ArticleThe Journal of biological chemistry2010
Activation of JAK2-V617F by components of heterodimeric cytokine receptors.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Structural Analysis of Janus Tyrosine Kinase Variants in Hematological Malignancies: Implications for Drug Development and Opportunities for Novel Therapeutic Strategies.International journal of molecular sciences · 2023Article
- Article
- MPL overexpression induces a high level of mutant-CALR/MPL complex: a novel mechanism of ruxolitinib resistance in myeloproliferative neoplasms with CALR mutations.International journal of hematology · 2021Article
- Competitive binding of STATs to receptor phospho-Tyr motifs accounts for altered cytokine responses.eLife · 2021Article
- JAK2 Inhibition by Fedratinib Reduces Osteoblast Differentiation and Mineralisation of Human Mesenchymal Stem Cells.Molecules (Basel, Switzerland) · 2021Article
- Article
- Characterization of epidermal growth factor receptor (EGFR) P848L, an unusual EGFR variant present in lung cancer patients, in a murine Ba/F3 model.FEBS open bio · 2019Article
- JAK2V617F but not CALR mutations confer increased molecular responses to interferon-α via JAK1/STAT1 activation.Leukemia · 2019Article
- Activating JAK2 mutants reveal cytokine receptor coupling differences that impact outcomes in myeloproliferative neoplasm.Leukemia · 2017Article
- JAK2 V617F stimulates proliferation of erythropoietin-dependent erythroid progenitors and delays their differentiation by activating Stat1 and other nonerythroid signaling pathways.Experimental hematology · 2016Article
- IL-27 Promotes Proliferation of Human Leukemic Cell Lines Through the MAPK/ERK Signaling Pathway and Suppresses Sensitivity to Chemotherapeutic Drugs.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2016Article
- Article
- Potential clinical application of interleukin-27 as an antitumor agent.Cancer science · 2015Review
- c-Abl activates janus kinase 2 in normal hematopoietic cells.The Journal of biological chemistry · 2014Article
- Identification of a novel function of the clathrin-coated structure at the plasma membrane in facilitating GM-CSF receptor-mediated activation of JAK2.Cell cycle (Georgetown, Tex.) · 2012Article
- Article
- Random mutagenesis reveals residues of JAK2 critical in evading inhibition by a tyrosine kinase inhibitor.PloS one · 2012Article
- Mutations in the transmembrane and juxtamembrane domains enhance IL27R transforming activity.The Biochemical journal · 2011Article
- Transforming JAK1 mutations exhibit differential signalling, FERM domain requirements and growth responses to interferon-γ.The Biochemical journal · 2010Article
- Structure-function correlation of G6, a novel small molecule inhibitor of Jak2: indispensability of the stilbenoid core.The Journal of biological chemistry · 2010Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The JAK2-V617F mutation is an important etiologic factor for the development of myeloproliferative neoplasms. The mechanism by which this mutated tyrosine kinase initiates deregulated signals in cells is not completely understood. It is believed that JAK2-V617F requires interactions with homodimeric cytokine receptors to elicit its transforming signal. In this study, we demonstrate that components of heterodimeric cytokine receptors can also activate JAK2-V617F. Expression of IL27Ra, a heterodimeric receptor component, enhanced the activation of JAK2-V617F and subsequent downstream signaling to activation of STAT5 and ERK. In addition, expression of components of the interleukin-3 receptor, IL3Ra and the common beta chain, activated JAK2-V617F as well as STAT5 and ERK. Importantly, expression of IL27Ra functionally replaced the requirement of a homodimeric cytokine receptor to promote the activation and transforming activity of JAK2-V617F in BaF3 cells. Tyrosine phosphorylation of IL27Ra was not required to induce activation of JAK2-V617F or STAT5, or to enhance the transforming activity of JAK2-V617F. Expression of IL3Ra or the common beta chain in BaF3 cells also enhanced the ability of JAK2-V617F to transform these hematopoietic cells. However, the heterodimeric receptor component IL12RB1 did not enhance the activation or transforming signals of JAK2-V617F in BaF3 cells. IL27Ra also activated the K539L and R683G JAK2 mutants. Together our data demonstrate that in addition to homodimeric receptors, some heterodimeric receptor components can support the activation and transforming signals of JAK2-V617F and other JAK2 mutants. Therefore, heterodimeric receptors may play unappreciated roles in JAK2 activation in the development of hematopoietic diseases including myeloproliferative neoplasms.
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