Expression data from neutrophils from wild-type and Jdp2-/- mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE42063 | GEO | 2012/11/30
SECONDARY ACCESSION(S): PRJNA179067
REPOSITORIES: GEO
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Project description:Jdp2 is a member of the AP-1 family and suppresses histone acetyltransferase activity. We used microarrays to examine the gene expression pattern of neutrophil form Jdp2-/- mice. Bone marrow CD11b+Ly6Clo Ly6G+ neutrophils form wild-type and Jdp2-/-mice were sorted by FACS, followed by RNA extraction. Affymetrix microarrays were used to analyze the mRNA expression.
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2018-06-18 | GSE115465 | GEO
Project description:A substantial subset of patients with T-cell acute lymphoblastic leukemia (T-ALL) develops resistance to steroids and succumb 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 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 shRNA knockdown leads to apoptosis. Mechanistically, JDP2 regulates pro-survival 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.
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Project description:Acute myeloid leukemia (AML) is a hematological malignancy characterized by the abnormal proliferation and accumulation of immature myeloid cells in the bone marrow. Inflammation plays a crucial role in AML progression, but excessive activation of inflammatory pathways can also trigger cell death. IRF2BP2 is a chromatin regulator that has been implicated in AML pathogenesis, although its precise role in this disease is not fully understood. In this study, we demonstrate that in AML cells IRF2BP2 interacts with the transcriptional heterodimer ATF7/JDP2, which is involved to activate inflammatory pathways in AML cells. We show that IRF2BP2 is recruited by the ATF7/JDP2 dimer to chromatin and counteracts its gene activating function. Loss of IRF2BP2 leads to the overactivation of inflammatory pathways, resulting in immediate cell death. Our findings suggest that a delicate balance of activating and repressive transcriptional mechanisms establishes a pro-oncogenic inflammatory set-up in AML cells, and that manipulation of the ATF7/JDP2-IRF2BP2 regulatory axis may offer a potential vulnerability for AML treatment. Thus, our study provides new insights into the molecular mechanisms underlying AML pathogenesis and identifies a potential therapeutic target for AML treatment.
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