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G-CSFR / CD114 / CSF3R Antibody, Mouse MAb

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    Human CD114/G-CSFR Antibody Product Information
    Immunogen:Human cell-derived rhG-CSFR extracellular domain (Catalog#10218-HCCH)
    Clone ID:2D9G1E3
    Ig Type:Mouse IgG1
    Concentration:
    Endotoxin:
    Formulation:0.2 μm filtered solution in PBS with 5% trehalose
    Preparation:This antibody was produced from a hybridoma resulting from the fusion of a mouse myeloma with B cells obtained from a mouse immunized with purified, recombinant Human G-CSFR extracellular domain (rhG-CSFR; Catalog #10218-HCCH; aa 1-621; NP_000751.1). The IgG fraction of the cell culture supernatant was purified by Protein A affinity chromatography.
    Other CD114/G-CSFR Antibody Products
    Reactivity: Human  
    Application: FCM  
    • Slide 1
    10218-MM06-P-50
    10218-MM06-P-100
    50 Tests 
    100 Tests 
    Add to Cart
    Reactivity: Human  
    Application: IF  ICC/IF  
    • Slide 1
    10218-MM03-50
    10218-MM03-200
    10218-MM03-100
    50 µg 
    200 µg 
    100 µg 
    Add to Cart
    Reactivity: Human  
    Application: IF  ICC/IF  
    • Slide 1
    10218-MM06-50
    10218-MM06-200
    10218-MM06-100
    50 µg 
    200 µg 
    100 µg 
    Add to Cart
    Reactivity: Human  
    Application: FCM  
    • Slide 1
    10218-MM06-A-50
    10218-MM06-A-100
    50 Tests 
    100 Tests 
    Add to Cart
    Reactivity: Human  
    Application: FCM  
    • Slide 1
    10433-R048-F-50
    10433-R048-F-100
    50 Tests 
    100 Tests 
    Add to Cart
    G-CSF R/CD114/CSF3R Background

    Granulocyte Colony Stimulating Factor Receptor (G-CSFR), also known as CD114, which belongs to the cytokine receptor superfamily, is a cell surface receptor for colony stimulating factor 3 (CSF3). It is a critical regulator of granulopoiesis. This type I membrane protein has a composite structure consisting of an immunoglobulin(Ig)-like domain, a cytokine receptor-homologous (CRH) domain and three fibronectin type III (FNIII) domains in the extracellular region. Mutations in the G-CSF receptor leading to carboxy-terminal truncation transduce hyperproliferative growth responses, and are implicated in the pathological progression of severe congenital neutropenia (SCN) to acute myelogenous leukemia (AML). Additionally, autocrine/paracrine stimulation of G-CSFR may be important in the biology of solid tumors, including metastasis.

    Human G-CSF R/CD114/CSF3R References
  • Kasper B, et al. (1999) Association of src-kinase Lyn and non-src-kinase Syk with the granulocyte colony-stimulating factor receptor (G-CSFR) is not abrogated in neutrophils from severe congenital neutropenia patients with point mutations in the G-CSFR mRNA. Int J Hematol. 70(4): 241-7.
  • Hollenstein U, et al. (2000) Endotoxin down-modulates granulocyte colony-stimulating factor receptor (CD114) on human neutrophils. J Infect Dis. 182(1): 343-6.
  • Kindwall-Keller TL, et al. (2008) Role of the proteasome in modulating native G-CSFR expression. Cytokine. 43(2): 114-23.
  • Beel K, et al. (2009) G-CSF receptor (CSF3R) mutations in X-linked neutropenia evolving to acute myeloid leukemia or myelodysplasia. Haematologica. 94(10): 1449-52.
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    G-CSFR/CD114 related areas, pathways, and other information

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    Please note: All products are "FOR RESEARCH USE ONLY AND ARE NOT INTENDED FOR DIAGNOSTIC OR THERAPEUTIC USE"