Render Target: STATIC
Render Timestamp: 2024-11-22T12:08:12.112Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-09-30 01:56:24.286
Product last modified at: 2024-11-15T13:00:12.205Z
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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.

Insulin Receptor α (D3U7I) Rabbit mAb #74118

Filter:
  • WB

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa) 135, 220
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    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

    Insulin Receptor α (D3U7I) Rabbit mAb recognizes endogenous levels of total insulin receptor α chain.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Asn170 of human insulin receptor protein.

    Background

    Insulin receptor (InsR) is a heterodimeric membrane receptor tyrosine kinase. It is composed of an extracellular α-subunit containing the ligand binding domain, a β-subunit containing an extracellular domain, a transmembrane domain, and a cytoplasmic tyrosine kinase domain (1). Binding of insulin to InsR results in receptor autophosphorylation and subsequent tyrosine kinase activation (2). This provides a docking site for various adaptor molecules, including insulin receptor substrate (IRS), Gab, and Shc, phosphorylation of which promotes subsequent activation of multiple downstream signaling pathways, including MAPK, PI3K, and TC10 (3,4). These events lead to increased glucose uptake and metabolism, and can promote cell growth. Loss-of-function mutation or desensitization of the InsR are two major contributors to insulin resistance and Type 2 diabetes (5).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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