Colony stimulating factor-1 (CSF-1) is the primary regulator of the mononuclear phagocytic lineage acting through its transmembrane tyrosine kinase receptor, CSF-1R, that is the product of the c-fms proto-oncogene. Null mutations in either the ligand or the receptor genes result in a severe osteopet
Colony-stimulating factor-1 receptor (c-fms)
β Scribed by Charles J. Sherr; Martine F. Roussel; Carl W. Rettenmier
- Publisher
- John Wiley and Sons
- Year
- 1988
- Tongue
- English
- Weight
- 706 KB
- Volume
- 38
- Category
- Article
- ISSN
- 0730-2312
No coin nor oath required. For personal study only.
β¦ Synopsis
The macrophage colony-stimulating factor, CSF-1 (M-CSF), is a homodimeric glycoprotein required for the lineage-specific growth of cells of the mononuclear phagocyte series. Apart from its role in stimulating the proliferation of bone marrowderived precursors of monocytes and macrophages, CSF-1 acts as a survival factor and primes mature macrophages to cany out differentiated functions. Each of the actions of CSF-I are mediated through its binding to a single class of high-affinity receptors expressed on monocytes, macrophages, and their committed progenitors. The CSF-I receptor (CSF-1R) is encoded by the c-fmr proto-oncogene, and is one of a family of growth factor receptors that exhibits an intrinsic tyrosine-specific protein kinase activity. Transduction of c-fms sequences as a viral oncogene (v-fms) in the McDonough (SM) and HZ-5 strains of feline sarcoma virus has resulted in alterations in receptor coding sequences that affect its activity as a tyrosine kinase and provide persistent signals for cell growth in the absence of its ligand. The genetic alterations in the c-fms gene that unmask its latent transforming potential abrogate its lineage-specific activity and enable v-fms to transform a variety of cells that do not normally express CSF-I receptors.
π SIMILAR VOLUMES