ArticleBlood2007
Expression of oncogenic K-ras from its endogenous promoter leads to a partial block of erythroid differentiation and hyperactivation of cytokine-dependent signaling pathways.
Article in Blood, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Article
- Enhanced BRAF engagement by NRAS mutants capable of promoting melanoma initiation.Nature communications · 2022Article
- Embryonic Expression of NrasFrontiers in cell and developmental biology · 2021Article
- Differential effects of RASA3 mutations on hematopoiesis are profoundly influenced by genetic background and molecular variant.PLoS genetics · 2020Article
- Integrative proteomics reveals principles of dynamic phosphosignaling networks in human erythropoiesis.Molecular systems biology · 2020Article
- A Synthetic Lethal Interaction between Glutathione Synthesis and Mitochondrial Reactive Oxygen Species Provides a Tumor-Specific Vulnerability Dependent on STAT3.Molecular and cellular biology · 2015Article
- Review
- Article
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- Article
- Molecular targets for the treatment of juvenile myelomonocytic leukemia.Advances in hematology · 2012Article
- Role of Ras/Raf/MEK/ERK signaling in physiological hematopoiesis and leukemia development.Immunologic research · 2011Review
- KRAS(G12V) enhances proliferation and initiates myelomonocytic differentiation in human stem/progenitor cells via intrinsic and extrinsic pathways.The Journal of biological chemistry · 2011Article
- Hematopoiesis and leukemogenesis in mice expressing oncogenic NrasG12D from the endogenous locus.Blood · 2011Article
- BCR-ABL but not JAK2 V617F inhibits erythropoiesis through the Ras signal by inducing p21CIP1/WAF1.The Journal of biological chemistry · 2010Article
- Defective erythroid differentiation in miR-451 mutant mice mediated by 14-3-3zeta.Genes & development · 2010Article
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- Article
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Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
When overexpressed in primary erythroid progenitors, oncogenic Ras leads to the constitutive activation of its downstream signaling pathways, severe block of terminal erythroid differentiation, and cytokine-independent growth of primary erythroid progenitors. However, whether high-level expression of oncogenic Ras is required for these phenotypes is unknown. To address this issue, we expressed oncogenic K-ras (K-ras(G12D)) from its endogenous promoter using a tetracycline-inducible system. We show that endogenous K-ras(G12D) leads to a partial block of terminal erythroid differentiation in vivo. In contrast to results obtained when oncogenic Ras was overexpressed from retroviral vectors, endogenous levels of K-ras(G12D) fail to constitutively activate but rather hyperactivate cytokine-dependent signaling pathways, including Stat5, Akt, and p44/42 MAPK, in primary erythroid progenitors. This explains previous observations that hematopoietic progenitors expressing endogenous K-ras(G12D) display hypersensitivity to cytokine stimulation in various colony assays. Our results support efforts to modulate Ras signaling for treating hematopoietic malignancies.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.