Human G-CSFR / CD114 / CSF3R Protein (Fc Tag)

CD114,G-CSF R,GCSFR

100ug (NPP2142) Please inquiry

Catalog Number	P10218-H02H
Organism Species	Human
Host	Human Cells
Synonyms	CD114,G-CSF R,GCSFR
Molecular Weight	The mature recombinant human G-CSFR/Fc is a disulfide-linked homodimeric protein. The reduced monomer consists of 835 amino acids and predicts a molecular mass of 93.3 kDa. By SDS-PAGE under reducing conditions, the apparent molecular mass of rh GCSFR/Fc monomer is approximately 120-130 kDa due to glycosylation.
predicted N	Glu 25
SDS-PAGE
Purity	> 95 % as determined by SDS-PAGE
Protein Construction	A DNA sequence encoding the extracellular domain (Met 1-Pro 621) of human G-CSF receptor (NP_000751.1) precursor was expressed with the fused Fc region of human IgG1 at the C-terminus.
Bio-activity	Measured by its ability to inhibit GCSF-induced proliferation of NFS-60 mouse myeloid cells. The ED₅₀ for this effect is typically 1-4 ng/ml in the presence of 0.125 ng/ml of recombinant human GCSF.
Research Area	Cardiovascular \|Angiogenesis \|Growth Factor & Receptor \|Colony-Stimulating Factor (CSF) & Receptor \|CSF Receptor
Formulation	Lyophilized from sterile PBS, pH 7.4 1. Normally 5 % - 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
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.
Reference	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.