Render Target: STATIC
Render Timestamp: 2025-01-22T14:15:52.745Z
Commit: da7e4f2f0d1aed1f1f8e20e4e2ecab8f33cbd595
XML generation date: 2024-09-30 01:59:32.994
Product last modified at: 2025-01-01T09:01:57.681Z
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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.

NID1/Nidogen-1 (E9J3L) Rabbit mAb #86513

Filter:
  • WB

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 150
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Simple Western™ 1:50 - 1:250

    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

    NID1/Nidogen-1 (E9J3L) Rabbit mAb recognizes endogenous levels of total NID1/nidogen-1 protein. This antibody cross-reacts with a band of unknown origin at approximately 80 kDa.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Ala1186 of human NID1/nidogen-1 protein.

    Background

    All extracellular basement membrane contains four major components: type IV collagen, nidogens, laminins, and perlecan (1). Nidogens are a family of highly conserved, sulfated glycoproteins which interact with the laminin 1 short arm chain, type IV collagen, and perlecan. This linking effect contributes to basement membrane formation (2,3). There are two isoforms in the nidogen family, nidogen-1, and nidogen-2. They have a similar domain structure consisting of three globular domains separated by a link region and a rod region (3). The functions of the two isoforms are complementary. Knockout of both genes results in defective basement membrane formation and perinatal lethality due to abnormal lung/heart/limb development (4,5). In lung cancer, colorectal cancer, and ovarian cancer, increased nidogen-1 release contributes to tumor progression by promoting proliferation and migration/invasion, EMT, and metastasis (6-10).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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