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timp1  (Proteintech)


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    Proteintech timp1
    Myeloid-specific Nogo-B deficiency alleviates liver injury and fibrosis. ( A ) Breeding scheme used to generate mice with myeloid-specific Nogo-B deletion. ( B ) Identification of myeloid-specific Nogo-B-deficient mice. ( C ) Serum Nogo-B concentrations in the 3 liver fibrosis models, as determined by ELISA. ( D ) Measurement of ALT and AST in the serum of the mice. ( E ) Collagen I and α-SMA mRNA expression in the murine livers was evaluated through qRT-PCR. ( F–H ) Liver sections from the mice were subjected to H&E and Sirius Red staining and Masson staining and α-SMA IHC analysis, and the proportions of Sirius red-positive and Masson-positive and a-SMA-positive regions were quantified. ( I–K ) Hepatic protein levels of collagen I, MMP-9, α-SMA, and <t>TIMP-1</t> were assessed via Western blotting; GAPDH served as the loading control. The data are presented as the means ± SEMs; n = 6 per group; original magnification, 10×; scale bars, 200 μm; ∗∗ P < .01.
    Timp1, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 122 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/timp1/product/Proteintech
    Average 95 stars, based on 122 article reviews
    timp1 - by Bioz Stars, 2026-02
    95/100 stars

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    1) Product Images from "Macrophage Nogo-B Drives Liver Fibrosis"

    Article Title: Macrophage Nogo-B Drives Liver Fibrosis

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    doi: 10.1016/j.jcmgh.2025.101622

    Myeloid-specific Nogo-B deficiency alleviates liver injury and fibrosis. ( A ) Breeding scheme used to generate mice with myeloid-specific Nogo-B deletion. ( B ) Identification of myeloid-specific Nogo-B-deficient mice. ( C ) Serum Nogo-B concentrations in the 3 liver fibrosis models, as determined by ELISA. ( D ) Measurement of ALT and AST in the serum of the mice. ( E ) Collagen I and α-SMA mRNA expression in the murine livers was evaluated through qRT-PCR. ( F–H ) Liver sections from the mice were subjected to H&E and Sirius Red staining and Masson staining and α-SMA IHC analysis, and the proportions of Sirius red-positive and Masson-positive and a-SMA-positive regions were quantified. ( I–K ) Hepatic protein levels of collagen I, MMP-9, α-SMA, and TIMP-1 were assessed via Western blotting; GAPDH served as the loading control. The data are presented as the means ± SEMs; n = 6 per group; original magnification, 10×; scale bars, 200 μm; ∗∗ P < .01.
    Figure Legend Snippet: Myeloid-specific Nogo-B deficiency alleviates liver injury and fibrosis. ( A ) Breeding scheme used to generate mice with myeloid-specific Nogo-B deletion. ( B ) Identification of myeloid-specific Nogo-B-deficient mice. ( C ) Serum Nogo-B concentrations in the 3 liver fibrosis models, as determined by ELISA. ( D ) Measurement of ALT and AST in the serum of the mice. ( E ) Collagen I and α-SMA mRNA expression in the murine livers was evaluated through qRT-PCR. ( F–H ) Liver sections from the mice were subjected to H&E and Sirius Red staining and Masson staining and α-SMA IHC analysis, and the proportions of Sirius red-positive and Masson-positive and a-SMA-positive regions were quantified. ( I–K ) Hepatic protein levels of collagen I, MMP-9, α-SMA, and TIMP-1 were assessed via Western blotting; GAPDH served as the loading control. The data are presented as the means ± SEMs; n = 6 per group; original magnification, 10×; scale bars, 200 μm; ∗∗ P < .01.

    Techniques Used: Enzyme-linked Immunosorbent Assay, Expressing, Quantitative RT-PCR, Staining, Western Blot, Control



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    Myeloid-specific Nogo-B deficiency alleviates liver injury and fibrosis. ( A ) Breeding scheme used to generate mice with myeloid-specific Nogo-B deletion. ( B ) Identification of myeloid-specific Nogo-B-deficient mice. ( C ) Serum Nogo-B concentrations in the 3 liver fibrosis models, as determined by ELISA. ( D ) Measurement of ALT and AST in the serum of the mice. ( E ) Collagen I and α-SMA mRNA expression in the murine livers was evaluated through qRT-PCR. ( F–H ) Liver sections from the mice were subjected to H&E and Sirius Red staining and Masson staining and α-SMA IHC analysis, and the proportions of Sirius red-positive and Masson-positive and a-SMA-positive regions were quantified. ( I–K ) Hepatic protein levels of collagen I, MMP-9, α-SMA, and TIMP-1 were assessed via Western blotting; GAPDH served as the loading control. The data are presented as the means ± SEMs; n = 6 per group; original magnification, 10×; scale bars, 200 μm; ∗∗ P < .01.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Macrophage Nogo-B Drives Liver Fibrosis

    doi: 10.1016/j.jcmgh.2025.101622

    Figure Lengend Snippet: Myeloid-specific Nogo-B deficiency alleviates liver injury and fibrosis. ( A ) Breeding scheme used to generate mice with myeloid-specific Nogo-B deletion. ( B ) Identification of myeloid-specific Nogo-B-deficient mice. ( C ) Serum Nogo-B concentrations in the 3 liver fibrosis models, as determined by ELISA. ( D ) Measurement of ALT and AST in the serum of the mice. ( E ) Collagen I and α-SMA mRNA expression in the murine livers was evaluated through qRT-PCR. ( F–H ) Liver sections from the mice were subjected to H&E and Sirius Red staining and Masson staining and α-SMA IHC analysis, and the proportions of Sirius red-positive and Masson-positive and a-SMA-positive regions were quantified. ( I–K ) Hepatic protein levels of collagen I, MMP-9, α-SMA, and TIMP-1 were assessed via Western blotting; GAPDH served as the loading control. The data are presented as the means ± SEMs; n = 6 per group; original magnification, 10×; scale bars, 200 μm; ∗∗ P < .01.

    Article Snippet: The membranes were probed with the following primary antibodies: Nogo-B (rabbit mAb, Thermo Fisher), USP14, p-RIPK3, and p-MLKL (rabbit mAbs, Abcam); α-SMA, collagen I, TIMP1, MMP9, caspase-1, cleaved caspase-1, pro-IL-1β, cleaved IL-1β, GAPDH, RIPK3, MLKL, CD11b, and LY6G (rabbit mAbs, Cell Signaling Technology); RIPK3 (mouse mAb, Cell Signaling Technology); USP14, NLRP3, and ASC (mouse mAbs, Proteintech); and Trim28 and Prpf19 (rabbit mAbs, Proteintech).

    Techniques: Enzyme-linked Immunosorbent Assay, Expressing, Quantitative RT-PCR, Staining, Western Blot, Control