IRF4 silencing gene expression study
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1226622 | ENA |
REPOSITORIES: ENA
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Project description:A gene expression study was conducted to understand the role of IRF4 in ABC like lymphomas. For this, IRF4 was silenced in TMD8 cell line alongside a control vector. Treated and control cell lines were subjected to gene expression measurement. Pathway analysis of differentially expressed gens showed antigen presentation pathways to be differentially regulated.
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Project description:Multiple Myeloma (MM) arises through oncogenic transformation of immunoglobulin-secreting
plasma cells. MM often co-opts the endoplasmic-reticulum (ER) stress mitigator, inositol
requiring enzyme 1 (IRE1), to sustain malignant growth. While certain MMs require enzymatic
IRE1-dependent activation of the ER-homeostatic transcription factor XBP1s, others display
nonenzymatic dependency on IRE1 that is not yet mechanistically understood. Interferon
regulatory factor 4 (IRF4) stimulates gene programs that promote immune-cell proliferation and cell cycle control by IRE1 in MM. Here we show that IRF4 acts as a key conduit of nonenzymatic cell cycle control by IRE1 in MM. IRE1 silencing increased inhibitory phosphorylation of IRF4, disrupting its chromatin-binding activity and mRNA transcription. IRF4 knockdown recapitulated, whereas IRF4 repletion reversed the anti-proliferative phenotype of IRE1 silencing. Functional studies revealed that IRF4 engages the E2F1 and CDC25A genes and promotes CDK2 activation to drive cell cycle progression. Our results advance mechanistic understanding of IRE1 and IRF4 in MM.
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Project description:The aim of experiment was to study on genome-wide level IRF4 target genes in chicken DT40 B cell line, by comparizon of gene expression profiles of IRF4-deficient DT40 cells with WT IRF4 DT40 cells .
2017-01-01 | GSE56165 | GEO
Project description:Multiple myeloma (MM) is an incurable malignancy of plasma cells that exploits transcriptional networks driven by IRF4. To discover unique molecular vulnerabilities in MM centered on IRF4, we employ a multi-omics approach integrating functional genomics screening, spatial proteomics, and global chromatin mapping. We find that ARID1A, a member of the SWI/SNF chromatin remodeling complex, is both required for IRF4 expression and functionally associated with IRF4 protein on chromatin. Deletion of Arid1a in activated murine B cells thwarts subsequent plasma cell differentiation by disrupting IRF4-dependent transcriptional networks, therefore defining ARID1A as a novel plasma cell vulnerability. Targeting ARID1A-dependent SWI/SNF activity via SMARCA2/4 inhibition induces a rapid loss of IRF4-target gene expression and quenches global amplification of oncogenic gene expression driven by MYC, resulting in profound toxicity to MM cells. Notably, MM patients with aggressive disease have markers of SWI/SNF activity, and SMARCA2/4 inhibitors retain their activity in immunomodulatory drug (IMiD)-resistant MM cells. To fully harness the potential of these drugs, we use combinatorial drug screens to uncover profound synergistic toxicity between SMARCA2/4 and MEK inhibitors. Thus, targeting SWI/SNF activity potently represses an IRF4-MYC feed forward loop and provides a feasible path to effectively treat this incurable disease.
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Project description:Gene expression profiling of murine irf4-/- and irf4+/+ splenic B cells identifies genes regulated by the transcription factor IRF4 in quiescent mature B cells.
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Project description:The goal of this gene expression study was to identify genes whose expression depends on the transription factor IRF4 by knocking down it's expression using shRNA in two IRF4+ myeloma cell lines. Keywords: time series design
2008-07-07 | GSE9067 | GEO
Project description:The goal of this gene expression study was to identify genes whose expression depends on the transription factor IRF4 by knocking down it's expression using shRNA in two IRF4+ myeloma cell lines. Keywords: time series design Two myeloma lines were analyzed over a time course of IRF4-targeted shRNA induction. There are 3 time courses: two using KMS12 (biological replicates) and one with SKMM1. Within each time course there are technical replicates.
2010-05-26 | E-GEOD-9067 | biostudies-arrayexpress
Project description:Transcriptional profiling of T-cells isolated from spleen of IRF4 -/- mice and cultured under Th17 polarizing conditions for 42 hrs compared to cells similarly isolated and cultured from spleen of IRF4 +/- mice. The aim of the study was to identify global misexpression of genes in IRF4 -/- cells and hence identify key pathways regulated by IRF4 during Th17 differentiation. Two-condition experiment, IRF4 -/- vs IRF4 +/- Th17 cells at 42hrs. Biological replicates: 3 for each condition
2012-09-13 | E-GEOD-40726 | biostudies-arrayexpress