Constitutive JunB expression, associated with the JAK2 V617F mutation, stimulates proliferation of the erythroid lineage

dc.creatorMonte-Mor, BDR
dc.creatorPlo, I
dc.creatorda Cunha, AF
dc.creatorCosta, GGL
dc.creatorde Albuquerque, DM
dc.creatorJedidi, A
dc.creatorVilleval, JL
dc.creatorBadaoui, S
dc.creatorLorand-Metze, I
dc.creatorPagnano, KBB
dc.creatorSaad, STO
dc.creatorVainchenker, W
dc.creatorCosta, FF
dc.date2009
dc.dateJAN
dc.date2014-11-17T09:15:19Z
dc.date2015-11-26T17:20:33Z
dc.date2014-11-17T09:15:19Z
dc.date2015-11-26T17:20:33Z
dc.date.accessioned2018-03-29T00:08:09Z
dc.date.available2018-03-29T00:08:09Z
dc.identifierLeukemia. Nature Publishing Group, v. 23, n. 1, n. 144, n. 152, 2009.
dc.identifier0887-6924
dc.identifierWOS:000262470700017
dc.identifier10.1038/leu.2008.275
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/56805
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/56805
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/56805
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1283161
dc.descriptionCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionThe JAK2 V617F mutation, present in the majority of polycythemia vera (PV) patients, causes constitutive activation of JAK2 and seems to be responsible for the PV phenotype. However, the transcriptional changes triggered by the mutation have not yet been totally characterized. In this study, we performed a large-scale gene expression study using serial analysis of gene expression in bone marrow cells of a newly diagnosed PV patient harboring the JAK2 V617F mutation and in normal bone marrow cells of healthy donors. JUNB was one of the genes upregulated in PV, and we confirmed, by quantitative real-time PCR, an overexpression of JUNB in hematopoietic cells of other JAK2 V617F PV patients. Using Ba/F3-EPOR cell lines and primary human erythroblast cultures, we found that JUNB was transcriptionally induced after erythropoietin addition and that JAK2 V617F constitutively induced JunB protein expression. Furthermore, JUNB knockdown reduced not only the growth of Ba/F3 cells by inducing apoptosis, but also the clonogenic and proliferative potential of human erythroid progenitors. These results establish a role for JunB in normal erythropoiesis and indicate that JunB may play a major role in the development of JAK2 V617F myeloproliferative disorders.
dc.description23
dc.description1
dc.description144
dc.description152
dc.descriptionCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionFRM
dc.descriptionLigue Nationale Contre le Cancer
dc.descriptionINCa
dc.descriptionINSERM
dc.descriptionCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.languageen
dc.publisherNature Publishing Group
dc.publisherLondon
dc.publisherInglaterra
dc.relationLeukemia
dc.relationLeukemia
dc.rightsfechado
dc.sourceWeb of Science
dc.subjectJunB
dc.subjectJAK2 V617F
dc.subjecterythropoiesis
dc.subjectHematopoietic Stem-cells
dc.subjectMyeloid-leukemia Cells
dc.subjectTyrosine Kinase Jak2
dc.subjectMice Lacking Junb
dc.subjectPolycythemia-vera
dc.subjectMyeloproliferative Disorders
dc.subjectGene-expression
dc.subjectC-jun
dc.subjectSignal-transduction
dc.subjectActivation
dc.titleConstitutive JunB expression, associated with the JAK2 V617F mutation, stimulates proliferation of the erythroid lineage
dc.typeArtículos de revistas


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