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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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SPIB and BATF provide alternate determinants of IRF4 occupancy in Diffuse Large B-cell Lymphoma linked to disease heterogeneity.

ABSTRACT: Gene expression from OCI-LY3 cells 48hrs after knock down of SPIB. 2 samples analysed (scramble and siRNA knock down), each with a single repeat.

ORGANISM(S): Homo sapiens

SUBMITTER: Matthew Care

PROVIDER: E-GEOD-50015 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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SPIB and BATF provide alternate determinants of IRF4 occupancy in diffuse large B-cell lymphoma linked to disease heterogeneity.

Care Matthew A MA Cocco Mario M Laye Jon P JP Barnes Nicholas N Huang Yuanxue Y Wang Ming M Barrans Sharon S Du Ming M Jack Andrew A Westhead David R DR Doody Gina M GM Tooze Reuben M RM

Nucleic acids research 20140529 12

Interferon regulatory factor 4 (IRF4) is central to the transcriptional network of activated B-cell-like diffuse large B-cell lymphoma (ABC-DLBCL), an aggressive lymphoma subgroup defined by gene expression profiling. Since cofactor association modifies transcriptional regulatory input by IRF4, we assessed genome occupancy by IRF4 and endogenous cofactors in ABC-DLBCL cell lines. IRF4 partners with SPIB, PU.1 and BATF genome-wide, but SPIB provides the dominant IRF4 partner in this context. Upon ...[more]

PMID: 24875472

Similar Datasets

SPIB and BATF provide alternate determinants of IRF4 occupancy in Diffuse Large B-cell Lymphoma linked to disease heterogeneity

Project description:ChIP-seq data for the transcription factors (TFs) IRF4, PU.1 and SPIB from the cell lines OCI-LY3, OCI-LY10 and H929, and BATF from the cell lines OCI-Ly3 and OCI-Ly10. In addition ChIP-seq for the TFs IRF4, PU.1 and SPIB from the cell line OCI-LY3 following transfections of scramble/SPIB-siRNA. ChIP-seq data for the transcription factors (TFs) IRF4, PU.1 and SPIB from the cell lines OCI-LY3, OCI-LY10 and H929, and BATF from the cell lines OCI-Ly3 and OCI-Ly10. In addition ChIP-seq for the TFs IRF4, PU.1 and SPIB from the cell line OCI-LY3 following transfections of scramble/SPIB-siRNA.

2014-06-03 | E-GEOD-56857 | biostudies-arrayexpress

SPIB and BATF provide alternate determinants of IRF4 occupancy in Diffuse Large B-cell Lymphoma linked to disease heterogeneity.

Project description:Gene expression from OCI-LY3 cells 48hrs after knock down of SPIB.

2014-06-03 | GSE50015 | GEO

SPIB and BATF provide alternate determinants of IRF4 occupancy in Diffuse Large B-cell Lymphoma linked to disease heterogeneity

2014-06-03 | GSE56857 | GEO

SPIB and BATF provide alternate determinants of IRF4 occupancy in diffuse large B-cell lymphoma linked to disease heterogeneity.

Project description: Not available

| S-EPMC4081075 | biostudies-literature

BATF-JUN is critical for IRF4-mediated transcription in T cells

Project description:Interferon regulatory factor 4 (IRF4) is an IRF family transcription factor with critical roles in lymphoid development and in regulating the immune response. IRF4 binds DNA weakly owing to a carboxy-terminal auto-inhibitory domain, but cooperative binding with factors such as PU.1 or SPIB in B cells increases binding affinity, allowing IRF4 to regulate genes containing ETS–IRF composite elements (EICEs; 5'-GGAAnnGAAA-3'). Here we show that in mouse CD4+ T cells, where PU.1/SPIB expression is low, and in B cells, where PU.1 is well expressed, IRF4 unexpectedly can cooperate with activator protein-1 (AP1) complexes to bind to AP1–IRF4 composite (5'-TGAnTCA/GAAA-3') motifs that we denote as AP1–IRF composite elements (AICEs). Moreover, BATF–JUN family protein complexes cooperate with IRF4 in binding to AICEs in pre-activated CD4+ T cells stimulated with IL-21 and in TH17 differentiated cells. Importantly, BATF binding was diminished in Irf4-/- T cells and IRF4 binding was diminished in Batf-/- T cells, consistent with functional cooperation between these factors. Moreover, we show that AP1 and IRF complexes cooperatively promote transcription of the Il10 gene, which is expressed in TH17 cells and potently regulated by IL-21. These findings reveal that IRF4 can signal via complexes containing ETS or AP1 motifs depending on the cellular context, thus indicating new approaches for modulating IRF4-dependent transcription. Genome-wide transcription factors mapping and binding of IRF4, BATF, IRF8, STAT3, JUN etc in WT, Irf4-/- and Batf-/- mice in different cell types (B cells, CD4+ T cells and TH17 cells) cultured with or without IL-21 was conducted. RNA-Seq is conducted in mouse B cells, CD4+ T cells, TH1/TH2/TH9/TH17/Treg.

2012-09-18 | E-GEOD-39756 | biostudies-arrayexpress

BATF-JUN is critical for IRF4-mediated transcription in T cells

2012-09-18 | GSE39756 | GEO

BATF-JUN is critical for IRF4-mediated transcription in T cells.

Project description: Not available

| S-EPMC3537508 | biostudies-literature

BATF and IRF4 cooperate to counter exhaustion in tumor-infiltrating CAR T cells.

Project description: Not available

| S-EPMC8319109 | biostudies-literature

Co-addiction to IRF4 and SPIB in ABC-DLBCL

Project description:RNA interference screens identified the transcription factor IRF4 as essential for the survival of the activated B-cell-like subtype of diffuse large B-cell lymphoma (ABC-DLBCL). Analysis of IRF4 genomic targets in ABC-DLBCL and Multiple Myeloma (MM) revealed that IRF4 regulates distinct networks in these cancers. IRF4 peaks in ABC-DLBCL, but not MM, were enriched for a composite ETS-IRF DNA motif that can be bound by heterodimers of IRF4 and the ETS-family transcription factor SPIB, whose expression is also essential for ABC-DLBCL survival. Gene expression and ChIP-Seq analysis identified essential genes co-regulated by IRF4 and SPIB. Together, these factors regulate a critical oncogenic loop by activating CARD11, which controls ABC-DLBCL survival via the NF-kB pathway. The interaction between IRF4 and SPIB presents an attractive therapeutic target in this aggressive lymphoma.

2012-08-16 | GSE32456 | GEO

Epstein-Barr virus nuclear antigen 3C binds to BATF/IRF4 or SPI1/IRF4 composite sites and recruits Sin3A to repress CDKN2A.

Project description: Not available

| S-EPMC3890834 | biostudies-literature