| First Author | Zhang J | Year | 2007 |
| Journal | Cell Cycle | Volume | 6 |
| Issue | 16 | Pages | 1970-3 |
| PubMed ID | 17721087 | Mgi Jnum | J:266120 |
| Mgi Id | MGI:6214787 | Doi | 10.4161/cc.6.16.4577 |
| Citation | Zhang J, et al. (2007) Endogenous K-ras signaling in erythroid differentiation. Cell Cycle 6(16):1970-3 |
| abstractText | K-ras is one of the most frequently mutated genes in virtually all types of human cancers. Using mouse fetal liver erythroid progenitors as a model system, we studied the role of endogenous K-ras signaling in erythroid differentiation. When oncogenic K-ras is expressed from its endogenous promoter, it hyperactivates cytokine-dependent signaling pathways and results in a partial block in erythroid differentiation. In erythroid progenitors deficient in K-ras, cytokine-dependent Akt activation is greatly reduced, leading to delays in erythroid differentiation. Thus, both loss- and gain-of-Kras functions affect erythroid differentiation through modulation of cytokine signaling. These results support the notion that in human cancer patients oncogenic Ras signaling might be controlled by antagonizing essential cytokines. |
