CSF1R Protein, Mouse (HEK293, Fc)

CSF1R protein, a tyrosine-protein kinase, serves as a cell-surface receptor for CSF1 and IL34, exerting pivotal control over the survival, proliferation, and differentiation of hematopoietic precursor cells, particularly mononuclear phagocytes like macrophages and monocytes. Its role in innate immunity and inflammatory processes is underscored by its promotion of the release of pro-inflammatory chemokines in response to IL34 and CSF1. Additionally, CSF1R plays a critical role in the regulation of osteoclast proliferation and differentiation, bone resorption, and is indispensable for normal bone and tooth development. It is essential for normal fertility in both males and females, as well as for the development of milk ducts and acinar structures in the mammary gland during pregnancy. Notably, CSF1R influences the reorganization of the actin cytoskeleton, regulates the formation of membrane ruffles, cell adhesion, cell migration, and facilitates cancer cell invasion. Upon ligand binding, CSF1R activates multiple signaling pathways, including ERK1/2, JNK, PI3K/AKT, MAP kinases (MAPK1/ERK2 and/or MAPK3/ERK1), and SRC family kinases (SRC, FYN, YES1). Its downstream effects involve the phosphorylation of various target proteins, such as PIK3R1, PLCG2, GRB2, SLA2, and CBL. Furthermore, CSF1R mediates the activation of STAT family members (STAT3, STAT5A, and/or STAT5B) and promotes tyrosine phosphorylation of SHC1 and INPP5D/SHIP-1. The receptor signaling is tightly regulated by protein phosphatases, including INPP5D/SHIP-1, and by the rapid internalization of the activated receptor. In the central nervous system, CSF1R may contribute to the development of microglia macrophages.