevant receptors and ligands of EMT-derived cell ( E ) or stromal cell ( F ) with other cell types. The size of the dot represents the level of significance. The color of the dot indicates the mean of the average expression level of interacting molecule 1 in EMT-derived cells ( E ) or stromal cells ( F ) and molecule 2 in other cell types. ( G ) Proximity ligation assay (PLA) validating the interactions of SEMA3A-NRP1 and CD46-JAG1 in the CTRL, SEC and WOI assembloids. Red signals the interaction of two proteins. Nuclei were counterstained with DAPI. Scale bar = 20 μm.

Article Snippet: Antibody , Jagged1 (28H8) Rabbit mAb (Rabbit monoclonal) , Cell Signaling , Cat#: 2620T RRID: AB_10693295 , PLA (1:1000).

Techniques: Single Cell, Derivative Assay, Gene Expression, Expressing, Proximity Ligation Assay

( A and B ) JAG1 expression in scRNA-seq data of cancer cells from different subtypes of breast cancer. n = 15,816 cells from 31 patients in all cases, n = 10,427 cells from 15 patients in ER+, n = 176 cells from 3 patients in HER2+, and n = 5213 cells from 13 patients in TNBC. UMAP, uniform manifold approximation projection. ( C ) Relapse-free survival of patients with a low (black) or high (red) expression of Jag1 in different subtypes of breast cancer in the Kaplan-Meier Plotter database . HR, hazard ratio. ( D ) Tumor masses of MDA-MB-231 WT (Jag1WT) and Jag1 knockout (Jag1KO) cell chick CAM xenograft models. P values are calculated by a two-tailed unpaired t test. n = 10 tumors for Jag1WT and n = 12 for Jag1KO. ( E ) Representative images of zebrafish embryos injected intravenously with fluorescently labeled cancer cells. The magenta arrowhead denotes an example of an individual cancer cell in the tail of the embryo, and cyan arrowheads mark a cluster of three cells. ( F ) Quantification of cells that have invaded into the tails of zebrafish embryos. The P value is calculated by a two-tailed unpaired Mann-Whitney test. n = 30 embryos for Jag1WT and n = 42 for Jag1KO. ( G ) Normalized fluorescence intensity of cells invaded to the heads of zebrafish embryos. The P value is calculated by a two-tailed unpaired t test. n = 30 embryos for Jag1WT and n = 44 for Jag1KO.

Journal: Science Advances

Article Title: Jagged1 regulates extracellular matrix deposition and remodeling in triple-negative breast cancer

doi: 10.1126/sciadv.aea9562

Figure Lengend Snippet: ( A and B ) JAG1 expression in scRNA-seq data of cancer cells from different subtypes of breast cancer. n = 15,816 cells from 31 patients in all cases, n = 10,427 cells from 15 patients in ER+, n = 176 cells from 3 patients in HER2+, and n = 5213 cells from 13 patients in TNBC. UMAP, uniform manifold approximation projection. ( C ) Relapse-free survival of patients with a low (black) or high (red) expression of Jag1 in different subtypes of breast cancer in the Kaplan-Meier Plotter database . HR, hazard ratio. ( D ) Tumor masses of MDA-MB-231 WT (Jag1WT) and Jag1 knockout (Jag1KO) cell chick CAM xenograft models. P values are calculated by a two-tailed unpaired t test. n = 10 tumors for Jag1WT and n = 12 for Jag1KO. ( E ) Representative images of zebrafish embryos injected intravenously with fluorescently labeled cancer cells. The magenta arrowhead denotes an example of an individual cancer cell in the tail of the embryo, and cyan arrowheads mark a cluster of three cells. ( F ) Quantification of cells that have invaded into the tails of zebrafish embryos. The P value is calculated by a two-tailed unpaired Mann-Whitney test. n = 30 embryos for Jag1WT and n = 42 for Jag1KO. ( G ) Normalized fluorescence intensity of cells invaded to the heads of zebrafish embryos. The P value is calculated by a two-tailed unpaired t test. n = 30 embryos for Jag1WT and n = 44 for Jag1KO.

Article Snippet: The following antibodies and dilutions were used: 1:1000 Jagged1 (Cell Signaling Technology, cat. no. 2620, RRID: AB_10693295), 1:1000 phospho-Smad2 (Ser 465/467 )/Smad3 (Ser 423/425 ) (Cell Signaling Technology, cat. no. 8828, RRID: AB_2631089), 1:1000 Smad2/3 (Santa Cruz Biotechnology, cat. no. sc-133098, RRID: AB_2193048), 1:1000 αSMA (Cell Signaling Technology, cat. no. 19245, RRID: AB_2734735), 1:2500 FN (BD Biosciences, cat. no. 610077, RRID: AB_2105706), 1:1000 ERα (Santa Cruz Biotechnology, cat. no. sc-8002, RRID: AB_627558), 1:1000 β-tubulin (Cell Signaling Technology, cat. no. 86298, RRID: AB_2715541), 1:200,000 β-actin (Sigma-Aldrich, cat. no. A1978, RRID: AB_4766922), and 1:5000 HSC70 (Enzo Life Sciences, cat. no. ADI-SPA-815, RRID: AB_10617277).

Techniques: Expressing, Knock-Out, Two Tailed Test, Injection, Labeling, MANN-WHITNEY, Fluorescence

( A ) Percentage of cancer cells with high JAG1 expression in scRNA-seq data of different breast cancer subtypes. ( B ) UMAP visualization of TNBC cells in the scRNA-seq data split into Jag1-high and Jag1-low populations on the basis of the JAG1 expression level. n = 719 Jag1-high TNBC cells and n = 4494 Jag1-low TNBC cells. ( C ) GSEA of genes differentially expressed between Jag1-high and Jag1-low TNBC cells in scRNA-seq data (fdr < 0.01 and average log 2 fold change >0.500). Examples of ( D ) Notch pathway genes, ( E ) breast CSC markers, and ( F ) EMT markers differentially expressed between Jag1-high and Jag1-low TNBC cells in scRNA-seq data. P values are calculated by a Wilcoxon rank sum test with Benjamini-Hochberg adjustment. ns, not significant. ( G ) Representative images of MDA-MB-231 Jag1WT and Jag1KO 3D spheroids and a Western blot showing Jag1 expression in the cell lines. Scale bar, 200 μm. ( H ) Clustered heatmap of a genome-wide transcriptome analysis showing z -scores of genes differentially expressed between spheroid samples of Jag1WT and Jag1KO cells, Jag1KO cells transfected with Jag1-containing plasmid (Jag1KO + rescue) or an empty vector plasmid (Jag1KO + ctrl), and Jag1WT cells transfected with nontargeting siRNA (siCtrl) or Jag1-targeting siRNA (siJag1) (fdr < 0.05 and fold change >1.5). n = 3 biological replicates. ( I ) GSEA of genes differentially expressed between Jag1WT and Jag1KO spheroids (fdr < 0.05). ( J ) GSEA of genes either positively (red) or negatively (blue) correlating with JAG1 expression (Spearman’s correlation coefficient >0.300 or <−0.300, respectively) in an mRNA expression dataset of patients with breast cancer (TCGA, Cell 2015, n = 817) .

Journal: Science Advances

Article Title: Jagged1 regulates extracellular matrix deposition and remodeling in triple-negative breast cancer

doi: 10.1126/sciadv.aea9562

Figure Lengend Snippet: ( A ) Percentage of cancer cells with high JAG1 expression in scRNA-seq data of different breast cancer subtypes. ( B ) UMAP visualization of TNBC cells in the scRNA-seq data split into Jag1-high and Jag1-low populations on the basis of the JAG1 expression level. n = 719 Jag1-high TNBC cells and n = 4494 Jag1-low TNBC cells. ( C ) GSEA of genes differentially expressed between Jag1-high and Jag1-low TNBC cells in scRNA-seq data (fdr < 0.01 and average log 2 fold change >0.500). Examples of ( D ) Notch pathway genes, ( E ) breast CSC markers, and ( F ) EMT markers differentially expressed between Jag1-high and Jag1-low TNBC cells in scRNA-seq data. P values are calculated by a Wilcoxon rank sum test with Benjamini-Hochberg adjustment. ns, not significant. ( G ) Representative images of MDA-MB-231 Jag1WT and Jag1KO 3D spheroids and a Western blot showing Jag1 expression in the cell lines. Scale bar, 200 μm. ( H ) Clustered heatmap of a genome-wide transcriptome analysis showing z -scores of genes differentially expressed between spheroid samples of Jag1WT and Jag1KO cells, Jag1KO cells transfected with Jag1-containing plasmid (Jag1KO + rescue) or an empty vector plasmid (Jag1KO + ctrl), and Jag1WT cells transfected with nontargeting siRNA (siCtrl) or Jag1-targeting siRNA (siJag1) (fdr < 0.05 and fold change >1.5). n = 3 biological replicates. ( I ) GSEA of genes differentially expressed between Jag1WT and Jag1KO spheroids (fdr < 0.05). ( J ) GSEA of genes either positively (red) or negatively (blue) correlating with JAG1 expression (Spearman’s correlation coefficient >0.300 or <−0.300, respectively) in an mRNA expression dataset of patients with breast cancer (TCGA, Cell 2015, n = 817) .

Techniques: Expressing, Western Blot, Genome Wide, Transfection, Plasmid Preparation

( A ) Percentage of cancer cells with high JAG1 expression in scRNA-seq data of TNBC samples from individual patients. ( B ) UMAP visualization of fibroblasts from patients with either high or low Jag1 in cancer cells. n = 881 of Jag1-high fibroblasts and n = 1530 of Jag1-low fibroblasts. ( C ) GSEA of genes differentially expressed between fibroblasts from patients with high or low Jag1 in cancer cells (fdr < 0.01 and average log 2 fold change >0.500). Expression of ( D ) Notch pathway genes, ( E ) TGFβ pathway genes, and ( F ) myofibroblast markers in fibroblasts from patients with high or low Jag1 in cancer cells. P values are calculated by a Wilcoxon rank sum test with Benjamini-Hochberg adjustment. ( G ) UMAP visualization of fibroblast clusters. ( H ) Percentage of fibroblasts from each individual patient in fibroblast clusters.

Journal: Science Advances

Article Title: Jagged1 regulates extracellular matrix deposition and remodeling in triple-negative breast cancer

doi: 10.1126/sciadv.aea9562

Figure Lengend Snippet: ( A ) Percentage of cancer cells with high JAG1 expression in scRNA-seq data of TNBC samples from individual patients. ( B ) UMAP visualization of fibroblasts from patients with either high or low Jag1 in cancer cells. n = 881 of Jag1-high fibroblasts and n = 1530 of Jag1-low fibroblasts. ( C ) GSEA of genes differentially expressed between fibroblasts from patients with high or low Jag1 in cancer cells (fdr < 0.01 and average log 2 fold change >0.500). Expression of ( D ) Notch pathway genes, ( E ) TGFβ pathway genes, and ( F ) myofibroblast markers in fibroblasts from patients with high or low Jag1 in cancer cells. P values are calculated by a Wilcoxon rank sum test with Benjamini-Hochberg adjustment. ( G ) UMAP visualization of fibroblast clusters. ( H ) Percentage of fibroblasts from each individual patient in fibroblast clusters.

Techniques: Expressing

( A ) Representative images of MCF7 and MDA-MB-231 WT cells grown on increasing substrate stiffness. Western blot analysis of Jag1 levels in ( B ) MCF7 and ( C ) MDA-MB-231 cells grown on increasing substrate stiffness. Quantifications of three independent experiments are shown to the right. Data are presented as the means ± SEM. P values are calculated by a one-way ANOVA with Tukey’s multiple comparisons test.

Journal: Science Advances

Article Title: Jagged1 regulates extracellular matrix deposition and remodeling in triple-negative breast cancer

doi: 10.1126/sciadv.aea9562

Figure Lengend Snippet: ( A ) Representative images of MCF7 and MDA-MB-231 WT cells grown on increasing substrate stiffness. Western blot analysis of Jag1 levels in ( B ) MCF7 and ( C ) MDA-MB-231 cells grown on increasing substrate stiffness. Quantifications of three independent experiments are shown to the right. Data are presented as the means ± SEM. P values are calculated by a one-way ANOVA with Tukey’s multiple comparisons test.

Techniques: Western Blot

( A ) Tumor masses of MDA-MB-231 Jag1WT or Jag1KO cell cocultures with MEF cells in the chick CAM xenograft model. P values are calculated by a two-tailed unpaired t test. n = 37 tumors for Jag1WT and n = 40 for Jag1KO. ( B ) Hematoxylin and eosin–stained tissue sections of CAM tumors in (A). Scale bars, 100 μm. CAM tumor cryosections stained for ( C ) collagen (CNA35; green in merge), FN (magenta in merge), actin (phalloidin; orange in merge), and nuclei (DAPI; blue in merge); ( D ) phosphorylated SMAD2 (Ser 465/467 )/SMAD3 (Ser 423/425 ) (p-SMAD); and ( E ) collagen (CNA35; green in merge), pan-cytokeratin (pan-cKRT; magenta in merge), αSMA (orange in merge), and nuclei (DAPI; blue in merge). Scale bars, 500 μm. ( F ) Quantifications of αSMA, p-SMAD, CNA35, and FN fluorescence integrated densities in CAM tumor cryosections. n = 4 tumors for αSMA and p-SMAD and n = 3 tumors for CNA35 and FN in each group. αSMA was quantified from glandular structures containing fibroblasts, and CNA35, FN, and p-SMAD were quantified from the whole-tumor area, excluding possible surrounding CAM. Data are presented as the means ± SEM. P values are calculated by a two-tailed unpaired t test. ( G ) mRNA expression level correlation with Jag1 mRNA expression in patients with breast cancer (TCGA, Cell 2015, n = 817) and ( H ) relapse-free survival of patients with low (black) or high (red) expression of ACTA2 , FN1 , COL1A2 , or COL3A1 in all breast cancer cases and in basal breast cancer separately in the Kaplan-Meier Plotter database .

Journal: Science Advances

Article Title: Jagged1 regulates extracellular matrix deposition and remodeling in triple-negative breast cancer

doi: 10.1126/sciadv.aea9562

Figure Lengend Snippet: ( A ) Tumor masses of MDA-MB-231 Jag1WT or Jag1KO cell cocultures with MEF cells in the chick CAM xenograft model. P values are calculated by a two-tailed unpaired t test. n = 37 tumors for Jag1WT and n = 40 for Jag1KO. ( B ) Hematoxylin and eosin–stained tissue sections of CAM tumors in (A). Scale bars, 100 μm. CAM tumor cryosections stained for ( C ) collagen (CNA35; green in merge), FN (magenta in merge), actin (phalloidin; orange in merge), and nuclei (DAPI; blue in merge); ( D ) phosphorylated SMAD2 (Ser 465/467 )/SMAD3 (Ser 423/425 ) (p-SMAD); and ( E ) collagen (CNA35; green in merge), pan-cytokeratin (pan-cKRT; magenta in merge), αSMA (orange in merge), and nuclei (DAPI; blue in merge). Scale bars, 500 μm. ( F ) Quantifications of αSMA, p-SMAD, CNA35, and FN fluorescence integrated densities in CAM tumor cryosections. n = 4 tumors for αSMA and p-SMAD and n = 3 tumors for CNA35 and FN in each group. αSMA was quantified from glandular structures containing fibroblasts, and CNA35, FN, and p-SMAD were quantified from the whole-tumor area, excluding possible surrounding CAM. Data are presented as the means ± SEM. P values are calculated by a two-tailed unpaired t test. ( G ) mRNA expression level correlation with Jag1 mRNA expression in patients with breast cancer (TCGA, Cell 2015, n = 817) and ( H ) relapse-free survival of patients with low (black) or high (red) expression of ACTA2 , FN1 , COL1A2 , or COL3A1 in all breast cancer cases and in basal breast cancer separately in the Kaplan-Meier Plotter database .

Techniques: Two Tailed Test, Staining, Fluorescence, Expressing

High Jagged1 expression promotes CSC-like features, EMT, and invasiveness of TNBC cells, thus enhancing tumor formation and metastasis. Jagged1 expressed by cancer cells activates Notch in the surrounding fibroblasts and increases TGFβ activity. Fibroblasts interacting with Jagged1-expressing cancer cells transdifferentiate into contractile myCAFs with increased deposition of ECM, especially collagen, and an increased capability of tumorigenic remodeling and aligning of the ECM fibers. In cancer cells, increased stiffness of the surrounding tissue and TGFβ activity induce further expression of Jagged1, leading to a tumor-promoting feed-forward loop. Jagged1 is a central modulator of the TNBC tissue structure, acting upstream of TGFβ. Created in BioRender. M. Parikainen (2025), https://biorender.com/o4se15z .

Journal: Science Advances

Article Title: Jagged1 regulates extracellular matrix deposition and remodeling in triple-negative breast cancer

doi: 10.1126/sciadv.aea9562

Figure Lengend Snippet: High Jagged1 expression promotes CSC-like features, EMT, and invasiveness of TNBC cells, thus enhancing tumor formation and metastasis. Jagged1 expressed by cancer cells activates Notch in the surrounding fibroblasts and increases TGFβ activity. Fibroblasts interacting with Jagged1-expressing cancer cells transdifferentiate into contractile myCAFs with increased deposition of ECM, especially collagen, and an increased capability of tumorigenic remodeling and aligning of the ECM fibers. In cancer cells, increased stiffness of the surrounding tissue and TGFβ activity induce further expression of Jagged1, leading to a tumor-promoting feed-forward loop. Jagged1 is a central modulator of the TNBC tissue structure, acting upstream of TGFβ. Created in BioRender. M. Parikainen (2025), https://biorender.com/o4se15z .

Techniques: Expressing, Activity Assay

Hybrid AECs display morphological and molecular features intermediate between epithelial and mesenchymal states (A) Representative bright-field and immunofluorescence images of freshly isolated AECs, hyAECs (hyAECs), and mesenchymal AECs (mAECs). Freshly isolated AECs display a typical cobblestone-like epithelial morphology and are positive for E-Cadherin (green) while negative for α-smooth muscle actin (α-SMA, red). In contrast, mAECs exhibit a spindle-shaped mesenchymal morphology with strong α-SMA expression and reduced E-Cadherin. HyAECs show intermediate morphological features with mixed cobblestone and elongated profiles and co-express both E-Cadherin and α-SMA, consistent with a hybrid epithelial/mesenchymal phenotype. Nuclei are counterstained with DAPI (blue). Scale bars, 25μm. (B) Western blot analysis of epithelial (E-Cadherin), mesenchymal (Vimentin, α-SMA), and hybrid-associated phenotypic stability factors (Jagged1, Nrf2) in amniotic membrane (AM), hyAECs, and mAECs. Tubulin was used as a loading control. Quantification of band intensities (normalized to tubulin) is shown in the accompanying graphs. E-Cadherin expression is highest in AM and decreases progressively across the EMP spectrum. Vimentin, α-SMA, Jagged1, and Nrf2 levels increase from AM to hyAECs and peak in mAECs, reflecting the transition from epithelial to mesenchymal identity. Data (mean ± SD) represent 3 independent sets of experiments (n = at least 3 biological replicates in each group per set; each biological replicate assayed in at least 3 technical replicates). Statistical significance was determined using one-way ANOVA with post hoc comparisons (∗ p < 0.05, ∗∗ p < 0.01).

Journal: iScience

Article Title: Progesterone-driven stabilization of hybrid E/M states in amniotic epithelial cells enhances regeneration and immune modulatory capacities

doi: 10.1016/j.isci.2026.114867

Figure Lengend Snippet: Hybrid AECs display morphological and molecular features intermediate between epithelial and mesenchymal states (A) Representative bright-field and immunofluorescence images of freshly isolated AECs, hyAECs (hyAECs), and mesenchymal AECs (mAECs). Freshly isolated AECs display a typical cobblestone-like epithelial morphology and are positive for E-Cadherin (green) while negative for α-smooth muscle actin (α-SMA, red). In contrast, mAECs exhibit a spindle-shaped mesenchymal morphology with strong α-SMA expression and reduced E-Cadherin. HyAECs show intermediate morphological features with mixed cobblestone and elongated profiles and co-express both E-Cadherin and α-SMA, consistent with a hybrid epithelial/mesenchymal phenotype. Nuclei are counterstained with DAPI (blue). Scale bars, 25μm. (B) Western blot analysis of epithelial (E-Cadherin), mesenchymal (Vimentin, α-SMA), and hybrid-associated phenotypic stability factors (Jagged1, Nrf2) in amniotic membrane (AM), hyAECs, and mAECs. Tubulin was used as a loading control. Quantification of band intensities (normalized to tubulin) is shown in the accompanying graphs. E-Cadherin expression is highest in AM and decreases progressively across the EMP spectrum. Vimentin, α-SMA, Jagged1, and Nrf2 levels increase from AM to hyAECs and peak in mAECs, reflecting the transition from epithelial to mesenchymal identity. Data (mean ± SD) represent 3 independent sets of experiments (n = at least 3 biological replicates in each group per set; each biological replicate assayed in at least 3 technical replicates). Statistical significance was determined using one-way ANOVA with post hoc comparisons (∗ p < 0.05, ∗∗ p < 0.01).

Article Snippet: Primary antibodies against Polyclonal Goat anti-Human CDH1/E Cadherin Antibody (aa750-850, WB) (1:300; LS-C204222; LSBio, Newark, CA 94560 USA), Jagged1 (D4Y1R) XP® Rabbit mAb (1:300; #70109T; Cell Signaling technology, Danvers, MA 01923, USA), Nrf2 (1:300; NBP1-32822; Novus Biologicals, Centennial, CO 80112 USA), Anti-alpha smooth muscle Actin, clone 1A4 (1:300; ab7817, Abcam, Cambridge, UK), Vimentin, clone V9 (1:300; M0725; Dako, Santa Clara, CA 95051, USA), α-Tubulin, clone DM1A (1:300; #3873; Cell Signaling technology, Danvers, MA 01923, USA), Oct4 (1:300; ab18976; Abcam, Cambridge, UK), Sox2 (1:300; ab59776; Abcam, Cambridge, UK), Nanog (1:300; AB9220; Sigma-Aldrich, St. Louis, MO, USA), Tenomodulin (1:300; ab203676; Abcam, Cambridge, UK), Collagen I (1:300; ab292; Abcam, Cambridge, UK), CD86, BU63 (1:300; MCA1118SBV610; Bio-Rad Laboratories, Milan, Italy), MMR/CD206 (1:300; AF2535; R&D Systems, Minneapolis, MN 55413, USA) were diluted in 1× TBS containing 1% Casein Blocker (#1610782; Bio-Rad Laboratories, Milan, Italy) and incubated overnight at 4 °C.

Techniques: Immunofluorescence, Isolation, Expressing, Western Blot, Membrane, Control

Mechano-regulation of CAF-CD8 + T cell NOTCH signaling interactions (A and B) Ultrasound elastography (A) shows a significant reduction in tumor stiffness with the combination group (12.95 ± 2.18 kPa) compared with controls (57.19 ± 15.02 kPa, ∗∗∗ p < 0.005) and VNP /ARG-GV monotherapy (46.82 ± 8.13 kPa, ∗∗ p < 0.01), LIFUS monotherapy group (36.93 ± 6.812 kPa), and the control group (57.19 ± 15.02 kPa, ∗ p < 0.05) ( n = 4) (B). (C) AFM further confirms reduced matrix elastic modulus ( n = 12). (D) Collagen I distribution secreted by fibroblasts in B supported the hypothesized changes in fibroblasts within the TME. Quantitative assessment (D) showed a significant reduction in the combined therapy group (42.24 ± 8.46 mm 2 ) compared with the control group (248.62 ± 9.19 mm 2 , ∗∗∗∗ p < 0.0001; n = 3). (E) The differential analysis visualizes changes in interaction numbers and strength, where red indicates enhanced and blue indicates reduced interactions in the combined group vs. control. The highlighted box reveals Cd8t_04 in the differential number of interactions and Cd8t_00 in differential interaction strength with reduced interactions with CAF. (F) Relative information flow of major stromal-immune signaling pathways. Relative contribution of fibroblast-derived signaling pathways to Cd8t_04 cells in control and combination treatment groups, normalized to a scale of 0–1. The dashed line at 0.5 indicates equal contribution between groups. NOTCH signaling dominates CAF–Cd8t_04 cell communication in control tumors and is selectively reduced following combination treatment, whereas CXCL and IFN-II pathways show a relative increase. (G–I) Notch1 and Jagged1 expression at the transcript (G and H) ( n = 6) and protein levels (I) are significantly reduced after combination therapy. Data are representative of three independent experiments. Data are mean ± SD. Statistical analysis was performed using one-way ANOVA (B–D) or two-tailed unpaired Student’s t test (G and H). See also .

Journal: Cell Reports Medicine

Article Title: LIFUS-driven engineered bacteria reprogram immunosuppressive niches via mechano-NOTCH signaling

doi: 10.1016/j.xcrm.2026.102658

Figure Lengend Snippet: Mechano-regulation of CAF-CD8 + T cell NOTCH signaling interactions (A and B) Ultrasound elastography (A) shows a significant reduction in tumor stiffness with the combination group (12.95 ± 2.18 kPa) compared with controls (57.19 ± 15.02 kPa, ∗∗∗ p < 0.005) and VNP /ARG-GV monotherapy (46.82 ± 8.13 kPa, ∗∗ p < 0.01), LIFUS monotherapy group (36.93 ± 6.812 kPa), and the control group (57.19 ± 15.02 kPa, ∗ p < 0.05) ( n = 4) (B). (C) AFM further confirms reduced matrix elastic modulus ( n = 12). (D) Collagen I distribution secreted by fibroblasts in B supported the hypothesized changes in fibroblasts within the TME. Quantitative assessment (D) showed a significant reduction in the combined therapy group (42.24 ± 8.46 mm 2 ) compared with the control group (248.62 ± 9.19 mm 2 , ∗∗∗∗ p < 0.0001; n = 3). (E) The differential analysis visualizes changes in interaction numbers and strength, where red indicates enhanced and blue indicates reduced interactions in the combined group vs. control. The highlighted box reveals Cd8t_04 in the differential number of interactions and Cd8t_00 in differential interaction strength with reduced interactions with CAF. (F) Relative information flow of major stromal-immune signaling pathways. Relative contribution of fibroblast-derived signaling pathways to Cd8t_04 cells in control and combination treatment groups, normalized to a scale of 0–1. The dashed line at 0.5 indicates equal contribution between groups. NOTCH signaling dominates CAF–Cd8t_04 cell communication in control tumors and is selectively reduced following combination treatment, whereas CXCL and IFN-II pathways show a relative increase. (G–I) Notch1 and Jagged1 expression at the transcript (G and H) ( n = 6) and protein levels (I) are significantly reduced after combination therapy. Data are representative of three independent experiments. Data are mean ± SD. Statistical analysis was performed using one-way ANOVA (B–D) or two-tailed unpaired Student’s t test (G and H). See also .

Article Snippet: Anti-Jagged1 antibody , Proteintech , Cat# 66890-1-Ig; RRID: AB_2882220.

Techniques: Control, Protein-Protein interactions, Derivative Assay, Expressing, Two Tailed Test

Dual mechanotransductive regulation of CAFs-CD8 + T cell crosstalk via NOTCH signaling (A) The schematic diagram of co-culture systems of CAFs and CD8 + T cells with GVs responsive to LIFUS constructs in vitro . Before 60 s of LIFUS exposure, cell co-incubation with purified GVs allowed sufficient GV-cell contact. (B and C) Confocal imaging revealed a significant reduction in Notch1 receptor and Jagged1 ligand expression in CAFs exposed to LIFUS-driven GVs (GVs + LIFUS group) compared to unstimulated controls (GVs − LIFUS group). Scale bars, 100 μm. (D and E) In CD8 + T cells, Jagged1 expression was decreased following LIFUS-driven GV stimulation (GVs + LIFUS group), whereas Notch1 receptor levels remained unchanged, indicating asymmetric NOTCH pathway modulation between CAF and CD8 + T cell. Scale bars, 100 μm. (F) Experimental workflow for assessing CAFs’ functional changes following LIFUS-driven GV treatment. (G and H) Transwell migration assays revealed significantly reduced CAF motility in the LIFUS treatment group (56 ± 4.0 cells/field) compared with the control group (150.67 ± 15.04 cells/field, ∗∗∗∗ p < 0.0001) and CAFs exposed to treatment without LIFUS (101.67 ± 3.79 cells/field, ∗∗ p < 0.01; n = 3). Scale bars, 100 μm. (I and J) ELISA quantification of CAF-secreted factors showed decreased TGF-β (0.39 ± 0.07 vs. 0.68 ± 0.38 ng/mL in control, ∗∗∗ p < 0.005) ( n = 3) (I) and collagen I (0.27 ± 0.11 vs. 0.76 ± 0.06 ng/mL in control, ∗∗ p < 0.01) ( n = 3) (J) after LIFUS-driven GV stimulation, consistent with reduced CAF activation. (K) Schematic of co-culture assay evaluating CD8 + T cell (precondition with or without LIFUS-driven GVs) and 4T1 tumor cell interactions. (L and M) CD8 + T cells stimulated by LIFUS-driven GVs exhibited significantly enhanced adhesion to 4T1 tumor cells (51.89% ± 10.47% adherent cells/field) compared with control (3.25% ± 1.19%, ∗∗∗ p < 0.005) and GV-only groups (15.72% ± 7.53%, ∗∗ p < 0.01) ( n = 3). Scale bars, 100 μm. (N) Functional validation showed the cytotoxicity of CD8 + T cells to 4T1-Luc cells ( C); the luminescence intensity, which represented the apoptosis of 4T1-Luc tumor cells, showed significant luminescence change at 12 h between CD8 + T −LIFUS ((48 ± 6.3) × 10 5 ps −1 cm −2 sr −1 ) and CD8 + T +LIFUS ((17 ± 5.2) × 10 5 ps −1 cm −2 sr −1 , ∗∗ p < 0.01) group, and a stronger decrease at 36 h compared to control group (∗∗∗∗ p < 0.0001) ( n = 3). A representative image is shown in C. Data are representative of three independent experiments. Data are mean ± SD. Statistical analysis was performed using one-way ANOVA (H–J and M) or two-way ANOVA (N). Also see A–S5C.

Journal: Cell Reports Medicine

Article Title: LIFUS-driven engineered bacteria reprogram immunosuppressive niches via mechano-NOTCH signaling

doi: 10.1016/j.xcrm.2026.102658

Figure Lengend Snippet: Dual mechanotransductive regulation of CAFs-CD8 + T cell crosstalk via NOTCH signaling (A) The schematic diagram of co-culture systems of CAFs and CD8 + T cells with GVs responsive to LIFUS constructs in vitro . Before 60 s of LIFUS exposure, cell co-incubation with purified GVs allowed sufficient GV-cell contact. (B and C) Confocal imaging revealed a significant reduction in Notch1 receptor and Jagged1 ligand expression in CAFs exposed to LIFUS-driven GVs (GVs + LIFUS group) compared to unstimulated controls (GVs − LIFUS group). Scale bars, 100 μm. (D and E) In CD8 + T cells, Jagged1 expression was decreased following LIFUS-driven GV stimulation (GVs + LIFUS group), whereas Notch1 receptor levels remained unchanged, indicating asymmetric NOTCH pathway modulation between CAF and CD8 + T cell. Scale bars, 100 μm. (F) Experimental workflow for assessing CAFs’ functional changes following LIFUS-driven GV treatment. (G and H) Transwell migration assays revealed significantly reduced CAF motility in the LIFUS treatment group (56 ± 4.0 cells/field) compared with the control group (150.67 ± 15.04 cells/field, ∗∗∗∗ p < 0.0001) and CAFs exposed to treatment without LIFUS (101.67 ± 3.79 cells/field, ∗∗ p < 0.01; n = 3). Scale bars, 100 μm. (I and J) ELISA quantification of CAF-secreted factors showed decreased TGF-β (0.39 ± 0.07 vs. 0.68 ± 0.38 ng/mL in control, ∗∗∗ p < 0.005) ( n = 3) (I) and collagen I (0.27 ± 0.11 vs. 0.76 ± 0.06 ng/mL in control, ∗∗ p < 0.01) ( n = 3) (J) after LIFUS-driven GV stimulation, consistent with reduced CAF activation. (K) Schematic of co-culture assay evaluating CD8 + T cell (precondition with or without LIFUS-driven GVs) and 4T1 tumor cell interactions. (L and M) CD8 + T cells stimulated by LIFUS-driven GVs exhibited significantly enhanced adhesion to 4T1 tumor cells (51.89% ± 10.47% adherent cells/field) compared with control (3.25% ± 1.19%, ∗∗∗ p < 0.005) and GV-only groups (15.72% ± 7.53%, ∗∗ p < 0.01) ( n = 3). Scale bars, 100 μm. (N) Functional validation showed the cytotoxicity of CD8 + T cells to 4T1-Luc cells ( C); the luminescence intensity, which represented the apoptosis of 4T1-Luc tumor cells, showed significant luminescence change at 12 h between CD8 + T −LIFUS ((48 ± 6.3) × 10 5 ps −1 cm −2 sr −1 ) and CD8 + T +LIFUS ((17 ± 5.2) × 10 5 ps −1 cm −2 sr −1 , ∗∗ p < 0.01) group, and a stronger decrease at 36 h compared to control group (∗∗∗∗ p < 0.0001) ( n = 3). A representative image is shown in C. Data are representative of three independent experiments. Data are mean ± SD. Statistical analysis was performed using one-way ANOVA (H–J and M) or two-way ANOVA (N). Also see A–S5C.

Article Snippet: Anti-Jagged1 antibody , Proteintech , Cat# 66890-1-Ig; RRID: AB_2882220.

Techniques: Co-Culture Assay, Construct, In Vitro, Incubation, Purification, Imaging, Expressing, Functional Assay, Migration, Control, Enzyme-linked Immunosorbent Assay, Activation Assay, Co-culture Assay, Biomarker Discovery

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