Anti-Mouse CD115 (CSF-1R) – FITC

Not available

This Fluorescein (FITC) conjugate is formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.4, 1% BSA and 0.09% sodium azide as a preservative.

This Fluorescein conjugate is stable when stored at 2-8°C. Do not freeze.

Next Day 2-8°C

Blue Laser (490 nm)

Clone AFS98 recognizes an epitope on mouse CD115.

CD115 antibody, clone AFS98, recognizes CD115, also known as mouse colony-stimulating factor 1 receptor (CSF-1R and macrophage colony-stimulating factor receptor (M-CSFR). CD115 is a 150kDa single-pass type I membrane protein encoded by the c-fms gene that belongs to the type III protein tyrosine kinase receptor family. CD115 has an immunoglobulin-like extracellular domain, transmembrane domain, and C-terminal tail receptor and is expressed by monocytes, macrophages, plasmacytoid and conventional dendritic cells (DCs), osteoclasts, and their precursors. CD115 is the receptor for CSF1, also known as M-CSF, and IL-34. Binding and signaling through CD115 regulates the proliferation, differentiation, survival, and cytokine-production of monocytes and macrophages^1,2. In addition, CD115 plays a key role in the differentiation and proliferation of osteoclasts as well as their bone resorption activity³. Mutations in CSF-1R are associated with cancer, including myeloid malignancies, Alzheimer’s disease, and other inflammatory and autoimmune diseases⁴. The presence of tumor-associated macrophages (TAMs) expressing CSF-1R correlates with poor survival in various tumor types^5,6, and efforts to eliminate these TAMs using CSF1R small-molecule inhibitors and monoclonal antibodies are currently in clinical trials⁷.

CD115 is expressed on monocytes, macrophages, plasmacytoid and conventional dendritic cells, osteoclasts, and peritoneal exudate cells.

Macrophage colony stimulating factor (M-CSF), IL-34

1. Stanley ER., et al. (1982) Cell. 28:71–81
2. Roussel MF., at al. (1988) Cold Spring Harb Symp Quant Biol. 53:521–530
3. Park-Min, KH., et al. (2020) Exp Mol Med 52, 1239–1254
4. Tak, P. P., at al. (2016) Nat. Rev. Drug Disco. 16, 53–70
5. d’Amore F. (2014) Histopathology. 65:490–500
6. Wei YQ., et al. (2012) PLoS One. 7:e50946
7. Rüttinger D., et al. (2017) J Immunother Cancer. 5(1):53