ArticleOncogene1999
Myeloproliferative disorder and leukaemia in mice induced by different classes of constitutive mutants of the human IL-3/IL-5/GM-CSF receptor common beta subunit.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Hhex induces promyelocyte self-renewal and cooperates with growth factor independence to cause myeloid leukemia in mice.Blood advances · 2018Article
- The GM-CSF receptor utilizes β-catenin and Tcf4 to specify macrophage lineage differentiation.Differentiation; research in biological diversity · 2012Article
- Host-derived interleukin-5 promotes adenocarcinoma-induced malignant pleural effusion.American journal of respiratory and critical care medicine · 2010Article
- Alternative modes of GM-CSF receptor activation revealed using activated mutants of the common beta-subunit.Blood · 2010Article
- Repression of Gadd45alpha by activated FLT3 and GM-CSF receptor mutants contributes to growth, survival and blocked differentiation.Leukemia · 2009Article
- Regulation of myeloproliferation and M2 macrophage programming in mice by Lyn/Hck, SHIP, and Stat5.The Journal of clinical investigation · 2008Article
- IL-3 receptor signaling is dispensable for BCR-ABL-induced myeloproliferative disease.Proceedings of the National Academy of Sciences of the United States of America · 2003Article
- Cytokine signaling and hematopoietic homeostasis are disrupted in Lnk-deficient mice.The Journal of experimental medicine · 2002Article
- The Raf/MEK/ERK signal transduction cascade as a target for chemotherapeutic intervention in leukemia.Leukemia · 2002Review
- Modeling Philadelphia chromosome positive leukemias.Oncogene · 2001Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several constitutively active mutant forms of the common beta subunit of the human IL-3, IL-5 and GM-CSF receptors (hbetac), which enable it to signal in the absence of ligand, have recently been described. Two of these, V449E and I374N, are amino acid substitutions in the transmembrane and extracellular regions of hbetac, respectively. A third, FIDelta, contains a 37 amino acid duplication in the extracellular domain. We have shown previously that when expressed in primary murine haemopoietic cells, the extracellular mutants confer factor-independence on cells of the neutrophil and monocyte lineages only, whereas V449E does so on all cell types of the myeloid and erythroid compartments. To study the in vivo effects and leukaemic potential of these mutants, we have expressed all three in mice by bone marrow reconstitution using retrovirally infected donor cells. Expression of the extracellular mutants leads to an early onset, chronic myeloproliferative disorder marked by elevations in the neutrophil, monocyte, erythrocyte and platelet lineages. In contrast, expression of V449E leads to an acute leukaemia-like syndrome of anaemia, thrombocytopaenia and blast cell expansion. These data support the possibility that activating mutations in hbetac are involved in haemopoietic disorders in man.
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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.