Render Target: SSR
Render Timestamp: 2024-11-14T22:42:09.930Z
Commit: 3c1f305a63297e594ac8d7bb5424007d592d68be
XML generation date: 2024-09-30 01:55:17.526
Product last modified at: 2024-11-07T18:45:10.609Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

COL1A1 (E6A8E) Rabbit mAb #39952

Filter:
  • WB
  • IP
  • IF

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 220
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • IF-Immunofluorescence 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:50
    Immunofluorescence (Immunocytochemistry) 1:400 - 1:1600

    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.

    Protocol

    Specificity / Sensitivity

    COL1A1 (E6A8E) Rabbit 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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