ArticleMolecular and cellular biology1989
Tyrosine kinase oncogenes abrogate interleukin-3 dependence of murine myeloid cells through signaling pathways involving c-myc: conditional regulation of c-myc transcription by temperature-sensitive v-abl.
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 45 papers.
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Who cites it
45 citing papers in PubMed, 130 citations in OpenAlex.
- Differences in growth promotion, drug response and intracellular protein trafficking of FLT3 mutants.Iranian journal of basic medical sciences · 2014Article
- Regulation of c-Myc ubiquitination controls chronic myelogenous leukemia initiation and progression.Cancer cell · 2013Article
- Tyrosine kinase inhibitor AG1024 exerts antileukaemic effects on STI571-resistant Bcr-Abl expressing cells and decreases AKT phosphorylation.British journal of cancer · 2004Article
- The role of translation in neoplastic transformation from a pathologist's point of view.Oncogene · 2004Review
- Molecular mechanisms associated with the regulation of apoptosis by the two alternatively spliced products of c-Myb.Molecular and cellular biology · 2003Article
- Chronic myelogenous leukemia as a paradigm of early cancer and possible curative strategies.Leukemia · 2003Review
- Review
- Activated Fes protein tyrosine kinase induces terminal macrophage differentiation of myeloid progenitors (U937 cells) and activation of the transcription factor PU.1.Molecular and cellular biology · 2002Article
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- Modeling Philadelphia chromosome positive leukemias.Oncogene · 2001Review
- Apoptosis suppression by Raf-1 and MEK1 requires MEK- and phosphatidylinositol 3-kinase-dependent signals.Molecular and cellular biology · 2001Article
- Identification and characterization of an activating TrkA deletion mutation in acute myeloid leukemia.Molecular and cellular biology · 2000Article
- Review
- Article
- The survival function of the Bcr-Abl oncogene is mediated by Bad-dependent and -independent pathways: roles for phosphatidylinositol 3-kinase and Raf.Molecular and cellular biology · 2000Article
- Cytokine receptor common beta chain as a potential activator of cytokine withdrawal-induced apoptosis.Molecular and cellular biology · 1999Article
- Expression of BCR - ABL in M1 myeloid leukemia cells induces differentiation without arresting proliferation.Oncogene · 1999Article
- STAT3 is required for the gp130-mediated full activation of the c-myc gene.The Journal of experimental medicine · 1999Article
- Direct interaction of Jak1 and v-Abl is required for v-Abl-induced activation of STATs and proliferation.Molecular and cellular biology · 1998Article
- p19(Arf) induces p53-dependent apoptosis during abelson virus-mediated pre-B cell transformation.Proceedings of the National Academy of Sciences of the United States of America · 1998Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Retroviral expression vectors carrying the tyrosine kinase oncogenes abl, fms, src, and trk abrogate the requirements of murine myeloid FDC-P1 cells for interleukin-3 (IL-3). Factor-independent clones constitutively express c-myc in the absence of IL-3, whereas in parental cultures c-myc transcription requires the presence of the ligand. To directly test the effect of a tyrosine kinase oncogene on c-myc expression, retroviral constructs containing three different temperature-sensitive mutants of v-abl were introduced into myeloid IL-3-dependent FDC-P1 and 32D cells. At the permissive temperature, clones expressing temperature-sensitive abl behaved like wild-type abl-containing cells in their growth properties and expressed c-myc constitutively. Temperature shift experiments demonstrated that both IL-3 abrogation and the regulation of c-myc expression correlated with the presence of functional v-abl. Induction of c-myc expression by reactivation of temperature-sensitive v-abl mimicked c-myc induction by IL-3 in that it did not require protein synthesis and occurred at the level of transcription, with effects on both initiation and a transcription elongation block. However, v-abl-regulated FDC-P1 cell growth differed from IL-3-regulated growth in that c-fos and junB, which are normally induced by IL-3, were not induced by activation of v-abl.
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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.