ArticleMolecular and cellular biology1989
A v-H-ras-dependent hemopoietic tumor model involving progression from a clonal stage of transformation competence to autocrine interleukin 3 production.
Article in Molecular and cellular biology, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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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Who cites it
19 citing papers in PubMed, 37 citations in OpenAlex.
- Subthreshold IKK activation modulates the effector functions of primary mast cells and allows specific targeting of transformed mast cells.Oncotarget · 2015Article
- Isolation and characterization of dominant and recessive IL-3-independent hematopoietic transformants.Oncogene · 2006Article
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- A constitutive decay element promotes tumor necrosis factor alpha mRNA degradation via an AU-rich element-independent pathway.Molecular and cellular biology · 2003Article
- Global analysis of differential gene expression after transformation with the v-H-ras oncogene in a murine tumor model.Oncogene · 2001Article
- Somatic mRNA turnover mutants implicate tristetraprolin in the interleukin-3 mRNA degradation pathway.Molecular and cellular biology · 2000Article
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- Cyclosporin A promotes translational silencing of autocrine interleukin-3 via ribosome-associated deadenylation.Molecular and cellular biology · 1999Article
- c-jun N-terminal kinase is involved in AUUUA-mediated interleukin-3 mRNA turnover in mast cells.The EMBO journal · 1998Article
- Rapamycin destabilizes interleukin-3 mRNA in autocrine tumor cells by a mechanism requiring an intact 3' untranslated region.Molecular and cellular biology · 1997Article
- Direct identification of differentially expressed genes by cycle sequencing and cycle labelling using the differential display PCR primers.Nucleic acids research · 1997Article
- Suppressible and nonsuppressible autocrine mast cell tumors are distinguished by insertion of an endogenous retroviral element (IAP) into the interleukin 3 gene.The Journal of experimental medicine · 1993Article
- 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
- In vivo transformation of factor-dependent hemopoietic cells: role of intracisternal A-particle transposition for growth factor gene activation.The EMBO journal · 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
- Reversible abrogation of IL-3 dependence by an inducible H-ras oncogene.The EMBO journal · 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
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autocrine interleukin 3 (IL-3)-secreting tumors were generated from an IL-3-dependent mouse mast cell line (PB-3c) after introduction of the v-H-ras oncogene. Tumor progression was characterized by four distinct phenotypes. The first corresponded to immortalized mast cells unresponsive to the oncogenic effect of v-H-ras. The second was expressed in a clonable subpopulation of PB-3c cells and was marked by the competence to form v-H-ras-dependent tumors (immortalized transformation competence). The third was a direct effect of v-H-ras expression on all PB-3c cells and was characterized in vitro by a reduced IL-3 requirement. Upon injection of v-H-ras-expressing, transformation-competent cells into mice, the final, fully malignant phenotype developed with a long latency period and was marked in vitro by independence of exogenous IL-3 and by autocrine IL-3 stimulation. Northern (RNA) blot analysis and an RNase A-T1 protection assay showed that IL-3 production was strictly associated with the tumor phenotype. Two of six tumors showed an alteration at the 5' region of the IL-3 gene. We conclude that v-H-ras required complementation by IL-3 gene rearrangement or an alternate event to generate autocrine mastocytomas.
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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.