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antibodies against collagen i  (Bioss)


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    Structured Review

    Bioss antibodies against collagen i
    Antibodies Against Collagen I, supplied by Bioss, used in various techniques. Bioz Stars score: 95/100, based on 114 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/antibodies against collagen i/product/Bioss
    Average 95 stars, based on 114 article reviews
    antibodies against collagen i - by Bioz Stars, 2026-06
    95/100 stars

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    BIG improves cardiac function after I/RI by inhibiting the inflammatory response and myofibroblast fibrosis. (A, B, C, D, E, F, H and I) The relative expressions of MMP2, MMP9, TNF‒α, IL-1β, IL-6, BCL-2, BAX and c-caspase-3 (n=6). (G) WB results showing the expression of related proteins. (J) Representative microphotographs of TUNEL (blue, DAPI; green, TUNEL‒positive cardiomyocytes) staining of cardiomyocytes (n= 6). Scale bar: 20 μm. (K) The number of TUNEL‒positive cells represents the apoptosis rate in Sham, I/RI and BIG treated mice (n= 6). (L and M) The number of <t>Col6a3-</t> and TGF‒β‒positive myofibroblasts in the myocardial infarction area (n= 6). (N) Immunofluorescent colocalization of Col6a3, TGF‒β and vimentin in mice subjected to Sham, I/RI or BIG treatment (red, Col6a3 or TGF‒β; green, VIM; blue, DAPI). Scale bar: 50 μm. (O) Immunofluorescent colocalization of Col6a3, TGF‒β and TNNI3 in mice subjected to Sham, I/RI and BIG treatment (red, Col6a3 or TGF‒β; green, TNNI3; blue, DAPI). Scale bar: 50 μm. (P and Q) The number of Col6a3- and TGF‒β‒positive cardiomyocytes in the myocardial infarction area (n= 6). The data are presented as the means ± SEMs, and one-way ANOVA with Tukey’s multiple comparisons test was used for multiple groups comparisons, ***P < 0.001
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    Proteintech collagen i
    BIG improves cardiac function after I/RI by inhibiting the inflammatory response and myofibroblast fibrosis. (A, B, C, D, E, F, H and I) The relative expressions of MMP2, MMP9, TNF‒α, IL-1β, IL-6, BCL-2, BAX and c-caspase-3 (n=6). (G) WB results showing the expression of related proteins. (J) Representative microphotographs of TUNEL (blue, DAPI; green, TUNEL‒positive cardiomyocytes) staining of cardiomyocytes (n= 6). Scale bar: 20 μm. (K) The number of TUNEL‒positive cells represents the apoptosis rate in Sham, I/RI and BIG treated mice (n= 6). (L and M) The number of <t>Col6a3-</t> and TGF‒β‒positive myofibroblasts in the myocardial infarction area (n= 6). (N) Immunofluorescent colocalization of Col6a3, TGF‒β and vimentin in mice subjected to Sham, I/RI or BIG treatment (red, Col6a3 or TGF‒β; green, VIM; blue, DAPI). Scale bar: 50 μm. (O) Immunofluorescent colocalization of Col6a3, TGF‒β and TNNI3 in mice subjected to Sham, I/RI and BIG treatment (red, Col6a3 or TGF‒β; green, TNNI3; blue, DAPI). Scale bar: 50 μm. (P and Q) The number of Col6a3- and TGF‒β‒positive cardiomyocytes in the myocardial infarction area (n= 6). The data are presented as the means ± SEMs, and one-way ANOVA with Tukey’s multiple comparisons test was used for multiple groups comparisons, ***P < 0.001
    Collagen I, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    BIG improves cardiac function after I/RI by inhibiting the inflammatory response and myofibroblast fibrosis. (A, B, C, D, E, F, H and I) The relative expressions of MMP2, MMP9, TNF‒α, IL-1β, IL-6, BCL-2, BAX and c-caspase-3 (n=6). (G) WB results showing the expression of related proteins. (J) Representative microphotographs of TUNEL (blue, DAPI; green, TUNEL‒positive cardiomyocytes) staining of cardiomyocytes (n= 6). Scale bar: 20 μm. (K) The number of TUNEL‒positive cells represents the apoptosis rate in Sham, I/RI and BIG treated mice (n= 6). (L and M) The number of <t>Col6a3-</t> and TGF‒β‒positive myofibroblasts in the myocardial infarction area (n= 6). (N) Immunofluorescent colocalization of Col6a3, TGF‒β and vimentin in mice subjected to Sham, I/RI or BIG treatment (red, Col6a3 or TGF‒β; green, VIM; blue, DAPI). Scale bar: 50 μm. (O) Immunofluorescent colocalization of Col6a3, TGF‒β and TNNI3 in mice subjected to Sham, I/RI and BIG treatment (red, Col6a3 or TGF‒β; green, TNNI3; blue, DAPI). Scale bar: 50 μm. (P and Q) The number of Col6a3- and TGF‒β‒positive cardiomyocytes in the myocardial infarction area (n= 6). The data are presented as the means ± SEMs, and one-way ANOVA with Tukey’s multiple comparisons test was used for multiple groups comparisons, ***P < 0.001
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    Proteintech runx2 rabbit monoclonal
    In vitro evaluation of osteogenic differentiation capacity . (A–B) Representative photographs of ALP staining on day 14. (C) Quantitative analysis of ALP activity of ADSCs on day 14. (D–E) Representative photographs of ARS staining on day 21. (F–H) RT-qPCR results for the mRNA expression of Collagen-I, <t>Runx2,</t> OPN. Data are presented as the mean ± SEM; n = 3; ∗significant difference between selected groups, ∗ p < 0.05, ∗∗ p < 0.01 and ∗∗∗ p < 0.001.
    Runx2 Rabbit Monoclonal, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Bioss collagen 1 polyclonal antibody
    In vitro evaluation of osteogenic differentiation capacity . (A–B) Representative photographs of ALP staining on day 14. (C) Quantitative analysis of ALP activity of ADSCs on day 14. (D–E) Representative photographs of ARS staining on day 21. (F–H) RT-qPCR results for the mRNA expression of Collagen-I, <t>Runx2,</t> OPN. Data are presented as the mean ± SEM; n = 3; ∗significant difference between selected groups, ∗ p < 0.05, ∗∗ p < 0.01 and ∗∗∗ p < 0.001.
    Collagen 1 Polyclonal Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    BIG improves cardiac function after I/RI by inhibiting the inflammatory response and myofibroblast fibrosis. (A, B, C, D, E, F, H and I) The relative expressions of MMP2, MMP9, TNF‒α, IL-1β, IL-6, BCL-2, BAX and c-caspase-3 (n=6). (G) WB results showing the expression of related proteins. (J) Representative microphotographs of TUNEL (blue, DAPI; green, TUNEL‒positive cardiomyocytes) staining of cardiomyocytes (n= 6). Scale bar: 20 μm. (K) The number of TUNEL‒positive cells represents the apoptosis rate in Sham, I/RI and BIG treated mice (n= 6). (L and M) The number of Col6a3- and TGF‒β‒positive myofibroblasts in the myocardial infarction area (n= 6). (N) Immunofluorescent colocalization of Col6a3, TGF‒β and vimentin in mice subjected to Sham, I/RI or BIG treatment (red, Col6a3 or TGF‒β; green, VIM; blue, DAPI). Scale bar: 50 μm. (O) Immunofluorescent colocalization of Col6a3, TGF‒β and TNNI3 in mice subjected to Sham, I/RI and BIG treatment (red, Col6a3 or TGF‒β; green, TNNI3; blue, DAPI). Scale bar: 50 μm. (P and Q) The number of Col6a3- and TGF‒β‒positive cardiomyocytes in the myocardial infarction area (n= 6). The data are presented as the means ± SEMs, and one-way ANOVA with Tukey’s multiple comparisons test was used for multiple groups comparisons, ***P < 0.001

    Journal: Dose-Response

    Article Title: 4,8-Dicarboxyl-8,9-Iridoid-1-Glycoside Alleviates Cardiac Dysfunction After Myocardial Ischaemia-Reperfusion Injury by Activating the PI3K/AKT Pathway

    doi: 10.1177/15593258261444840

    Figure Lengend Snippet: BIG improves cardiac function after I/RI by inhibiting the inflammatory response and myofibroblast fibrosis. (A, B, C, D, E, F, H and I) The relative expressions of MMP2, MMP9, TNF‒α, IL-1β, IL-6, BCL-2, BAX and c-caspase-3 (n=6). (G) WB results showing the expression of related proteins. (J) Representative microphotographs of TUNEL (blue, DAPI; green, TUNEL‒positive cardiomyocytes) staining of cardiomyocytes (n= 6). Scale bar: 20 μm. (K) The number of TUNEL‒positive cells represents the apoptosis rate in Sham, I/RI and BIG treated mice (n= 6). (L and M) The number of Col6a3- and TGF‒β‒positive myofibroblasts in the myocardial infarction area (n= 6). (N) Immunofluorescent colocalization of Col6a3, TGF‒β and vimentin in mice subjected to Sham, I/RI or BIG treatment (red, Col6a3 or TGF‒β; green, VIM; blue, DAPI). Scale bar: 50 μm. (O) Immunofluorescent colocalization of Col6a3, TGF‒β and TNNI3 in mice subjected to Sham, I/RI and BIG treatment (red, Col6a3 or TGF‒β; green, TNNI3; blue, DAPI). Scale bar: 50 μm. (P and Q) The number of Col6a3- and TGF‒β‒positive cardiomyocytes in the myocardial infarction area (n= 6). The data are presented as the means ± SEMs, and one-way ANOVA with Tukey’s multiple comparisons test was used for multiple groups comparisons, ***P < 0.001

    Article Snippet: The blocking solution was removed, and the myocardial cells were treated with primary antibodies against TNNI3 (1:50) (Bioss, BD-PE0227), Col6a3 (1:100) (Bioss, bs-0553R), and TGF-β (1:200) (Affinity, AF1027); the myocardial fibroblasts were then treated with primary antibodies against vimentin (1:100) (Bioss, BD-PE1985), Col6a3 (1:100), and TGF-β (1:200).

    Techniques: Expressing, TUNEL Assay, Staining

    Changes in the multiomic map after myocardial infarction. (A) UMAP of the snRNA‒seq data from all the samples (n = 191,795). (B) Differential expression of Col6a3 in cardiac fibroblasts (n = 47,309) and cardiomyocytes (n = 64,510). (C) Volcano plot of the expression of all genes in myocardial fibroblasts and cardiomyocytes in the infarct area. Red, upregulated; green, downregulated; grey, no difference. (D) KEGG of differentially expressed genes. (E) The expressions of Col6a3 and TGF‒β in the myocardial tissue of the infarct area in the Sham, I/RI, and BIG treated mice (n = 6). The data are presented as the means ± SEMs, and one-way ANOVA with Tukey’s multiple comparisons test was used for multiple groups comparisons, ***P < 0.001

    Journal: Dose-Response

    Article Title: 4,8-Dicarboxyl-8,9-Iridoid-1-Glycoside Alleviates Cardiac Dysfunction After Myocardial Ischaemia-Reperfusion Injury by Activating the PI3K/AKT Pathway

    doi: 10.1177/15593258261444840

    Figure Lengend Snippet: Changes in the multiomic map after myocardial infarction. (A) UMAP of the snRNA‒seq data from all the samples (n = 191,795). (B) Differential expression of Col6a3 in cardiac fibroblasts (n = 47,309) and cardiomyocytes (n = 64,510). (C) Volcano plot of the expression of all genes in myocardial fibroblasts and cardiomyocytes in the infarct area. Red, upregulated; green, downregulated; grey, no difference. (D) KEGG of differentially expressed genes. (E) The expressions of Col6a3 and TGF‒β in the myocardial tissue of the infarct area in the Sham, I/RI, and BIG treated mice (n = 6). The data are presented as the means ± SEMs, and one-way ANOVA with Tukey’s multiple comparisons test was used for multiple groups comparisons, ***P < 0.001

    Article Snippet: The blocking solution was removed, and the myocardial cells were treated with primary antibodies against TNNI3 (1:50) (Bioss, BD-PE0227), Col6a3 (1:100) (Bioss, bs-0553R), and TGF-β (1:200) (Affinity, AF1027); the myocardial fibroblasts were then treated with primary antibodies against vimentin (1:100) (Bioss, BD-PE1985), Col6a3 (1:100), and TGF-β (1:200).

    Techniques: Quantitative Proteomics, Expressing

    In vitro evaluation of osteogenic differentiation capacity . (A–B) Representative photographs of ALP staining on day 14. (C) Quantitative analysis of ALP activity of ADSCs on day 14. (D–E) Representative photographs of ARS staining on day 21. (F–H) RT-qPCR results for the mRNA expression of Collagen-I, Runx2, OPN. Data are presented as the mean ± SEM; n = 3; ∗significant difference between selected groups, ∗ p < 0.05, ∗∗ p < 0.01 and ∗∗∗ p < 0.001.

    Journal: Materials Today Bio

    Article Title: Ultrasound-activated piezoelectric Silk-PVDF hydrogel reprograms the osteoimmune microenvironment via NRF2 signaling for accelerated bone regeneration

    doi: 10.1016/j.mtbio.2026.102779

    Figure Lengend Snippet: In vitro evaluation of osteogenic differentiation capacity . (A–B) Representative photographs of ALP staining on day 14. (C) Quantitative analysis of ALP activity of ADSCs on day 14. (D–E) Representative photographs of ARS staining on day 21. (F–H) RT-qPCR results for the mRNA expression of Collagen-I, Runx2, OPN. Data are presented as the mean ± SEM; n = 3; ∗significant difference between selected groups, ∗ p < 0.05, ∗∗ p < 0.01 and ∗∗∗ p < 0.001.

    Article Snippet: Membranes were blocked with 5 % non-fat milk (BD DifcoTM, #232100) in TBST (Beyotime, #ST673) for 1 h at 25 °C and incubated overnight at 4 °C with the following primary antibodies: Osteopontin (OPN) : • Rabbit monoclonal (Proteintech, 22952-1-AP), 1:1000 • Collagen I (COL1A1): Rabbit polyclonal (Proteintech, 14695-1-AP), 1:1000 • RUNX2: Rabbit monoclonal (Proteintech, 20700-1-AP), 1:1000 • NRF2: Rabbit monoclonal (Proteintech, 16396-1-AP), 1:2000 • NQO1: Mouse monoclonal (Proteintech, 67240-1-Ig), 1:2000 • Beta Actin: Mouse monoclonal (Proteintech, 66009-1-Ig), 1:20,000 After three 10-min TBST washes, membranes were incubated with HRP-conjugated goat anti-rabbit/mouse IgG (Beyotime, #A0208/#A0216, 1:5000) for 2 h at 25 °C.

    Techniques: In Vitro, Staining, Activity Assay, Quantitative RT-PCR, Expressing

    In vitro evaluation of osteogenesis related proteins and genes. (A) The relative protein expression levels of C1, Runx2 and OPN. (B–D) Semi-quantitative analysis of immunoblotting results of C1, Runx2 and OPN. (E) Immunofluorescence staining of OPN. (F) Immunofluorescence staining of OCN. (G) The relative protein expression levels of C1, Runx2 and OPN. (H–J) Semi-quantitative analysis of immunoblotting results of C1, Runx2 and OPN. Data are presented as the mean ± SEM; n = 3; ∗significant difference between selected groups, ∗ p < 0.05, ∗∗ p < 0.01 and ∗∗∗ p < 0.001.

    Journal: Materials Today Bio

    Article Title: Ultrasound-activated piezoelectric Silk-PVDF hydrogel reprograms the osteoimmune microenvironment via NRF2 signaling for accelerated bone regeneration

    doi: 10.1016/j.mtbio.2026.102779

    Figure Lengend Snippet: In vitro evaluation of osteogenesis related proteins and genes. (A) The relative protein expression levels of C1, Runx2 and OPN. (B–D) Semi-quantitative analysis of immunoblotting results of C1, Runx2 and OPN. (E) Immunofluorescence staining of OPN. (F) Immunofluorescence staining of OCN. (G) The relative protein expression levels of C1, Runx2 and OPN. (H–J) Semi-quantitative analysis of immunoblotting results of C1, Runx2 and OPN. Data are presented as the mean ± SEM; n = 3; ∗significant difference between selected groups, ∗ p < 0.05, ∗∗ p < 0.01 and ∗∗∗ p < 0.001.

    Article Snippet: Membranes were blocked with 5 % non-fat milk (BD DifcoTM, #232100) in TBST (Beyotime, #ST673) for 1 h at 25 °C and incubated overnight at 4 °C with the following primary antibodies: Osteopontin (OPN) : • Rabbit monoclonal (Proteintech, 22952-1-AP), 1:1000 • Collagen I (COL1A1): Rabbit polyclonal (Proteintech, 14695-1-AP), 1:1000 • RUNX2: Rabbit monoclonal (Proteintech, 20700-1-AP), 1:1000 • NRF2: Rabbit monoclonal (Proteintech, 16396-1-AP), 1:2000 • NQO1: Mouse monoclonal (Proteintech, 67240-1-Ig), 1:2000 • Beta Actin: Mouse monoclonal (Proteintech, 66009-1-Ig), 1:20,000 After three 10-min TBST washes, membranes were incubated with HRP-conjugated goat anti-rabbit/mouse IgG (Beyotime, #A0208/#A0216, 1:5000) for 2 h at 25 °C.

    Techniques: In Vitro, Expressing, Western Blot, Immunofluorescence, Staining