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R&D Systems anti human timp 1 antibody
Anti Human Timp 1 Antibody, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 68 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+human+timp+1/Human+TIMP-1+Antibody/pm41354972-57-18-32
Average 93 stars, based on 68 article reviews

anti human timp 1 antibody - by Bioz Stars, 2026-09

93/100 stars

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Enzyme-linked Immunosorbent Assay:

Article Title: Gelatinases and their tissue inhibitors are associated with oxidative stress: a potential set of markers connected with male infertility
Article Snippet: The expression and activity of matrix metalloproteinases (MMPs) may be regulated by oxidative stress in various pathophysiological processes; therefore, the aim of the present study was to analyse the associations between the expression of the gelatinases MMP-9 and MMP-2 and their tissue inhibitors TIMP-1, TIMP-2 and levels of total antioxidant capacity (TAC) and advanced oxidation protein products (AOPP) in seminal plasma prepared for artificial insemination.. Levels ofMMPs and TIMPswere evaluated using ELISA,whereas TAC andAOPP in the seminal plasma of 131 childless men and 38 fertile volunteers were determined spectrophotometrically.. Seminal MMP-9 expression was higher in childless men than in fertile subjects, whereas there was no significant differences inMMP-2 expression between the analysed seminal groups.

Article Title: Red blood cells increase secretion of matrix metalloproteinases from human lung fibroblasts in vitro.
Article Snippet: K. Fredriksson, X. D. Liu, J. Lundahl, J. Klominek, S. I. Rennard, and C. M. Skold Karolinska Institutet, Department of Medicine, Division of Respiratory Medicine, Karolinska University Hospital Solna, Stockholm, Sweden; Pulmonary, Critical Care and Sleep Medicine, Department Internal Medicine, University of Nebraska Medical Center, Omaha, Nebraska; and Karolinska Institutet, Department of Medicine, Division of Clinical Immunology, Karolinska University Hospital Huddinge, Stockholm, Sweden

Article Title: Vitamin D Inhibits Expression and Activity of Matrix Metalloproteinase in Human Lung Fibroblasts (HFL-1) Cells
Article Snippet: .. Ninety-six-well ELISA plates were coated overnight at 4°C with 100 μL of anti-human TIMP-1 or TIMP-2 antibodies (R&D Systems) diluted in Voler's buffer (pH 9.6). ..

Neutralization:

Article Title: Breast Cancer Cells Induce Cancer-Associated Fibroblasts to Secrete Hepatocyte Growth Factor to Enhance Breast Tumorigenesis
Article Snippet: .. For neutralization of cytokines and growth factors, mouse anti-human HGF, anti-human TIMP-1 and anti-human IGFBP-3 antibodies (R&D Systems) were added into the medium and mixed with the agar. ..

Isolation:

Article Title: Involvement of TIMP-1 in PECAM-1-mediated tumor dissemination
Article Snippet: .. The following antibodies were used in the present study: Anti-mouse TIMP-1 (cat. no. AF980) and anti-human TIMP-1 (cat. no. AF970) (both from R&D Systems, Inc., Minneapolis, MN, USA); anti-GAPDH (cat. no. sc-25778; Santa Cruz Biotechnology, Inc., Dallas, TX, USA); anti-PECAM-1 antibodies: 390, isolated from hybridoma ( ) and Mec 13.3 (cat. no. NB600-1475; Novus Biologicals, LLC, Littleton, CO, USA); anti-mouse cluster of differentiation (CD)16/32 (cat. no. 101319) and rat IgG2a, κ isotype control (cat. no. 400511) (both from BioLegend, Inc., San Diego, CA, USA); rabbit polyclonal anti-proliferating cell nuclear antigen (PCNA) (cat. no. ab18197; Abcam, Cambridge, MA, USA); and biotinylated donkey anti-goat antibody (cat. no. 705-065-147) and biotinylated goat anti-rabbit antibody (cat. no. 111-065-144) (from Jackson ImmunoResearch Laboratories, Inc., West Grove, PA, USA). .. Murine EC (MEC) lines, H5V , provided by Dr Cecilia Garlanda (Humanitas University, Rozzano, Milan, Italy) through Dr Steven Albelda (University of Pennsylvania, Philadelphia, PA, USA) and CD3 , provided by Dr Clement Diglio, (Wayne State University, Detroit, MI, USA), as well as the B16-F10 murine melanoma [CRL-6475, American Type Culture Collection (ATCC), Manassas, VA, USA] and 4T1 murine breast cancer (CRL-2539, ATCC) cell lines were maintained at 37°C in an atmosphere containing 5% CO 2 .

Control:

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snRNA-seq identifies epithelial-subtype-specific CISS upregulation toward TIMP-1 hi basal-like PDAC (A) UMAP embedding of PDAC patient tumor ( n = 17) snRNA-seq and post-hoc cell-type annotation. CAF, cancer-associated fibroblasts; VSMC, vascular smooth muscle cells. (B) Selected marker genes ( Z scores) and proportion of positive cells in indicated cell types. (C) Non-epithelial cell UMAP embeddings and post-hoc cell-type annotation (see B–S3F). (D) Epithelial cell UMAP embeddings and post-hoc cell-type annotation. (E) Selected marker genes ( Z scores) and proportion of positive cells in epithelial subsets. (F and G) RNA velocity analysis to infer transcriptional dynamics in acinar/ductal cells (F) and cell state progression across neoplastic/malignant cells (G). Statistics (G) by Kruskal-Wallis and Dunn’s test compared to PanIN. (H) CISS expression in epithelial subsets and induction compared to acinar cells by Kruskal-Wallis and Dunn’s test. (I) (Left) CISS factor expression in epithelial subsets normalized to acinar (mean ±95% CI). (Right) Heatmap and statistics of CISS factors by Kruskal-Wallis and Dunn’s test. (J) Normalized TIMP1 expression on the UMAP embedding. (K) (Left) TIMP1 prevalence within the CISS by comparing norm. CISS expression with TIMP1 (red) or without TIMP1 (black) (mean ±95% CI). Statistics by Mann-Whitney tests. (Right) Volcano plot of TIMP1 prevalence across epithelial clusters identified TIMP1 lo classical, TIMP1 int basal-like, and TIMP1 hi basal-like cancer cells. Groups identified by log2 fold-changes and significance of TIMP1 prevalences within CISS pattern (left). (L) TIMP1 expression and proportion of individual cell subtypes within epithelial compartment across patient tumors. For all statistics: n.s., non-significant; ∗ p < 0.05, ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001.

Journal: Cell Reports Medicine

Article Title: Multimodal profiling of pancreatic cancer reveals a TIMP-1-dominated secretory profile determining pro-tumor immunoinstruction in human cancers

doi: 10.1016/j.xcrm.2025.102546

Figure Lengend Snippet: snRNA-seq identifies epithelial-subtype-specific CISS upregulation toward TIMP-1 hi basal-like PDAC (A) UMAP embedding of PDAC patient tumor ( n = 17) snRNA-seq and post-hoc cell-type annotation. CAF, cancer-associated fibroblasts; VSMC, vascular smooth muscle cells. (B) Selected marker genes ( Z scores) and proportion of positive cells in indicated cell types. (C) Non-epithelial cell UMAP embeddings and post-hoc cell-type annotation (see B–S3F). (D) Epithelial cell UMAP embeddings and post-hoc cell-type annotation. (E) Selected marker genes ( Z scores) and proportion of positive cells in epithelial subsets. (F and G) RNA velocity analysis to infer transcriptional dynamics in acinar/ductal cells (F) and cell state progression across neoplastic/malignant cells (G). Statistics (G) by Kruskal-Wallis and Dunn’s test compared to PanIN. (H) CISS expression in epithelial subsets and induction compared to acinar cells by Kruskal-Wallis and Dunn’s test. (I) (Left) CISS factor expression in epithelial subsets normalized to acinar (mean ±95% CI). (Right) Heatmap and statistics of CISS factors by Kruskal-Wallis and Dunn’s test. (J) Normalized TIMP1 expression on the UMAP embedding. (K) (Left) TIMP1 prevalence within the CISS by comparing norm. CISS expression with TIMP1 (red) or without TIMP1 (black) (mean ±95% CI). Statistics by Mann-Whitney tests. (Right) Volcano plot of TIMP1 prevalence across epithelial clusters identified TIMP1 lo classical, TIMP1 int basal-like, and TIMP1 hi basal-like cancer cells. Groups identified by log2 fold-changes and significance of TIMP1 prevalences within CISS pattern (left). (L) TIMP1 expression and proportion of individual cell subtypes within epithelial compartment across patient tumors. For all statistics: n.s., non-significant; ∗ p < 0.05, ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001.

Article Snippet: TIMP-1 anti-human mAb (rabbit) , Cell Signaling , CAT# 8946; clone D10E6; RRID: AB_10891805.

Techniques: Marker, Expressing, MANN-WHITNEY

$CISS-prevalent TIMP-1 is causal for PDAC-cell-induced NK cell suppression (A) PCA integrating epithelial (red) and immune (blue) cell fractions, fractions of CISS-expressing epithelial cells, and epithelial TIMP1 . (B) Pearson correlation between PCA-standardized variables (A) (∗ p < 0.05, ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001). (C) Comparison of correlations between epithelial and immune subtypes (A and B) by paired Student’s t test between indicated groups. (D–F) Workflow (D) to identify canonical pathways [GSEA; (E)] and immune cell profiles [CIBERSORTx; (F)] correlated with TIMP1 expression (TCGA-PAAD). For GSEA, genes were ranked by correlation coefficients (Spearman) with TIMP1 expression. Reference gene set: C2:CP. (G–I) Workflow (G) for MIA PaCa-2-cell-derived secreted factors suppressing NK cell killing of K562 targets (H) and degranulation (I) at indicated effector-to-target ratios (E:T). Comparison to control media [no cancer conditioning; shared with (O,P)] by unpaired Student’s t tests. (J) Workflow for CRISPR-Cas9-based TIMP-1 knockout in MIA PaCa-2 cells and RNA-seq. (K) PCA of RNA-seq data [ n = 3 per cell line; (J)]. (L) TIMP-1-dependent DEGs (DESeq2) in MIA PaCa-2 cells. Intersection shows DEGs between TIMP-1 WT and TIMP-1 KO (1 and 2) cells, independent of CRISPR-Cas9 (CRISPR Control). (M) GSEA of TIMP-1-dependent biological processes in MIA PaCa-2 cells. log2 fold-changes of DEGs (L) between means of TIMP-1-competent (“TIMP-1 WT”/“ CRISPR Control”) cells and TIMP-1-deficient (“TIMP-1 KO 1/2”) cells. Reference gene set: GO:BP. Enriched gene sets (FDR q < 0.05) were categorized (see G). (N–P) Workflow (N) of TIMP-1-dependent NK cell suppression of CRISPR-Cas9-derived MIA PaCa-2 cell lines (J) on K562 target cell killing (O) and degranulation (P) at indicated E:T. Statistics by one-way ANOVA and Tukey test for indicated groups. Data in (H, I, K, O, and P) showing biological replicates as box and whiskers plots (H, I, O, and P). (D, G, J, and N) Created with BioRender.com .$

Journal: Cell Reports Medicine

Article Title: Multimodal profiling of pancreatic cancer reveals a TIMP-1-dominated secretory profile determining pro-tumor immunoinstruction in human cancers

doi: 10.1016/j.xcrm.2025.102546

Figure Lengend Snippet: CISS-prevalent TIMP-1 is causal for PDAC-cell-induced NK cell suppression (A) PCA integrating epithelial (red) and immune (blue) cell fractions, fractions of CISS-expressing epithelial cells, and epithelial TIMP1 . (B) Pearson correlation between PCA-standardized variables (A) (∗ p < 0.05, ∗∗ p < 0.01; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001). (C) Comparison of correlations between epithelial and immune subtypes (A and B) by paired Student’s t test between indicated groups. (D–F) Workflow (D) to identify canonical pathways [GSEA; (E)] and immune cell profiles [CIBERSORTx; (F)] correlated with TIMP1 expression (TCGA-PAAD). For GSEA, genes were ranked by correlation coefficients (Spearman) with TIMP1 expression. Reference gene set: C2:CP. (G–I) Workflow (G) for MIA PaCa-2-cell-derived secreted factors suppressing NK cell killing of K562 targets (H) and degranulation (I) at indicated effector-to-target ratios (E:T). Comparison to control media [no cancer conditioning; shared with (O,P)] by unpaired Student’s t tests. (J) Workflow for CRISPR-Cas9-based TIMP-1 knockout in MIA PaCa-2 cells and RNA-seq. (K) PCA of RNA-seq data [ n = 3 per cell line; (J)]. (L) TIMP-1-dependent DEGs (DESeq2) in MIA PaCa-2 cells. Intersection shows DEGs between TIMP-1 WT and TIMP-1 KO (1 and 2) cells, independent of CRISPR-Cas9 (CRISPR Control). (M) GSEA of TIMP-1-dependent biological processes in MIA PaCa-2 cells. log2 fold-changes of DEGs (L) between means of TIMP-1-competent (“TIMP-1 WT”/“ CRISPR Control”) cells and TIMP-1-deficient (“TIMP-1 KO 1/2”) cells. Reference gene set: GO:BP. Enriched gene sets (FDR q < 0.05) were categorized (see G). (N–P) Workflow (N) of TIMP-1-dependent NK cell suppression of CRISPR-Cas9-derived MIA PaCa-2 cell lines (J) on K562 target cell killing (O) and degranulation (P) at indicated E:T. Statistics by one-way ANOVA and Tukey test for indicated groups. Data in (H, I, K, O, and P) showing biological replicates as box and whiskers plots (H, I, O, and P). (D, G, J, and N) Created with BioRender.com .

Article Snippet: TIMP-1 anti-human mAb (rabbit) , Cell Signaling , CAT# 8946; clone D10E6; RRID: AB_10891805.

Techniques: Expressing, Comparison, Derivative Assay, Control, CRISPR, Knock-Out, RNA Sequencing

CISS-prevalent TIMP-1 is sufficient to suppress cytotoxic capacity in NK cells via CD74 signaling (A–F) Workflow (A) to identify NK cell clusters in TUM Cohort (B, C, and F) and Steele Cohort (D and E). (B and D) NK cell UMAP embeddings, post-hoc annotations, and selected marker genes ( Z scores) (C and D, bottom). ctx, cytotoxicity. KLRC, killer cell lectin like receptor C gene family. (E and F, right) GZMB and PRF1 expression on the UMAP (B and D). (F, left) RNA velocity to infer transcriptional dynamics in NK cell clusters. (G–I) NK cell granzyme B and perforin levels upon exposure to (G) rhWT-TIMP-1 (granzyme B: UNT, n = 17; 50 ng/mL, n = 6; 100 ng/mL, n = 6; 250 ng/mL, n = 10; 500 ng/mL, n = 14; perforin: UNT, n = 12; 50 ng/mL, n = 6; 100 ng/mL, n = 6; 250 ng/mL, n = 6; 500 ng/mL, n = 11). (H) 500 ng/mL WT-TIMP-1 vs. equimolar N-TIMP-1 (granzyme B: UNT, n = 32; WT-TIMP-1, n = 30; N-TIMP-1, n = 24; perforin: UNT, n = 27; WT-TIMP-1, n = 27; N-TIMP-1, n = 24); (I) 500 ng/mL WT-TIMP-1 vs. equimolar N-TIMP-1 with or without α-CD74 antibody milatuzumab or immunoglobulin G (IgG) control (granzyme B: IgG alone, n = 23; IgG + WT-TIMP-1, n = 25; IgG + N-TIMP-1, n = 20; α-CD74 alone, n = 26; α-CD74 + WT-TIMP-1, n = 24; α-CD74 + N-TIMP-1, n = 20; perforin: IgG alone, n = 19; IgG + WT-TIMP-1, n = 20; IgG + N-TIMP-1, n = 20; α-CD74 alone, n = 19; α-CD74 + WT-TIMP-1, n = 20; α-CD74 + N-TIMP-1, n = 20). Data (G–I) pooled from four independent experiments show biological replicates (box and whiskers plots) derived from six healthy donors. Statistics by one-way ANOVA and Dunnett test (G) or one-way ANOVA and Tukey test (H and I) across indicated groups. (J and K) Proportions of NK (J) and epithelial (K) subsets within samples (TUM Cohort). (L) PCA of NK and epithelial subsets (J and K), NK cell CD74 , and cancer cell TIMP1 expression (small dots) across patients (large dots). Exp., expression. (M) Spearman correlation between TIMP1 hi basal-like cancer cells and ctx hi NK cells. (N) Inferred cancer cell-to-NK cell signaling by CellChat in tumors (J and K) (also see H). (A) Created with BioRender.com .

Journal: Cell Reports Medicine

Article Title: Multimodal profiling of pancreatic cancer reveals a TIMP-1-dominated secretory profile determining pro-tumor immunoinstruction in human cancers

doi: 10.1016/j.xcrm.2025.102546

Figure Lengend Snippet: CISS-prevalent TIMP-1 is sufficient to suppress cytotoxic capacity in NK cells via CD74 signaling (A–F) Workflow (A) to identify NK cell clusters in TUM Cohort (B, C, and F) and Steele Cohort (D and E). (B and D) NK cell UMAP embeddings, post-hoc annotations, and selected marker genes ( Z scores) (C and D, bottom). ctx, cytotoxicity. KLRC, killer cell lectin like receptor C gene family. (E and F, right) GZMB and PRF1 expression on the UMAP (B and D). (F, left) RNA velocity to infer transcriptional dynamics in NK cell clusters. (G–I) NK cell granzyme B and perforin levels upon exposure to (G) rhWT-TIMP-1 (granzyme B: UNT, n = 17; 50 ng/mL, n = 6; 100 ng/mL, n = 6; 250 ng/mL, n = 10; 500 ng/mL, n = 14; perforin: UNT, n = 12; 50 ng/mL, n = 6; 100 ng/mL, n = 6; 250 ng/mL, n = 6; 500 ng/mL, n = 11). (H) 500 ng/mL WT-TIMP-1 vs. equimolar N-TIMP-1 (granzyme B: UNT, n = 32; WT-TIMP-1, n = 30; N-TIMP-1, n = 24; perforin: UNT, n = 27; WT-TIMP-1, n = 27; N-TIMP-1, n = 24); (I) 500 ng/mL WT-TIMP-1 vs. equimolar N-TIMP-1 with or without α-CD74 antibody milatuzumab or immunoglobulin G (IgG) control (granzyme B: IgG alone, n = 23; IgG + WT-TIMP-1, n = 25; IgG + N-TIMP-1, n = 20; α-CD74 alone, n = 26; α-CD74 + WT-TIMP-1, n = 24; α-CD74 + N-TIMP-1, n = 20; perforin: IgG alone, n = 19; IgG + WT-TIMP-1, n = 20; IgG + N-TIMP-1, n = 20; α-CD74 alone, n = 19; α-CD74 + WT-TIMP-1, n = 20; α-CD74 + N-TIMP-1, n = 20). Data (G–I) pooled from four independent experiments show biological replicates (box and whiskers plots) derived from six healthy donors. Statistics by one-way ANOVA and Dunnett test (G) or one-way ANOVA and Tukey test (H and I) across indicated groups. (J and K) Proportions of NK (J) and epithelial (K) subsets within samples (TUM Cohort). (L) PCA of NK and epithelial subsets (J and K), NK cell CD74 , and cancer cell TIMP1 expression (small dots) across patients (large dots). Exp., expression. (M) Spearman correlation between TIMP1 hi basal-like cancer cells and ctx hi NK cells. (N) Inferred cancer cell-to-NK cell signaling by CellChat in tumors (J and K) (also see H). (A) Created with BioRender.com .

Article Snippet: TIMP-1 anti-human mAb (rabbit) , Cell Signaling , CAT# 8946; clone D10E6; RRID: AB_10891805.

Techniques: Marker, Expressing, Control, Derivative Assay

TIMP-1-dependent suppression of NK cell mTOR signaling links PDAC immunosuppression to clinical risk profiles (A–C) Workflow (A) to identify enriched pathways in NK_ctx hi C1 cluster vs. all other NK clusters in TUM Cohort (B) and Steele Cohort (C). DEGs (adj. p < 0.05) by Wilcoxon rank-sum test and auROC analysis. Mean odds ratios by pathway enrichment using Enrichr (Hallmark reference gene sets; see A and S6B , ). AKT, protein kinase B; IL-2, interleukin-2; mTORC1, mechanistic target of rapamycin complex 1; PI3K, phosphoinositide 3-kinase; STAT5, signal transducer and activator of transcription 5; UV, ultraviolet. (D–K) Workflow (D) to identify TIMP-1-dependent MIA PaCa-2-cell-mediated suppression of mTOR-signaling and IL-2 responses in NK cells, using co-culture [3 h (F); 24h (E and G)] or cancer-cell-conditioned media [24 h (H and I); 72 h (J and K)]. NK cell suppression with or without IL-2 activation assessed by (E) K562 killing (E:T 1:3; killing for 3 h); (F–H) p-mTOR(Ser2448)/p-S6(Ser235/236) signaling; (I) intracellular NK cell IFN-γ and TNF-α; (J) cell growth; (K) neutral lipid content; norm. to IL-2-free controls (H–J). Statistics between indicated groups: one-way ANOVA and Dunnett test (E–G, upper), one-way ANOVA and Tukey test (H, J, and K), unpaired Student’s t tests (E–G, lower; I). (L and M) NK cell (L) p-mTOR and (M) p-S6 levels upon exposure to rhWT-TIMP-1. Statistics by two-way ANOVA and Dunnett test. Data (E–M) shown as biological replicates [box and whiskers plots (E–I, and K–M) or mean ± SEM (J)]. (N–P) Cox-regression-based TIMP1 /NK risk score for recurrence-free (RFS) or metastasis-free survival (MFS) (TCGA-PAAD, n = 137), (N) For MFS, patient hazard ratios (HRs), and risk groups separated by quartiles. Statistics between linear predictors of TIMP1 expression and NK cell activity by Spearman correlation. (O) For MFS, survival probabilities by Kaplan-Meier curves (±95% CI). Statistics: global differences by KONP test, restricted mean survival time (RMST; τ = 0.9) between high (H) and low (L) risk groups by Wald test. (P) Heatmaps showing HRs (upper) and significance (lower) for the TIMP1 /NK score, both factors individually, and CISS by Cox regression analyses and G squared log likelihood ratio (∗ p < 0.05; ∗∗ p < 0.01). (A and D) Created with BioRender.com .

Journal: Cell Reports Medicine

Article Title: Multimodal profiling of pancreatic cancer reveals a TIMP-1-dominated secretory profile determining pro-tumor immunoinstruction in human cancers

doi: 10.1016/j.xcrm.2025.102546

Figure Lengend Snippet: TIMP-1-dependent suppression of NK cell mTOR signaling links PDAC immunosuppression to clinical risk profiles (A–C) Workflow (A) to identify enriched pathways in NK_ctx hi C1 cluster vs. all other NK clusters in TUM Cohort (B) and Steele Cohort (C). DEGs (adj. p < 0.05) by Wilcoxon rank-sum test and auROC analysis. Mean odds ratios by pathway enrichment using Enrichr (Hallmark reference gene sets; see A and S6B , ). AKT, protein kinase B; IL-2, interleukin-2; mTORC1, mechanistic target of rapamycin complex 1; PI3K, phosphoinositide 3-kinase; STAT5, signal transducer and activator of transcription 5; UV, ultraviolet. (D–K) Workflow (D) to identify TIMP-1-dependent MIA PaCa-2-cell-mediated suppression of mTOR-signaling and IL-2 responses in NK cells, using co-culture [3 h (F); 24h (E and G)] or cancer-cell-conditioned media [24 h (H and I); 72 h (J and K)]. NK cell suppression with or without IL-2 activation assessed by (E) K562 killing (E:T 1:3; killing for 3 h); (F–H) p-mTOR(Ser2448)/p-S6(Ser235/236) signaling; (I) intracellular NK cell IFN-γ and TNF-α; (J) cell growth; (K) neutral lipid content; norm. to IL-2-free controls (H–J). Statistics between indicated groups: one-way ANOVA and Dunnett test (E–G, upper), one-way ANOVA and Tukey test (H, J, and K), unpaired Student’s t tests (E–G, lower; I). (L and M) NK cell (L) p-mTOR and (M) p-S6 levels upon exposure to rhWT-TIMP-1. Statistics by two-way ANOVA and Dunnett test. Data (E–M) shown as biological replicates [box and whiskers plots (E–I, and K–M) or mean ± SEM (J)]. (N–P) Cox-regression-based TIMP1 /NK risk score for recurrence-free (RFS) or metastasis-free survival (MFS) (TCGA-PAAD, n = 137), (N) For MFS, patient hazard ratios (HRs), and risk groups separated by quartiles. Statistics between linear predictors of TIMP1 expression and NK cell activity by Spearman correlation. (O) For MFS, survival probabilities by Kaplan-Meier curves (±95% CI). Statistics: global differences by KONP test, restricted mean survival time (RMST; τ = 0.9) between high (H) and low (L) risk groups by Wald test. (P) Heatmaps showing HRs (upper) and significance (lower) for the TIMP1 /NK score, both factors individually, and CISS by Cox regression analyses and G squared log likelihood ratio (∗ p < 0.05; ∗∗ p < 0.01). (A and D) Created with BioRender.com .

Article Snippet: TIMP-1 anti-human mAb (rabbit) , Cell Signaling , CAT# 8946; clone D10E6; RRID: AB_10891805.

Techniques: Co-Culture Assay, Activation Assay, Expressing, Activity Assay

Multikinase inhibition targets TIMP-1 and CISS and enhances NK cell cytotoxicity in TIMP1 hi /CISS hi basal-like PDAC in vivo (A) TIMP1 hi /CISS hi basal-like PDAC in patients based on TIMP1/CISS expression (see ). Statistics by Mann-Whitney tests. (B) Transcription factor targets (TFTs) and kinase perturbations correlated with TIMP1/CISS in basal-like PDAC. (Left) Genes correlating (Spearman; p < 0.05) with TIMP1 expression were ranked by coefficients for GSEA (reference: C3:TFT). DEGs (Wilcoxon rank-sum test and auROC analysis) between TIMP1 hi /CISS hi basal-like cancer and other epithelial cells tested for pathway enrichment by Enrichr (“Kinase perturbations from GEO UP” and “DOWN”). (C) UMAP embedding of TIMP1 expression (see J), ERK activity, and FGFR signaling. ERK activity (TFT:MAPK3_Target_Genes) and FGFR signaling (Reactome_Signaling_by_FGFR) calculated by UCell and correlated to TIMP1 expression (Spearman). (D) Western blot ( n = 3; biological replicates) of intracellular TIMP-1 in MIA PaCa-2 cells upon treatment with trametinib (T) and nintedanib (N). Statistics by one-way ANOVA and Dunnett test. (E) ZIP synergy map of TIMP-1 inhibition (intracellular TIMP-1) in MIA PaCa-2 cells using trametinib or nintedanib (see A). (F) Workflow to assess in vivo effect of trametinib, nintedanib, and a -PDL1 treatment on TIMP1/CISS and NK cells in orthotopic classical and basal-like PDAC transplantation mouse models. (G–J) UMAP embedding of all cells (G) or cancer cells (H) from scRNA-seq of PDAC tumors derived from (F) and post-hoc cell-type annotations (G), cancer cell type (H, upper), or Timp1 expression (H, lower). (I) Timp1 and (J) CISS expression in cancer cells. Statistics by Mann-Whitney tests. (K) CISS factors in PDAC cells upon indicated treatments vs. controls from snRNA-seq data (F–J). Changes in CISS factors calculated by pseudobulk limma-voom workflow. Statistics: one-way ANOVA for matched data (genes) and Dunnett test between indicated groups. (L and M) UMAP embedding of NK cell clusters (M) and proportions across treatments (F,G), assessed by frequencies (M, upper) and PCA (M, lower). (N and O) Pathways enriched (N; Enrichr using Hallmark reference gene set) and cytotoxicity gene expression (O) between treatment- enriched and - reduced NK clusters. Changes in cytotoxicity genes (O) calculated by Wilcoxon rank-sum test and auROC analysis. Statistics by paired Student’s t test. (F) Created with BioRender.com .

Journal: Cell Reports Medicine

Article Title: Multimodal profiling of pancreatic cancer reveals a TIMP-1-dominated secretory profile determining pro-tumor immunoinstruction in human cancers

doi: 10.1016/j.xcrm.2025.102546

Figure Lengend Snippet: Multikinase inhibition targets TIMP-1 and CISS and enhances NK cell cytotoxicity in TIMP1 hi /CISS hi basal-like PDAC in vivo (A) TIMP1 hi /CISS hi basal-like PDAC in patients based on TIMP1/CISS expression (see ). Statistics by Mann-Whitney tests. (B) Transcription factor targets (TFTs) and kinase perturbations correlated with TIMP1/CISS in basal-like PDAC. (Left) Genes correlating (Spearman; p < 0.05) with TIMP1 expression were ranked by coefficients for GSEA (reference: C3:TFT). DEGs (Wilcoxon rank-sum test and auROC analysis) between TIMP1 hi /CISS hi basal-like cancer and other epithelial cells tested for pathway enrichment by Enrichr (“Kinase perturbations from GEO UP” and “DOWN”). (C) UMAP embedding of TIMP1 expression (see J), ERK activity, and FGFR signaling. ERK activity (TFT:MAPK3_Target_Genes) and FGFR signaling (Reactome_Signaling_by_FGFR) calculated by UCell and correlated to TIMP1 expression (Spearman). (D) Western blot ( n = 3; biological replicates) of intracellular TIMP-1 in MIA PaCa-2 cells upon treatment with trametinib (T) and nintedanib (N). Statistics by one-way ANOVA and Dunnett test. (E) ZIP synergy map of TIMP-1 inhibition (intracellular TIMP-1) in MIA PaCa-2 cells using trametinib or nintedanib (see A). (F) Workflow to assess in vivo effect of trametinib, nintedanib, and a -PDL1 treatment on TIMP1/CISS and NK cells in orthotopic classical and basal-like PDAC transplantation mouse models. (G–J) UMAP embedding of all cells (G) or cancer cells (H) from scRNA-seq of PDAC tumors derived from (F) and post-hoc cell-type annotations (G), cancer cell type (H, upper), or Timp1 expression (H, lower). (I) Timp1 and (J) CISS expression in cancer cells. Statistics by Mann-Whitney tests. (K) CISS factors in PDAC cells upon indicated treatments vs. controls from snRNA-seq data (F–J). Changes in CISS factors calculated by pseudobulk limma-voom workflow. Statistics: one-way ANOVA for matched data (genes) and Dunnett test between indicated groups. (L and M) UMAP embedding of NK cell clusters (M) and proportions across treatments (F,G), assessed by frequencies (M, upper) and PCA (M, lower). (N and O) Pathways enriched (N; Enrichr using Hallmark reference gene set) and cytotoxicity gene expression (O) between treatment- enriched and - reduced NK clusters. Changes in cytotoxicity genes (O) calculated by Wilcoxon rank-sum test and auROC analysis. Statistics by paired Student’s t test. (F) Created with BioRender.com .

Article Snippet: TIMP-1 anti-human mAb (rabbit) , Cell Signaling , CAT# 8946; clone D10E6; RRID: AB_10891805.

Techniques: Inhibition, In Vivo, Expressing, MANN-WHITNEY, Activity Assay, Western Blot, Transplantation Assay, Derivative Assay, Gene Expression

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