1. Eva Van Overmeire; Benoît Stijlemans; Felix Heymann; Jiri Keirsse; Yannick Morias; Yvon Elkrim; Lea Brys; Chloé Abels; Qods Lahmar; Can Ergen; Lars Vereecke; Frank Tacke; Patrick De Baetselier; Jo A. Van Ginderachter; Damya Laoui: M-CSF and GM-CSF Receptor Signaling Differentially Regulate Monocyte Maturation and Macrophage Polarization in the Tumor Microenvironment. Cancer Res (2016) 76 (1): 35–42.
Colony stimulating factor 1 receptor (CSF1R) is also known as macrophage colony-stimulating factor receptor (M-CSFR), CD115 Cluster of Differentiation 115 (CD115), C-FMS, CSFR, FIM2, FMS, and is a member of the type Ⅲ subfamily of receptor tyrosine kinases. M-CSF receptor, the product of the c-fms proto-oncogene, is a member of the type III subfamily of receptor tyrosine kinases that also includes receptors for SCF and PDGF. These receptors each contain five immunoglobulin-like domains in their extracellular domain (ECD) and a split kinase domain in their intracellular region. M-CSF receptor is expressed primarily on cells of the monocyte/macrophage lineage, dendritic cells, stem cells and in the developing placenta. M-CSF R engagement is continuously required for macrophage survival and regulates lineage decisions and maturation of monocytes, macrophages, osteoclasts and DC. M-CSF R and integrin alpha v beta 3 share signaling pathways during osteoclastogenesis and deletion of either causes osteopetrosis. In the brain, microglia expressing increased M-CSF R are concentrated with Alzheimers a beta peptide, but their role in pathogenesis is unclear.
1μg (R: reducing condition, N: non-reducing condition).
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