Render Target: STATIC
Render Timestamp: 2024-12-02T11:11:48.708Z
Commit: cd2fae6ca3f811b1ddb1df24ac291ed56d5d501b
XML generation date: 2024-09-30 01:57:42.612
Product last modified at: 2024-11-22T13:30:23.194Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77

COL1A1 (E3E1X) Mouse mAb #66948

Filter:
  • WB
  • IHC
  • IF

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 220
    Source/Isotype Mouse IgG2a kappa
    Application Key:
    • WB-Western Blotting 
    • IHC-Immunohistochemistry 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    IHC Leica Bond 1:200 - 1:800
    Immunohistochemistry (Paraffin) 1:50 - 1:200
    Immunofluorescence (Immunocytochemistry) 1:50 - 1:200

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    For a carrier free (BSA and azide free) version of this product see product #66154.

    Protocol

    Specificity / Sensitivity

    COL1A1 (E3E1X) Mouse mAb recognizes endogenous levels of total COL1A1 protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Lys170 of human COL1A1 protein.

    Background

    Type 1 collagen is the most abundant collagen in many human tissues, including bone, skin, and tendons. It is a trimeric complex composed of two molecules of COL1A1 (alpha-1 type 1 collagen) and one molecule of COL1A2 (alpha-2 type 1 collagen) (1-3). The expression levels of COL1A1 are regulated by multiple mechanisms, including mRNA stability, translation, and post-translational modification (3-5). Overexpression of COL1A1 has been positively associated with tissue fibrosis disorders, including systemic sclerosis (6), while loss-of-function mutations in the COL1A1 gene are a major causative factor for osteogenesis imperfecta (brittle bone disease) (7). Notably, COL1A1 expression levels have also been associated with tumor development in gastric, lung, thyroid, and breast cancers. Research studies suggest that upregulation of COL1A1 can generate a modified extracellular matrix environment that promotes cancer cell survival, proliferation, metastasis, and invasion (8-11).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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