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Perspectives

Endogenous K-ras Signaling in Erythroid Differentiation

Jing Zhang and Harvey F. Lodish

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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.

Authors

Jing Zhang

Whitehead Institute for Biomedical Research; Cambridge, MA

Harvey F. Lodish

Whitehead Institute for Biomedical Research; Cambridge, MA

Purchase article for $19

Subscribe to this journal for $129/year