The v-mos oncogene product has the ability to induce differentiation in human monocytic leukemia U937 tells, thereby arresting cell proliferation, and also exhibits transforming activity in mouse NIH3T3 cells. Mutation in the v-mos gene consisting of one or two amino acid substitutions in the putative ATP-binding domain impaired its differentiation inducing activity although mutant proteins showed rather higher levels of autophosphorylation in vitro. Macrophage-specific characteristics such as their morphology, expression of C3b receptor and Fc receptor, and production of interleukin-1β and tumor necrosis factor α, were equally diminished in cells transfected with mutant mos genes when compared to those with intact v-mos. The ability of the gene to arrest the proliferation of U937 cells was likewise diminished, while the transforming efficiency of the intact and mutant mos genes were essentially the same. These results suggest that the mos product functions differently in cell differentiation and transformation.
|Number of pages||7|
|Journal||European Journal of Cell Biology|
|Publication status||Published - 01-01-1995|
All Science Journal Classification (ASJC) codes
- Pathology and Forensic Medicine
- Cell Biology