Colony stimulating factor 1 receptor
(Redirected from Macrophage colony-stimulating factor receptor)
Colony stimulating factor 1 receptor (CSF1R) is a protein that in humans is encoded by the CSF1R gene. This receptor is a member of the tyrosine kinase family of receptors and plays a crucial role in the regulation of macrophage production, differentiation, and function.
Structure[edit | edit source]
CSF1R is a transmembrane protein that consists of an extracellular domain, a single transmembrane helix, and an intracellular tyrosine kinase domain. The extracellular domain is responsible for binding to its ligand, colony stimulating factor 1 (CSF1), and interleukin-34 (IL-34).
Function[edit | edit source]
CSF1R is primarily expressed on the surface of macrophages and their precursors. Upon binding to its ligands, CSF1R undergoes dimerization and autophosphorylation, which activates its intrinsic tyrosine kinase activity. This activation triggers a cascade of downstream signaling pathways that promote the survival, proliferation, and differentiation of macrophages.
Role in Disease[edit | edit source]
Mutations in the CSF1R gene have been associated with several diseases, including hereditary diffuse leukoencephalopathy with spheroids (HDLS), a rare neurodegenerative disorder. Overexpression of CSF1R has also been implicated in certain types of cancer, such as breast cancer and prostate cancer, where it may contribute to tumor growth and metastasis.
Clinical Significance[edit | edit source]
CSF1R is a potential therapeutic target for diseases involving macrophage dysregulation. Inhibitors of CSF1R are being investigated for their potential to treat conditions such as rheumatoid arthritis, multiple sclerosis, and certain cancers.
Related Pages[edit | edit source]
- Macrophage
- Tyrosine kinase
- Colony stimulating factor 1
- Interleukin-34
- Hereditary diffuse leukoencephalopathy with spheroids
- Breast cancer
- Prostate cancer
- Rheumatoid arthritis
- Multiple sclerosis
References[edit | edit source]
External Links[edit | edit source]
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