期刊
CELL CYCLE
卷 6, 期 16, 页码 1970-1973出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cc.6.16.4577
关键词
K-ras; erythroid differentiation; cytokine; signal transduction; endogenous level
类别
资金
- NHLBI NIH HHS [P01 HL 32262] Funding Source: Medline
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.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据