MycoFold rHu Macrophage Colony-Stimulating Factor (M-CSF)

MycoFold™ Recombinant Human Macrophage-Colony Stimulating Factor (rHu M-CSF) protein is a growth factor that regulates the survival, proliferation, and differentiation of hematopoietic precursor cells towards the M2 phenotype.  Also known as CSF1, this protein is required for the control of monocyte and macrophage differentiation to adopt the M2 phenotype. 

Upon CSF1 binding, the CSF-1R (receptor) undergoes dimerization and autophosphorylation of several tyrosine residues, which initiate downstream signaling cascades.  The PI3K/AKT signaling pathway inactivates FOXO1, which otherwise restricts M2 activation.  Additionally, CSF-1R signaling increases IL-4R expression, priming macrophages to be more sensitive to STAT6-mediated M2 activation by cytokines such as IL-4 and IL-13.  In glial applications, CSF1 is a primary regulator of microglia development, survival, and maintenance predominantly in white matter regions.  CSR-1R is expressed on neural progenitor cells (NPCs), and CSF1 signaling in these suppresses self-renewal and enhances differentiation into mature neurons.            

Cytokine is a disulfide-linked homodimer (18.4 kDa) expressed via extracellular secretion of K. phaffii engineered yeast.  Chaperone-guided folding and engineered secretion pathways generate native tertiary 3D structures, thereby optimizing thermostability.  Priced for best-in-class bioactivity value (IUs/mg/$) to maximize research budgets. 

Key Research Applications

• Development and maintenance of tissue-resident macrophages (TRMs) (e.g., microglia, Kupffer cells, and osteoclasts)
• Differentiation of HSCs into macrophages, monocytes, and dendritic cells
• Hematopoietic stem and progenitor cells (HSPCs) research and transplantation
• Self-renewal capacity of certain tissue-resident macrophages (TRMs)
• Modulation of tumor-associated macrophages (TAMs)
• M2-like (anti-inflammatory/regulatory) phenotype polarization
• Activation of PI3K-Akt (survival/anti-apoptosis), MAPK/ERK (proliferation), and JAK-STAT (differentiation) pathways.