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antibodies against timp 1  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc antibodies against timp 1
    Antibodies Against Timp 1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 97 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies against timp 1/product/Cell Signaling Technology Inc
    Average 95 stars, based on 97 article reviews
    antibodies against timp 1 - by Bioz Stars, 2026-03
    95/100 stars

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    Image Search Results


    Fig. 3 A model constructed with 13 genes that accurately identify COPD. (A-B) ROC results demonstrate the performance of 20 different machine learning methods, based on the selected 13-gene model, in identifying COPD across GSE47460 (A) and GSE76925 (B). (C) ROC results indicated that the random forest and extra tree models constructed using GSE47460 and GSE76925 datasets were cross-validated against each other. (D) ROC results display AUC outcomes for validating the random forest and extra tree models using two external patients with COPD lung tissue sequencing data (GSE103174 and GSE239897). (E) The expression changes of the 13 genes (ANGPTL1, DUSP26, FGG, GAS2, VEGFD, BHLHE22, SYNGR1, TIMP4, CXCL12, GEMIN5, SV2B, HTR2B, and TMEM117) used to construct the model are indicated between control and COPD groups in GSE47460 and GSE76925 datasets. (F) Scatter plots reveal ing predicted versus observed FEV1% predicted values for each of the 13 regression models (AdaBoost, Decision Tree, ElasticNet, GLM, LASSO, Least.Angle, Linear, NeuralNet, RandomForest, Ridge, SGD, SVR, and voting) in GSE47460. Each point represents a sample in the test set. R-squared values and p-values are displayed for each model. Data indicated mean ± SD. P-values are indicated in charts determined by a two-tailed student test (E)

    Journal: Respiratory research

    Article Title: An integrated machine learning model of transcriptomic genes in multi-center chronic obstructive pulmonary disease reveals the causal role of TIMP4 in airway epithelial cell.

    doi: 10.1186/s12931-025-03238-1

    Figure Lengend Snippet: Fig. 3 A model constructed with 13 genes that accurately identify COPD. (A-B) ROC results demonstrate the performance of 20 different machine learning methods, based on the selected 13-gene model, in identifying COPD across GSE47460 (A) and GSE76925 (B). (C) ROC results indicated that the random forest and extra tree models constructed using GSE47460 and GSE76925 datasets were cross-validated against each other. (D) ROC results display AUC outcomes for validating the random forest and extra tree models using two external patients with COPD lung tissue sequencing data (GSE103174 and GSE239897). (E) The expression changes of the 13 genes (ANGPTL1, DUSP26, FGG, GAS2, VEGFD, BHLHE22, SYNGR1, TIMP4, CXCL12, GEMIN5, SV2B, HTR2B, and TMEM117) used to construct the model are indicated between control and COPD groups in GSE47460 and GSE76925 datasets. (F) Scatter plots reveal ing predicted versus observed FEV1% predicted values for each of the 13 regression models (AdaBoost, Decision Tree, ElasticNet, GLM, LASSO, Least.Angle, Linear, NeuralNet, RandomForest, Ridge, SGD, SVR, and voting) in GSE47460. Each point represents a sample in the test set. R-squared values and p-values are displayed for each model. Data indicated mean ± SD. P-values are indicated in charts determined by a two-tailed student test (E)

    Article Snippet: Membranes were blocked and incubated overnight at 4 °C with primary antibodies against TIMP4 (Catalog # 12326-1-AP, proteintech, China), MMP9 (Catalog # 13667, CST, USA), fibronectin-1 (FN1; Catalog # 26836, CST, USA), β-catenin (Catalog # 9562, CST, USA), nonp-β-catenin (Catalog # 4176, CST, USA), and GAPDH (Catalog # 60004-1-Ig, proteintech, China).

    Techniques: Construct, Sequencing, Expressing, Control, Two Tailed Test

    Fig. 8 TIMP4 overexpression reduces cilia in airway epithelial cells cultured at ALI and decreases ciliary gene expression. (A) Multiplex IF staining of human airway epithelial cells cultured at ALI. Green: α-tubulin; red: Muc5ac. Blue: DAPI (n = 5). (B) qRT-PCR analysis of RNA levels of TTLL6, DNAFF1, RFX3, and HYDIN in primary human cells cultured at ALI across four groups (n = 5). (C) WB analysis was conducted to assess the protein expression levels of FN1 and MMP9 across the four groups (n = 4). (D) WB analysis was conducted to assess the protein expression levels of β-catenin and non-p-β-catenin across the four groups (n = 4). Data are expressed as mean ± SD. P-values indicated in charts are determined by one-way analysis of variance (A–D). *p < 0.05, **p < 0.01 and ***p < 0.001

    Journal: Respiratory research

    Article Title: An integrated machine learning model of transcriptomic genes in multi-center chronic obstructive pulmonary disease reveals the causal role of TIMP4 in airway epithelial cell.

    doi: 10.1186/s12931-025-03238-1

    Figure Lengend Snippet: Fig. 8 TIMP4 overexpression reduces cilia in airway epithelial cells cultured at ALI and decreases ciliary gene expression. (A) Multiplex IF staining of human airway epithelial cells cultured at ALI. Green: α-tubulin; red: Muc5ac. Blue: DAPI (n = 5). (B) qRT-PCR analysis of RNA levels of TTLL6, DNAFF1, RFX3, and HYDIN in primary human cells cultured at ALI across four groups (n = 5). (C) WB analysis was conducted to assess the protein expression levels of FN1 and MMP9 across the four groups (n = 4). (D) WB analysis was conducted to assess the protein expression levels of β-catenin and non-p-β-catenin across the four groups (n = 4). Data are expressed as mean ± SD. P-values indicated in charts are determined by one-way analysis of variance (A–D). *p < 0.05, **p < 0.01 and ***p < 0.001

    Article Snippet: Membranes were blocked and incubated overnight at 4 °C with primary antibodies against TIMP4 (Catalog # 12326-1-AP, proteintech, China), MMP9 (Catalog # 13667, CST, USA), fibronectin-1 (FN1; Catalog # 26836, CST, USA), β-catenin (Catalog # 9562, CST, USA), nonp-β-catenin (Catalog # 4176, CST, USA), and GAPDH (Catalog # 60004-1-Ig, proteintech, China).

    Techniques: Over Expression, Cell Culture, Gene Expression, Multiplex Assay, Staining, Quantitative RT-PCR, Expressing

    TIMP3 is a target gene of miR-21-5p, and the expression of the miR-21-5p/TIMP3/PI3K/Akt/mTOR was affected by EMSCs-Endo in vitro. (A) Bioinformatic analysis of the differential expression of miR-21-5p in endometriosis. (B) The levels of miR-21-5p were significantly elevated in the eutopic and ectopic tissues of patients with endometriosis. (C) The TIMP3 3ʹ-UTR contains miR-21-5p binding sites. (D) Dual-luciferase reporter assays confirmed TIMP3 as a target gene of miR-21-5p. (E) The relative expression of miR-21-5p in cocultured HUVECs from each group. (F) Expression analysis of TIMP3/PI3K/Akt/mTOR in cocultured HUVECs from each group by Western blotting. (G-J) Quantification of protein levels of TIMP3 (G), p-PI3K (H), p-Akt (I), p-mTOR (J). The data are presented as the mean ± SD of n = 3 independent experiments. Statistical analysis was performed via 1-way ANOVA with Bonferroni post hoc correction (B, D, E, and G-J), * P < 0.05, *** P < 0.001.

    Journal: Stem Cells Translational Medicine

    Article Title: Endostatin-expressing endometrial mesenchymal stem cells inhibit angiogenesis in endometriosis through the miRNA-21-5p/TIMP3/PI3K/Akt/mTOR pathway

    doi: 10.1093/stcltm/szae079

    Figure Lengend Snippet: TIMP3 is a target gene of miR-21-5p, and the expression of the miR-21-5p/TIMP3/PI3K/Akt/mTOR was affected by EMSCs-Endo in vitro. (A) Bioinformatic analysis of the differential expression of miR-21-5p in endometriosis. (B) The levels of miR-21-5p were significantly elevated in the eutopic and ectopic tissues of patients with endometriosis. (C) The TIMP3 3ʹ-UTR contains miR-21-5p binding sites. (D) Dual-luciferase reporter assays confirmed TIMP3 as a target gene of miR-21-5p. (E) The relative expression of miR-21-5p in cocultured HUVECs from each group. (F) Expression analysis of TIMP3/PI3K/Akt/mTOR in cocultured HUVECs from each group by Western blotting. (G-J) Quantification of protein levels of TIMP3 (G), p-PI3K (H), p-Akt (I), p-mTOR (J). The data are presented as the mean ± SD of n = 3 independent experiments. Statistical analysis was performed via 1-way ANOVA with Bonferroni post hoc correction (B, D, E, and G-J), * P < 0.05, *** P < 0.001.

    Article Snippet: Next, each membrane was blocked overnight with 5% nonfat milk and then incubated with antibodies against TIMP3 (Proteintech Group, China), p-Akt (CST, USA), Akt (CST, USA), p-PI3K (Proteintech Group, China), PI3K (Proteintech Group, China), p-mTOR (Proteintech Group, China), mTOR (CST, USA), and GAPDH (Proteintech Group, China) at 4° C overnight.

    Techniques: Expressing, In Vitro, Quantitative Proteomics, Binding Assay, Luciferase, Western Blot

    The expression of miR-21-5p/TIMP3/p-PI3K/p-Akt/p-mTOR in mouse endometriotic lesions. (A) Expression analysis of TIMP3/p-PI3K/p-Akt/p-mTOR in the endometriotic lesions of each group by Western blotting. (B) Quantification of protein levels of TIMP3, p-PI3K, p-Akt, and p-mTOR. (C) Relative expression of miR-21-5p in the endometriotic lesions of each group. (D) Expression analysis of TIMP3/p-PI3K/p-Akt/p-mTOR in the endometriotic lesions of each group by means of immunohistochemistry. Scale bar = 25 μm. The data are presented as the mean ± SD. Statistical analysis was performed by means of 1-way ANOVA with the Bonferroni post hoc correction. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Journal: Stem Cells Translational Medicine

    Article Title: Endostatin-expressing endometrial mesenchymal stem cells inhibit angiogenesis in endometriosis through the miRNA-21-5p/TIMP3/PI3K/Akt/mTOR pathway

    doi: 10.1093/stcltm/szae079

    Figure Lengend Snippet: The expression of miR-21-5p/TIMP3/p-PI3K/p-Akt/p-mTOR in mouse endometriotic lesions. (A) Expression analysis of TIMP3/p-PI3K/p-Akt/p-mTOR in the endometriotic lesions of each group by Western blotting. (B) Quantification of protein levels of TIMP3, p-PI3K, p-Akt, and p-mTOR. (C) Relative expression of miR-21-5p in the endometriotic lesions of each group. (D) Expression analysis of TIMP3/p-PI3K/p-Akt/p-mTOR in the endometriotic lesions of each group by means of immunohistochemistry. Scale bar = 25 μm. The data are presented as the mean ± SD. Statistical analysis was performed by means of 1-way ANOVA with the Bonferroni post hoc correction. * P < 0.05, ** P < 0.01, *** P < 0.001.

    Article Snippet: Next, each membrane was blocked overnight with 5% nonfat milk and then incubated with antibodies against TIMP3 (Proteintech Group, China), p-Akt (CST, USA), Akt (CST, USA), p-PI3K (Proteintech Group, China), PI3K (Proteintech Group, China), p-mTOR (Proteintech Group, China), mTOR (CST, USA), and GAPDH (Proteintech Group, China) at 4° C overnight.

    Techniques: Expressing, Western Blot, Immunohistochemistry