AbstractThe c‐fmsproto‐oncogene encodes the receptor for the mononuclear phagocyte colony stimulating factor, CSF‐1. Although the tyrosine kinase activity of the CSF‐1 receptor is stimulated by its ligand, the viral oncogene, v‐fms, encodes a constitutive receptor kinase that can transform both fibroblasts and hematopoietic cells by a nonautocrine mechanism. Mutations in the c‐fmsgene as well as a critical alteration of the distal 3′ coding sequences appear to be responsible for fully activating its latent transforming potential. The v‐fmsgene can convert CSF‐1 or IL‐3 dependent hematopoietic cell lines to factor independence and render them tumorigenic. Expression of the v‐fmsgene product does not transmodulate the normal receptors for CSF‐1 or IL‐3 and affects neither their affinity, number, nor potential to be independently down‐regulated by their ligands or by phorbol esters. The ability of v‐fmsto transform hematopoietic target cells suggests that critical alterations in the c‐fmsproto‐oncogene might
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