分子量:92.8 kDa

纯度:>95% as determined by SDS-PAGE.

内毒素:Less than 1.0 EU per μg of the Human G-CSF R, Fc Tag by the LAL method.

Buffer:50 mM tris, 100 mM glycine, pH7.5

生物活性:Measured by its ability to inhibit the GCSF-induced proliferation of NFS-60 mouse myeloid cells.The ED50 for this effect is typically 1-5 ng /ml in the presence of 0.125 ng /ml of recombinant human GCSF.
Measured by its binding ability in a functional ELISA.Immobilized ActiveMax Human G-CSF (Cat# GCF-H5214) at 5 μg/mL (100 μL/well) can bind Human G-CSF R, Fc Tag (Cat# GCR-H5250 ).The EC50 is typically 0.6-6 ng/mL.

产品特性:Human G-CSF R, Fc Tag is fused with a human IgG1 Fc tag at the C-terminus, and has a calculated MW of 92.8 kDa. The predicted N-terminus is Glu 25. The reducing (R) protein migrates as 100-130 kDa in SDS-PAGE  due to glycosylation.

产品背景:Granulocyte Colony Stimulating Factor Receptor (G-CSFR) is also known as Cluster of Differentiation 114 (CD114), CSF3R and GCSF, is a cell-surface receptor for the granulocyte colony-stimulating factor (G-CSF), a cytokine that plays a critical role in the regulation of the activation, proliferation, differentiation, and survival of the neutrophilic granulocyte lineage. G-CSFR belongs to a family of cytokine receptors known as the hematopoietin receptor family. 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. G-CSFR is present mainly on precursor cells in the bone marrow, and, in response to stimulation by G-CSF, initiates cell proliferation and differentiation into mature neutrophilic granulocytes and macrophages. G-CSFR mediates the specific effect of GCSF through activating a variety of intracellular signaling cascades, including the Jak/Stat, PI3/Akt, Ras-Raf-MAP kinase, and Src family kinase pathways, and thus functions in defense against infection, inflammation and repair, and in the maintenance of steady state hematopoiesis. Mutations in this gene are a cause of Kostmann syndrome, also known as severe congenital neutropenia. Mutations in the intracellular part of this receptor are also associated with certain types of leukemia.