Anti-MCSF Receptor/CSF1R Antibody Picoband® Fluoro647 Conjugated

CSF1R (Colony-Stimulating Factor 1 Receptor) also known as MCSFR, FMS, c-FMS, CD115, ONCOGENE FMS or CD115 ANTIGEN, encodes a tyrosine kinase growth factor receptor for colony-stimulating factor-1, the macrophage-and monocyte-specific growth factor. The gene is located on long arm of chromosome 5 (5q32) on the Crick (minus) strand. The as-yet-unidentified  CSF1 Rpromoter/enhancer sequences may be confined to the nucleotides separating the 2 genes or could potentially lie within the PDGFR gene itself. The encoded protein is a single pass type I membrane protein and acts as the receptor for  colony stimulating factor 1, a cytokine which controls the production, differentiation, and function of  macrophages. The encoded protein is atyrosine kinase  transmembrane receptor  and member of the CSF1/PDGF receptor  family of tyrosine-protein kinases.  Kondo et al. (2000)   showed that the endogenous myelomonocytic cytokine receptors for GM-CSF and macrophage colony-stimulating factor (CSF1R) are expressed at low to moderate levels on the more primitive hematopoietic stem cells, are absent on common lymphoid progenitors, and are upregulated after myeloid lineage induction by IL2.

A synthetic peptide corresponding to a sequence at the C-terminus of human MCSF Receptor, different from the related mouse sequence by one amino acid and from the related rat sequence by two amino acids.

Angiogenesis, Cardiovascular, Cytokines, Immunology, Innate Immunity, Macrophage/Inflammation, Protein Phosphorylation, Ser/Thr Kinases, Signal Transduction

Tyrosine-protein kinase that acts as cell-surface receptor for CSF1 and IL34 and 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 in response to IL34 and CSF1, and thereby plays an important role in innate immunity and in inflammatory processes. Plays an important role in the regulation of osteoclast proliferation and differentiation, the regulation of bone resorption, and is required for normal bone and tooth development. Required for normal male and female fertility, and for normal development of milk ducts and acinar structures in the mammary gland during pregnancy. Promotes reorganization of the actin cytoskeleton, regulates formation of membrane ruffles, cell adhesion and cell migration, and promotes cancer cell invasion. Activates several signaling pathways in response to ligand binding. Phosphorylates PIK3R1, PLCG2, GRB2, SLA2 and CBL. Activation of PLCG2 leads to the production of the cellular signaling molecules diacylglycerol and inositol 1,4,5- trisphosphate, that then lead to the activation of protein kinase C family members, especially PRKCD. Phosphorylation of PIK3R1, the regulatory subunit of phosphatidylinositol 3-kinase, leads to activation of the AKT1 signaling pathway. Activated CSF1R also mediates activation of the MAP kinases MAPK1/ERK2 and/or MAPK3/ERK1, and of the SRC family kinases SRC, FYN and YES1. Activated CSF1R transmits signals both via proteins that ly interact with phosphorylated tyrosine residues in its intracellular domain, or via adapter proteins, such as GRB2. Promotes activation of STAT family members STAT3, STAT5A and/or STAT5B. Promotes tyrosine phosphorylation of SHC1 and INPP5D/SHIP- 1. Receptor signaling is down-regulated by protein phosphatases, such as INPP5D/SHIP-1, that dephosphorylate the receptor and its downstream effectors, and by rapid internalization of the activated receptor. .

1. Aikawa, Y., Katsumoto, T., Zhang, P., Shima, H., Shino, M., Terui, K., Ito, E., Ohno, H., Stanley, E. R., Singh, H., Tenen, D. G., Kitabayashi, I. PU.1-mediated upregulation of CSF1R is crucial for leukemia stem cell potential induced by MOZ-TIF2. (Letter) Nature Med. 16: 580-585, 2010. 2. Boultwood, J., Rack, K., Kelly, S., Madden, J., Sakaguchi, A. Y., Wang, L.-M., Oscier, D. G., Buckle, V. J., Wainscoat, J. S. Loss of both CSF1R (FMS) alleles in patients with myelodysplasia and a chromosome 5 deletion. Proc. Nat. Acad. Sci. 88: 6176-6180, 1991. 3. Kondo, M., Scherer, D. C., Miyamoto, T., King, A. G., Akashi, K., Sugamura, K., Weissman, I. L. Cell-fate conversion of lymphoid-committed progenitors by instructive actions of cytokines.Nature 407: 383-386, 2000.