ArticleThe EMBO journal1989
Reversible abrogation of IL-3 dependence by an inducible H-ras oncogene.
Article in The EMBO journal, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 48 citations in OpenAlex.
- Isolation and characterization of dominant and recessive IL-3-independent hematopoietic transformants.Oncogene · 2006Article
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- Mutant N-RAS induces erythroid lineage dysplasia in human CD34+ cells.The Journal of experimental medicine · 1997Article
- Regulation of the salvage pathway of deoxynucleotides synthesis in apoptosis induced by growth factor deprivation.The Biochemical journal · 1996Article
- Susceptibility to apoptosis is differentially regulated by c-myc and mutated Ha-ras oncogenes and is associated with endonuclease availability.British journal of cancer · 1993Article
- Autocrine stimulation by erythropoietin and autonomous growth of human erythroid leukemic cells in vitro.The Journal of clinical investigation · 1991Article
- Involvement of ras p21 protein in signal-transduction pathways from interleukin 2, interleukin 3, and granulocyte/macrophage colony-stimulating factor, but not from interleukin 4.Proceedings of the National Academy of Sciences of the United States of America · 1991Article
- Abrogation of the requirement for feeder cell interaction and T cell receptor stimulation of lymphocytes infected with retroviral vectors.The Journal of experimental medicine · 1990Article
- Regulation of interleukin 3 mRNA expression in mast cells occurs at the posttranscriptional level and is mediated by calcium ions.Proceedings of the National Academy of Sciences of the United States of America · 1990Article
- Tumor suppression involves down-regulation of interleukin 3 expression in hybrids between autocrine mastocytoma and interleukin 3-dependent parental mast cells.Proceedings of the National Academy of Sciences of the United States of America · 1989Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immortalized, interleukin-3 (IL-3)-dependent mouse mast cells (PB-3c) were transfected with a human activated c-H-ras gene under the transcriptional control of the mouse mammary tumor virus long terminal repeat. Addition of increasing amounts of dexamethasone resulted in a concentration-dependent increase in expression of the H-ras oncogene. The elevation of p21 ras protein concentrations was paralleled by progressive growth of the transfectants in the absence of exogenous IL-3, leading to complete abrogation of growth-factor requirement at high p21ras levels. The maintenance of the IL-3-independent state required the continuous expression of the H-ras oncogene, since dexamethasone removal was followed by rapid cell death. Expression of the H-ras oncogene induced PB-3c cells to produce IL-3 and granulocyte-macrophage colony-stimulating factor, suggesting that their IL-3-independent proliferation may be due to an autocrine mechanism.
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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.