Please use this identifier to cite or link to this item: https://doi.org/10.1084/jem.20170484
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dc.titleJDP2: An oncogenic bZIP transcription factor in T cell acute lymphoblastic leukemia
dc.contributor.authorMansour, M.R
dc.contributor.authorHe, S
dc.contributor.authorLi, Z
dc.contributor.authorLobbardi, R
dc.contributor.authorAbraham, B.J
dc.contributor.authorHug, C
dc.contributor.authorRahman, S
dc.contributor.authorLeon, T.E
dc.contributor.authorKuang, Y.-Y
dc.contributor.authorZimmerman, M.W
dc.contributor.authorBlonquist, T
dc.contributor.authorGjini, E
dc.contributor.authorGutierrez, A
dc.contributor.authorTang, Q
dc.contributor.authorGarcia Perez, L
dc.contributor.authorPike Overzet, K
dc.contributor.authorAnders, L
dc.contributor.authorBerezovskaya, A
dc.contributor.authorZhou, Y
dc.contributor.authorZon, L.I
dc.contributor.authorNeuberg, D
dc.contributor.authorFielding, A.K
dc.contributor.authorStaal, F.J.T
dc.contributor.authorLangenau, D.M
dc.contributor.authorSanda, T
dc.contributor.authorYoung, R.A
dc.contributor.authorLook, A.T
dc.date.accessioned2020-10-22T07:22:29Z
dc.date.available2020-10-22T07:22:29Z
dc.date.issued2018
dc.identifier.citationMansour, M.R, He, S, Li, Z, Lobbardi, R, Abraham, B.J, Hug, C, Rahman, S, Leon, T.E, Kuang, Y.-Y, Zimmerman, M.W, Blonquist, T, Gjini, E, Gutierrez, A, Tang, Q, Garcia Perez, L, Pike Overzet, K, Anders, L, Berezovskaya, A, Zhou, Y, Zon, L.I, Neuberg, D, Fielding, A.K, Staal, F.J.T, Langenau, D.M, Sanda, T, Young, R.A, Look, A.T (2018). JDP2: An oncogenic bZIP transcription factor in T cell acute lymphoblastic leukemia. Journal of Experimental Medicine 215 (7) : 1929-1945. ScholarBank@NUS Repository. https://doi.org/10.1084/jem.20170484
dc.identifier.issn00221007
dc.identifier.urihttps://scholarbank.nus.edu.sg/handle/10635/179029
dc.description.abstractA substantial subset of patients with T cell acute lymphoblastic leukemia (T-ALL) develops resistance to steroids and succumbs to their disease. JDP2 encodes a bZIP protein that has been implicated as a T-ALL oncogene from insertional mutagenesis studies in mice, but its role in human T-ALL pathogenesis has remained obscure. Here we show that JDP2 is aberrantly expressed in a subset of T-ALL patients and is associated with poor survival. JDP2 is required for T-ALL cell survival, as its depletion by short hairpin RNA knockdown leads to apoptosis. Mechanistically, JDP2 regulates prosurvival signaling through direct transcriptional regulation of MCL1. Furthermore, JDP2 is one of few oncogenes capable of initiating T-ALL in transgenic zebrafish. Notably, thymocytes from rag2:jdp2 transgenic zebrafish express high levels of mcl1 and demonstrate resistance to steroids in vivo. These studies establish JDP2 as a novel oncogene in high-risk T-ALL and implicate overexpression of MCL1 as a mechanism of steroid resistance in JDP2-overexpressing cells. © 2018 Mansour et al.
dc.publisherRockefeller University Press
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.sourceUnpaywall 20201031
dc.subjectbasic leucine zipper transcription factor
dc.subjectcaspase 3
dc.subjectccnd2 protein
dc.subjectdexamethasone
dc.subjectdoxycycline
dc.subjectglucocorticoid
dc.subjectjdp2 protein
dc.subjectmicroRNA 17 92
dc.subjectMyc protein
dc.subjectnicotinamide adenine dinucleotide adenosine diphosphate ribosyltransferase 1
dc.subjectNotch1 receptor
dc.subjectprotein
dc.subjectprotein kinase B
dc.subjectprotein kinase Pim 1
dc.subjectprotein mcl 1
dc.subjectprotein Myb
dc.subjectRAG2 protein
dc.subjectshort hairpin RNA
dc.subjectsteroid
dc.subjecttranscription factor RUNX2
dc.subjectunclassified drug
dc.subjectzinc finger E box binding homeobox 2
dc.subjectdexamethasone
dc.subjectglucocorticoid
dc.subjectJDP2 protein, human
dc.subjectMCL1 protein, human
dc.subjectMyc protein
dc.subjectprotein binding
dc.subjectprotein mcl 1
dc.subjectrepressor protein
dc.subjectzebrafish protein
dc.subjectacute lymphoblastic leukemia
dc.subjectanimal experiment
dc.subjectanimal model
dc.subjectapoptosis
dc.subjectArticle
dc.subjectcancer survival
dc.subjectcell survival
dc.subjectcontrolled study
dc.subjectdisease association
dc.subjectgenetic association
dc.subjecthuman
dc.subjecthuman tissue
dc.subjectin vivo study
dc.subjectnonhuman
dc.subjectoncogene
dc.subjectpriority journal
dc.subjectprotein expression
dc.subjectregulatory mechanism
dc.subjectsignal transduction
dc.subjectthymocyte
dc.subjecttransgenic zebrafish
dc.subjectupregulation
dc.subjectacute lymphoblastic leukemia
dc.subjectanimal
dc.subjectcancer transplantation
dc.subjectcell proliferation
dc.subjectdisease model
dc.subjectDNA responsive element
dc.subjectdrug effect
dc.subjectenhancer region
dc.subjectgene expression regulation
dc.subjectgenetics
dc.subjectinfant
dc.subjectmetabolism
dc.subjectmouse
dc.subjectnucleotide sequence
dc.subjectoncogene
dc.subjectpathology
dc.subjectpreschool child
dc.subjecttreatment outcome
dc.subjectzebra fish
dc.subjectAnimals
dc.subjectApoptosis
dc.subjectBase Sequence
dc.subjectCell Proliferation
dc.subjectCell Survival
dc.subjectChild, Preschool
dc.subjectDexamethasone
dc.subjectDisease Models, Animal
dc.subjectEnhancer Elements, Genetic
dc.subjectGene Expression Regulation, Leukemic
dc.subjectGlucocorticoids
dc.subjectHumans
dc.subjectInfant
dc.subjectMice
dc.subjectMutagenesis, Insertional
dc.subjectMyeloid Cell Leukemia Sequence 1 Protein
dc.subjectNeoplasm Transplantation
dc.subjectOncogenes
dc.subjectPrecursor T-Cell Lymphoblastic Leukemia-Lymphoma
dc.subjectProtein Binding
dc.subjectProto-Oncogene Proteins c-myc
dc.subjectRepressor Proteins
dc.subjectResponse Elements
dc.subjectThymocytes
dc.subjectTreatment Outcome
dc.subjectZebrafish
dc.subjectZebrafish Proteins
dc.typeArticle
dc.contributor.departmentMEDICINE
dc.description.doi10.1084/jem.20170484
dc.description.sourcetitleJournal of Experimental Medicine
dc.description.volume215
dc.description.issue7
dc.description.page1929-1945
dc.published.statePublished
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