Render Target: STATIC
Render Timestamp: 2024-11-21T13:05:17.341Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-10-18 00:01:06.906
Product last modified at: 2024-10-18T07:00:55.532Z
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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.

G-CSF-R (E8E7D) Rabbit mAb #10424

Filter:
  • WB
  • IP
  • F

    Supporting Data

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 50-80, 110-140
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    • IP-Immunoprecipitation 
    • F-Flow Cytometry 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000
    Immunoprecipitation 1:100
    Flow Cytometry (Live) 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.

    Protocol

    Specificity / Sensitivity

    G-CSF-R (E8E7D) Rabbit mAb recognizes endogenous levels of total G-CSF-R protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the extracellular domain of human G-CSF-R protein.

    Background

    Granulocyte colony-stimulating factor receptor (G-CSF-R) is a transmembrane protein comprised of an immunoglobulin-like (Ig-like) domain, a cytokine receptor-homologous (CRH) domain, and three fibronectin type III (FN III) domains (1). G-CSF-R is expressed on all granulocytic lineages, including progenitor cells, and has been detected on monocytes, T and B lymphocytes, as well as non-hematopoietic tissues including cardiomyocytes and neural stem cells (2-6). The primary ligand for G-CSF-R is the cytokine granulocyte colony-stimulating factor (G-CSF). G-CSF-R has no intrinsic tyrosine kinase activity; ligand binding induces conformational changes in the receptor, leading to activation of the Jak/Stat, PI3K/Akt, and MAPK pathways (7-10). G-CSF induces differentiation and proliferation of myeloid progenitor cells into neutrophils (11). Multiple diseases have been associated with mutations of the G-CSF-R gene, CSF3R, including severe congenital neutropenia (SCN), chronic neutrophilic leukemia (CNL), and atypical chronic myeloid leukemia (aCML) (12).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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