Render Target: STATIC
Render Timestamp: 2024-11-21T12:50:29.291Z
Commit: 5c4accf06eb7154018ba3f54329c7590f97f534a
XML generation date: 2024-08-01 15:24:02.367
Product last modified at: 2024-11-11T14:00:16.469Z
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PDP - Template Name: Polyclonal Antibody
PDP - Template ID: *******59c6464

Phospho-CSF-1R/M-CSF-R (Tyr723) Antibody #3151

Filter:
  • WB

    Supporting Data

    REACTIVITY H M
    SENSITIVITY Endogenous
    MW (kDa) 175
    SOURCE Rabbit
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 

    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 and 50% glycerol. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    Phospho-CSF-1R/M-CSF-R (Tyr723) Antibody detects endogenous CSF-1R/M-CSF-R only when phosphorylated at tyrosine 723.

    Species Reactivity:

    Human, Mouse

    Source / Purification

    Polyclonal antibodies are produced by immunizing animals with a synthetic phosphopeptide corresponding to residues surrounding Tyr723 of human CSF-1R/M-CSF-R. Antibodies are purified by protein A and peptide affinity chromatography.

    Background

    Macrophage-colony stimulating factor (M-CSF, CSF-1) receptor is an integral membrane tyrosine kinase encoded by the c-fms proto-oncogene. M-CSF receptor is expressed in monocytes (macrophages and their progenitors) and drives growth and development of this blood cell lineage (1-3). Binding of M-CSF to its receptor induces receptor dimerization, activation, and autophosphorylation of cytoplasmic tyrosine residues used as docking sites for SH2-containing signaling proteins (4). There are at least five major tyrosine autophosphorylation sites. Tyr723 (Tyr721 in mouse) is located in the kinase insert (KI) region. Phosphorylated Tyr723 binds the p85 subunit of PI3 kinase as well as PLCγ2 (5). Phosphorylation of Tyr809 provides a docking site for Shc (5). Overactivation of this receptor can lead to a malignant phenotype in various cell systems (6). The activated M-CSF receptor has been shown to be a predictor of poor outcome in advanced epithelial ovarian carcinoma (7) and breast cancer (8).
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