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anti col1 rabbit polyclonal antibody  (Boster Bio)


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    Boster Bio anti col1 rabbit polyclonal antibody
    Fig. 6. Proposed mechanism based on the observed results. Increased LOX(L) expression and activity promotes cartilage calcification (Anx, Enpp1, Pit1, Pit2, ALP). Both classical LOX(L) role (matrix cross-links) and non-classical roles are involved. The latter encompass: increased chondrocyte hypertrophy (Runx2, COL10), increased fibrosis <t>(Col1,</t> Col3), increased inflammation (IL-6) and increased oxidative stress (ROS). Finally, cartilage calcification can in turn induce increased LOX (L) activity.
    Anti Col1 Rabbit Polyclonal Antibody, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 23 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti col1 rabbit polyclonal antibody/product/Boster Bio
    Average 93 stars, based on 23 article reviews
    anti col1 rabbit polyclonal antibody - by Bioz Stars, 2026-02
    93/100 stars

    Images

    1) Product Images from "Inhibiting Lysyl Oxidases prevents pathologic cartilage calcification."

    Article Title: Inhibiting Lysyl Oxidases prevents pathologic cartilage calcification.

    Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

    doi: 10.1016/j.biopha.2023.116075

    Fig. 6. Proposed mechanism based on the observed results. Increased LOX(L) expression and activity promotes cartilage calcification (Anx, Enpp1, Pit1, Pit2, ALP). Both classical LOX(L) role (matrix cross-links) and non-classical roles are involved. The latter encompass: increased chondrocyte hypertrophy (Runx2, COL10), increased fibrosis (Col1, Col3), increased inflammation (IL-6) and increased oxidative stress (ROS). Finally, cartilage calcification can in turn induce increased LOX (L) activity.
    Figure Legend Snippet: Fig. 6. Proposed mechanism based on the observed results. Increased LOX(L) expression and activity promotes cartilage calcification (Anx, Enpp1, Pit1, Pit2, ALP). Both classical LOX(L) role (matrix cross-links) and non-classical roles are involved. The latter encompass: increased chondrocyte hypertrophy (Runx2, COL10), increased fibrosis (Col1, Col3), increased inflammation (IL-6) and increased oxidative stress (ROS). Finally, cartilage calcification can in turn induce increased LOX (L) activity.

    Techniques Used: Expressing, Activity Assay



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    Fig. 6. Proposed mechanism based on the observed results. Increased LOX(L) expression and activity promotes cartilage calcification (Anx, Enpp1, Pit1, Pit2, ALP). Both classical LOX(L) role (matrix cross-links) and non-classical roles are involved. The latter encompass: increased chondrocyte hypertrophy (Runx2, COL10), increased fibrosis <t>(Col1,</t> Col3), increased inflammation (IL-6) and increased oxidative stress (ROS). Finally, cartilage calcification can in turn induce increased LOX (L) activity.
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    rabbit anti-collagen 1 (col1) polyclonal antibody cl50151ap  (Cedarlane)
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    Fig. 6. Proposed mechanism based on the observed results. Increased LOX(L) expression and activity promotes cartilage calcification (Anx, Enpp1, Pit1, Pit2, ALP). Both classical LOX(L) role (matrix cross-links) and non-classical roles are involved. The latter encompass: increased chondrocyte hypertrophy (Runx2, COL10), increased fibrosis <t>(Col1,</t> Col3), increased inflammation (IL-6) and increased oxidative stress (ROS). Finally, cartilage calcification can in turn induce increased LOX (L) activity.
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    DOX inhibited the TGF-β1 induced expression of <t>COL1</t> in NIH3T3 cells but not in CFs. Western blot analysis of NIH3T3 cells ( A ) and CFs ( B ) probing COL1 protein levels with and without TGF-β1 stimulation and DOX. Densitometry results were normalized to the treatment of TGF-β and without DOX. Values represent mean ± standard error (n = 4). *, P -value < 0.05 compared to treatment stimulated with TGF- β1 without DOX (Student’s t-test). #, P -value < 0.05 compared to treatment group stimulated with TGF-β1 and DOX (Student’s t-test).
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    DOX inhibited the TGF-β1 induced expression of <t>COL1</t> in NIH3T3 cells but not in CFs. Western blot analysis of NIH3T3 cells ( A ) and CFs ( B ) probing COL1 protein levels with and without TGF-β1 stimulation and DOX. Densitometry results were normalized to the treatment of TGF-β and without DOX. Values represent mean ± standard error (n = 4). *, P -value < 0.05 compared to treatment stimulated with TGF- β1 without DOX (Student’s t-test). #, P -value < 0.05 compared to treatment group stimulated with TGF-β1 and DOX (Student’s t-test).
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    Image Search Results


    Fig. 6. Proposed mechanism based on the observed results. Increased LOX(L) expression and activity promotes cartilage calcification (Anx, Enpp1, Pit1, Pit2, ALP). Both classical LOX(L) role (matrix cross-links) and non-classical roles are involved. The latter encompass: increased chondrocyte hypertrophy (Runx2, COL10), increased fibrosis (Col1, Col3), increased inflammation (IL-6) and increased oxidative stress (ROS). Finally, cartilage calcification can in turn induce increased LOX (L) activity.

    Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

    Article Title: Inhibiting Lysyl Oxidases prevents pathologic cartilage calcification.

    doi: 10.1016/j.biopha.2023.116075

    Figure Lengend Snippet: Fig. 6. Proposed mechanism based on the observed results. Increased LOX(L) expression and activity promotes cartilage calcification (Anx, Enpp1, Pit1, Pit2, ALP). Both classical LOX(L) role (matrix cross-links) and non-classical roles are involved. The latter encompass: increased chondrocyte hypertrophy (Runx2, COL10), increased fibrosis (Col1, Col3), increased inflammation (IL-6) and increased oxidative stress (ROS). Finally, cartilage calcification can in turn induce increased LOX (L) activity.

    Article Snippet: Collagen 1 (COL1) and Collagen 3 (COL3) expression were evaluated using an anti-COL1 rabbit polyclonal antibody (Boster, PA2140–2) and an anti-COL3 rabbit polyclonal antibody (Origene, AP06517PU-N) respectively.

    Techniques: Expressing, Activity Assay

    DOX inhibited the TGF-β1 induced expression of COL1 in NIH3T3 cells but not in CFs. Western blot analysis of NIH3T3 cells ( A ) and CFs ( B ) probing COL1 protein levels with and without TGF-β1 stimulation and DOX. Densitometry results were normalized to the treatment of TGF-β and without DOX. Values represent mean ± standard error (n = 4). *, P -value < 0.05 compared to treatment stimulated with TGF- β1 without DOX (Student’s t-test). #, P -value < 0.05 compared to treatment group stimulated with TGF-β1 and DOX (Student’s t-test).

    Journal: Scientific Reports

    Article Title: Doxorubicin-induced modulation of TGF-β signaling cascade in mouse fibroblasts: insights into cardiotoxicity mechanisms

    doi: 10.1038/s41598-023-46216-7

    Figure Lengend Snippet: DOX inhibited the TGF-β1 induced expression of COL1 in NIH3T3 cells but not in CFs. Western blot analysis of NIH3T3 cells ( A ) and CFs ( B ) probing COL1 protein levels with and without TGF-β1 stimulation and DOX. Densitometry results were normalized to the treatment of TGF-β and without DOX. Values represent mean ± standard error (n = 4). *, P -value < 0.05 compared to treatment stimulated with TGF- β1 without DOX (Student’s t-test). #, P -value < 0.05 compared to treatment group stimulated with TGF-β1 and DOX (Student’s t-test).

    Article Snippet: Primary antibodies used in this study were: recombinant rabbit anti-cellular communication network factor 2 (CCN2) monoclonal antibody diluted to a concentration of 1:1,000 (Abcam, ab209780); rabbit anti-bone morphogenetic protein 1 (BMP1) polyclonal antibody diluted to a concentration of 1:1,000 (Thermo Fisher Scientific; PA5-103,660; RRID: AB_2852994); rabbit anti-collagen type I (COL1) polyclonal antibody diluted to a concentration of 1:1,000 (Thermo Fisher Scientific; PA1-26204; RRID: AB_2260734); rabbit anti-suppressors of mothers against decapentaplegic homolog 2 (SMAD2) polyclonal antibody diluted to a concentration of 1:1,000 (Thermo Fisher Scientific; 51–1300; RRID: AB_2533896); rabbit anti-phosphorylated SMAD2 (pSMAD2) monoclonal antibody diluted to a concentration of 1:1,000 (Thermo Fisher Scientific; MA5-15122; RRID: AB_10978317); and mouse anti-beta actin (β-actin) monoclonal antibody diluted to a concentration of 1:5,000 (Thermo Fisher Scientific; MA1-91399; RRID: AB_2273656).

    Techniques: Expressing, Western Blot

    Journal: iScience

    Article Title: Targeting endometrial inflammation in intrauterine adhesion ameliorates endometrial fibrosis by priming MSCs to secrete C1INH

    doi: 10.1016/j.isci.2023.107201

    Figure Lengend Snippet:

    Article Snippet: Rabbit polyclonal anti-Col1 , Proteintech , Cat# 14695-1-AP; RRID: AB_2082037.

    Techniques: Staining, Recombinant, Cell Counting, Enzyme-linked Immunosorbent Assay, Western Blot, Software