1. Immobilized Human M-CSF at 0.5μg/ml (100μl/Well) on the plate. Dose response curve for Human M-CSF R, hFc Tag with the EC50 42.8ng/ml determined by ELISA (QC Test). 2. Human M-CSF, No Tag immobilized on CM5 Chip can bind Human M-CSF R, hFc Tag with an affinity constant of 2.06 nM as determined in SPR assay. 3. Measured in a cell proliferation assay using RAW264.7 cells. The ED50 for this effect is 2.5 - 7.0 ng/mL (QC Test).

M-CSF/CSF1 Protein, Human, Recombinant (aa 33-190) is expressed in HEK293 mammalian cells. The predicted molecular weight is 20.5 kDa and the accession number is P09603-1.

Human

HEK293 Cells

MGC31930,M-CSF,MCSF,Lanimostim,CSF-1,CSF1

Glu33-Asn190

> 95% as determined by Tris-Bis PAGE; > 95% as determined by HPLC

Reconstitute the lyophilized protein in distilled water. The product concentration should not be less than 100 μg/ml. Before opening, centrifuge the tube to collect powder at the bottom. After adding the reconstitution buffer, avoid vortexing or pipetting for mixing.

It is recommended to store recombinant proteins at -20°C to -80°C for future use. Lyophilized powders can be stably stored for over 12 months, while liquid products can be stored for 6-12 months at -80°C. For reconstituted protein solutions, the solution can be stored at -20°C to -80°C for at least 3 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.

CSF-1, also known as M-CSF , is a four alpha -helical-bundle cytokine that is the primary regulator of macrophage survival, proliferation and differentiation. CSF-1 is also essential for the survival and proliferation of osteoclast progenitors.CSF-1 is cytokine that plays an essential role in the regulation of survival, proliferation and differentiation of hematopoietic precursor cells, especially mononuclear phagocytes, such as macrophages and monocytes. Promotes the release of proinflammatory chemokines, and thereby plays an important role in innate immunity and in inflammatory processes. This mutation leads to a deletion of exons 2-7 of the EGFR gene and renders the mutant receptor incapable of binding any known ligand.