ArticleProceedings of the National Academy of Sciences of the United States of America2005
Identification of K-ras as the major regulator for cytokine-dependent Akt activation in erythroid progenitors in vivo.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- PI3K: A Crucial Piece in the RAS Signaling Puzzle.Cold Spring Harbor perspectives in medicine · 2018Review
- Loss of the clock protein PER2 shortens the erythrocyte life span in mice.The Journal of biological chemistry · 2017Article
- Loss of wild-type Kras promotes activation of all Ras isoforms in oncogenic Kras-induced leukemogenesis.Leukemia · 2016Article
- Kras is Required for Adult Hematopoiesis.Stem cells (Dayton, Ohio) · 2016Article
- Multidimensional Screening Platform for Simultaneously Targeting Oncogenic KRAS and Hypoxia-Inducible Factors Pathways in Colorectal Cancer.ACS chemical biology · 2016Article
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- Genetically engineered mouse models shed new light on the pathogenesis of neurofibromatosis type I-related neoplasms of the peripheral nervous system.Brain research bulletin · 2012Review
- Nras overexpression results in granulocytosis, T-cell expansion and early lethality in mice.PloS one · 2012Article
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- Role of Ras/Raf/MEK/ERK signaling in physiological hematopoiesis and leukemia development.Immunologic research · 2011Review
- RAS Interaction with PI3K: More Than Just Another Effector Pathway.Genes & cancer · 2011Article
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- Defective erythroid differentiation in miR-451 mutant mice mediated by 14-3-3zeta.Genes & development · 2010Article
- The role of hypoxia in 2-butoxyethanol-induced hemangiosarcoma.Toxicological sciences : an official journal of the Society of Toxicology · 2010Article
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2 authors.
Funding
Abstract
Despite intensive investigation, controversial results have been obtained concerning the precise signaling pathway(s) regulated by K-ras in different cell types. We show that in primary fetal liver erythroid progenitors, erythropoietin activates all three Ras isoforms, but preferentially N- and K-ras. In K-ras(-/-) fetal liver cells (FLC), erythropoietin- or stem cell factor-dependent Akt activation is greatly reduced, whereas other pathways including Stat5 and p44/p42 MAP kinase are activated normally. We further studied the effects of reduced cytokine-dependent Akt activation in erythroid differentiation. We find that freshly isolated K-ras(-/-) FLC show an approximately 7-fold increase of apoptosis and delayed erythroid differentiation, but only at the stage of erythroid progenitors and very early erythroblasts. When K-ras(-/-) erythroid progenitors are cultured in vitro, there is a significant delay in erythroid differentiation but little increase in apoptosis. Furthermore, we show that partial pharmacologic inhibition of the phosphatidylinositol 3-kinase/Akt pathway in wild-type erythroid progenitors leads to a delay in erythroid differentiation similar to that observed in K-ras(-/-) FLC. Taken together, our data identify K-ras as the major regulator for cytokine-dependent Akt activation, which is important for erythroid differentiation in vivo.
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