anti human timp 1 antibody (R&D Systems)
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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+antibody/Human+TIMP-1+Antibody/pm41354972-57-18-32
Average 93 stars, based on 68 article reviews
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+antibody/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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Concentration Assay:Article Title: Primary human acute myelogenous leukemia cells release matrix metalloproteases and their inhibitors: release profile and pharmacological modulation. Article Snippet: matrix metalloproteases and their inhibitors: release profile and pharmacological modulation Håkon Reikvam, Kimberley J. Hatfield, Anne M. Øyan, Karl H. Kalland, Astrid O. Kittang, Øystein Bruserud Institute of Internal Medicine, Division for Hematology, University of Bergen, Bergen; Department of Medicine, Haukeland University Hospital, Bergen; The Gade Institute, University of Bergen, Bergen; Department of Microbiology, Haukeland University Hospital, Bergen, Norway Recombinant:Article Title: Primary human acute myelogenous leukemia cells release matrix metalloproteases and their inhibitors: release profile and pharmacological modulation. Article Snippet: matrix metalloproteases and their inhibitors: release profile and pharmacological modulation Håkon Reikvam, Kimberley J. Hatfield, Anne M. Øyan, Karl H. Kalland, Astrid O. Kittang, Øystein Bruserud Institute of Internal Medicine, Division for Hematology, University of Bergen, Bergen; Department of Medicine, Haukeland University Hospital, Bergen; The Gade Institute, University of Bergen, Bergen; Department of Microbiology, Haukeland University Hospital, Bergen, Norway Binding Assay:Article Title: Generation of antibodies recognizing an aberrant glycoform of human tissue inhibitor of metalloproteinase-1 (TIMP-1) using decoy immunization and phage display. Article Snippet: Aberrant glycosylation of human tissue inhibitor of metalloproteinase-1 (TIMP-1) by Nacetylglucosaminyltransferase-V (GnT-V) was previously reported to be related to cancer progression.. Here, we report on the antibodies recognizing the structural features initiated by an addition of N-linked (1,6)-N-acetylglucosamine (GlcNAc) branch by GnT-V on TIMP-1.. Two glycoforms of TIMP-1, TIMP1-L produced in Lec4 cells without GnT-V activity and TIMP1-B in GnT-V overexpressing transfectant cells, were purified from culture supernatant and used for generation of antibodies. Activity Assay:Article Title: Generation of antibodies recognizing an aberrant glycoform of human tissue inhibitor of metalloproteinase-1 (TIMP-1) using decoy immunization and phage display. Article Snippet: Aberrant glycosylation of human tissue inhibitor of metalloproteinase-1 (TIMP-1) by Nacetylglucosaminyltransferase-V (GnT-V) was previously reported to be related to cancer progression.. Here, we report on the antibodies recognizing the structural features initiated by an addition of N-linked (1,6)-N-acetylglucosamine (GlcNAc) branch by GnT-V on TIMP-1.. Two glycoforms of TIMP-1, TIMP1-L produced in Lec4 cells without GnT-V activity and TIMP1-B in GnT-V overexpressing transfectant cells, were purified from culture supernatant and used for generation of antibodies. Incubation:Article Title: Fibroblast-driven MMP-9/TIMP-1 imbalance in bronchoalveolar lavage reflects fibrotic progression in interstitial lung disease. Article Snippet: Immunofluorescence staining was performed on fibroblasts derived from ILD patients and grown in chamber slides (Thermo Fisher Scientific). .. Once fixed with 2% paraformaldehyde and treated with Triton X- 100, the cells were incubated overnight with an Bioprocessing:Article Title: Fibroblast-driven MMP-9/TIMP-1 imbalance in bronchoalveolar lavage reflects fibrotic progression in interstitial lung disease. Article Snippet: Immunofluorescence staining was performed on fibroblasts derived from ILD patients and grown in chamber slides (Thermo Fisher Scientific). .. Once fixed with 2% paraformaldehyde and treated with Triton X- 100, the cells were incubated overnight with an Blocking Assay:Article Title: Fibroblast-driven MMP-9/TIMP-1 imbalance in bronchoalveolar lavage reflects fibrotic progression in interstitial lung disease. Article Snippet: Immunofluorescence staining was performed on fibroblasts derived from ILD patients and grown in chamber slides (Thermo Fisher Scientific). .. Once fixed with 2% paraformaldehyde and treated with Triton X- 100, the cells were incubated overnight with an |
![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 .](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_6174/pmc12866174/pmc12866174__gr4.jpg)
![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 .](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_6174/pmc12866174/pmc12866174__gr6.jpg)
