Invitrogen™ Mouse M-CSF Recombinant Protein

M-CSF (Macrophage colony-stimulating factor, CSF-1) is a survival factor essential for the proliferation and development of monocytes, macrophages, and osteoclast progenitor cells. M-CSF also induces VEGF (vascular endothelial growth factor) secretion by macrophages, thereby mediating mobilization of endothelial progenitor cells and neovascularization. M-CSF is present as several bioactive isoforms that differ in potency and stability. The full-length protein is synthesized as a membrane-spanning protein that can be expressed on the cell surface or further cleaved and modified in the secretory vesicle. Further, M-CSF is a disulfide-bonded homodimer which is processed into one of two isoforms, a glycoprotein or a proteoglycan that has been modified by the addition of chondroitin sulfate to each subunit. Binding of M-CSF to its receptor, c-Fms (CSF-1R or CD115) induces dimerization of the receptor followed by internalization and degradation of the complex. Functionally, M-CSF is known to stimulate differentiation of hematopoietic stem cells to monocyte-macrophage cell populations in culture. M-CSF acts through the CSF receptor 1. Although human M-CSF shows activity on mouse cells, mouse CSF shows no activity on human cells. Recombinant mouse M-CSF is a disulfide-linked homodimer, containing two 156 amino acid chains, with a total molecular weight of 36.4 kDa. Purity is typically greater than 98% and endotoxin level less than 1 EU/ug. The expected biological activity (ED50) is determined by the dose-dependent induction of M-NFS-60 cell proliferation and is typically less than 2ng/mL. The specific activity of this protein is 5x10^5 units/mg. Reconstitute using sterile water at 0.1mg/mL and centrifuge prior to opening vial. Gently pipet solution down the sides of the vial. DO NOT VORTEX sample. Store reconstituted material at -20°C and add 0.1% BSA for additional stability. Amino acid sequence: MKEVSEHCSH MIGNGHLKVL QQLIDSQMET SCQIAFEFVD QEQLDDPVCY LKKAFFLVQD IIDETMRFKD NTPNANATER LQELSNNLNS CFTKDYEEQN KACVRTFHET PLQLLEKIKN FFNETKNLLE KDWNIFTKNC NNSFAKCSSR DVVTKP.