Render Target: STATIC
Render Timestamp: 2024-10-31T10:44:29.718Z
Commit: 23cb9f61fe67e1e9093fd644a533c4ff516a6463
XML generation date: 2024-08-09 16:16:09.080
Product last modified at: 2024-09-03T12:15:42.364Z
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PDP - Template Name: Monoclonal Antibody (Alexa Fluor Conjugate)
PDP - Template ID: *******c8ce56b
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

Insulin Receptor β (E9L5V) XP® Rabbit mAb (Alexa Fluor® 594 Conjugate) #98448

Filter:
  • IF
  • F

    Supporting Data

    REACTIVITY H M R
    SENSITIVITY Endogenous
    MW (kDa)
    Source/Isotype Rabbit IgG
    Application Key:
    • IF-Immunofluorescence 
    • F-Flow Cytometry 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 
    • R-Rat 

    Product Information

    Product Description

    This Cell Signaling Technology antibody is conjugated to Alexa Fluor® 594 fluorescent dye under optimal conditions and tested in-house for direct flow cytometric and immunofluorescent analysis in human cells and immunofluorescent analysis in mouse tissue. This antibody conjugate is expected to exhibit the same species cross-reactivity as the unconjugated Insulin Receptor β (E9L5V) XP® Rabbit mAb #23413.

    Product Usage Information

    Application Dilution
    Immunofluorescence (Frozen) 1:100 - 1:400
    Immunofluorescence (Immunocytochemistry) 1:100 - 1:400
    Flow Cytometry (Fixed/Permeabilized) 1:50

    Storage

    Supplied in PBS (pH 7.2), less than 0.1% sodium azide, and 2 mg/mL BSA. Store at 4°C. Do not aliquot the antibody. Protect from light. Do not freeze.

    Protocol

    Specificity / Sensitivity

    Insulin Receptor β (E9L5V) XP® Rabbit mAb (Alexa Fluor® 594 Conjugate) recognizes endogenous levels of total insulin receptor β.

    Species Reactivity:

    Human, Mouse, Rat

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu1374 of human insulin receptor.

    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.
    Cell Signaling Technology is a trademark of Cell Signaling Technology, Inc.
    XP is a registered trademark of Cell Signaling Technology, Inc.
    This product is provided under an intellectual property license from Life Technologies Corporation. The transfer of this product is conditioned on the buyer using the purchased product solely in research conducted by the buyer, excluding contract research or any fee for service research, and the buyer must not (1) use this product or its components for (a) diagnostic, therapeutic or prophylactic purposes; (b) testing, analysis or screening services, or information in return for compensation on a per-test basis; or (c) manufacturing or quality assurance or quality control, and/or (2) sell or transfer this product or its components for resale, whether or not resold for use in research. For information on purchasing a license to this product for purposes other than as described above, contact Life Technologies Corporation, 5791 Van Allen Way, Carlsbad, CA 92008 USA or [email protected].
    All other trademarks are the property of their respective owners. Visit our Trademark Information page.