Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

33 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A new type of pathogenic transcription factor mutation targeting interferon regulatory factor 4 (IRF4) in human lymphoma

ABSTRACT: RNA sequencing of mouse splenic B cell transfected with WT and T95R mutated IRF4. T95R mutation attenuates the plasma cell differentiation program in mouse splenic B cells

INSTRUMENT(S): Illumina HiSeq 4000

ORGANISM(S): Mus musculus

SUBMITTER: Vedran Franke

PROVIDER: E-MTAB-12352 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

A new type of pathogenic transcription factor mutation targeting interferon regulatory factor 4 (IRF4) in human lymphoma

Project description:We report the characterization of a recurrent somatic mutation c.295T>C (p.C99R) in the Interferon Regulatory Factor 4 (IRF4) gene in human lymphoma in the α3-recognition helix of the IRF4 DNA-binding domain. IRF4-C99R fundamentally alters IRF4 DNA-binding, combining loss-of-binding at canonical IRF motifs and neomorph gain-of-binding at canonical and non-canonical IRF composite elements (CEs). IRF4-C99R thoroughly modifies IRF4 function, blocking IRF4-dependent plasma cell induction, and specifically up-regulating lymphoma-specific genes in a degenerate Activator Protein-1 (AP-1)-IRF-CE (AICE)-dependent manner.

2023-07-21 | E-MTAB-12522 | biostudies-arrayexpress

Intrinsic transcriptional heterogeneity in B cells controls early class switching to IgE

Project description:'Non-coding transcripts originating upstream of the immunoglobulin constant region (I-transcripts) are required to direct activation-induced deaminase to initiate class switching in B cells. Differential regulation of I and I1 transcription in response to interleukin-4 (IL-4), hence class switching to IgE and IgG1, is not fully understood. Here we combine novel mouse reporters and single-cell RNA-seq to reveal the heterogeneity in IL-4 induced I-transcription. Transgenic mice were generated with one allele labelled with an eGFP fluorescent reporter gene in the first exon of the gamma-1 non-coding RNA and one allele with a tdTom fluorescent reporter gene in the first exon of the epsilon non-coding RNA. Ex vivo splenic B cells from these mice were stimulated with IL-4, lipopolysaccharide and B cell activating factor. After 24 hours culture, cell were sorted according to their fluorescence and used for single-cell mRNA-sequencing. Two independent experiments were performed (labelled as ''batch 1'' and ''batch 2'').'

2016-12-08 | E-MTAB-4825 | biostudies-arrayexpress

RNA-seq analyses of murine naïve B-cells transduced by retroviral vectors driving expression of MYD88 L265P and SPI1 (WT or mutant) alone or in combination

Project description:To investigate potential oncogenic cooperation of MYD88 and SPI1 mutations on cellular proliferation and B-cell differentiation

2019-05-03 | E-MTAB-7882 | biostudies-arrayexpress

microRNA expression profile of activated primary B cells and miR181b overexpressing primary B cells

Project description:This SuperSeries is composed of the following subset Series: GSE12156: Murine spleen B cells miR181b vs control (G4122A) GSE12158: Murine spleen B cells miR181b vs control (G4122F) GSE12176: microRNA expression profile of activated versus non activated primary B cells Refer to individual Series

2008-08-20 | E-GEOD-12186 | biostudies-arrayexpress

Differentiation of DLBCL induced by HDAC inhibitors is associated with sensitization to proteasome inhibition

Project description:Epigenetic modifying enzymes are commonly mutated in diffuse large B cell lymphoma (DLBCL), suggesting that epigenetic regulation is an important factor in DLBCL pathogenesis and a potential target for therapy. We developed resistant cell lines to histone deacetylase inhibitors (HDACi), one such epigenetic therapy, in order to define mechanisms of response and resistance. Strikingly, using gene expression and metabolic profiling, we found that development of HDACi resistance was associated with differentiation toward a plasmablast-like phenotype. Differentiation correlated with decreased B cell receptor signaling, increased ER stress and activation of the unfolded protein response, and increased sensitivity to proteasome inhibitors. Importantly, we found evidence of differentiation in lymphoma biopsies from patients treated with HDACi. Together, these data show, for the first time, that HDACi are differentiating agents in lymphoma and may be used to prime DLBCL for targeted therapy including proteasome inhibitors. Gene expression in DLBCL cells from tumor biopsies after 15 days panobinostat therapy

2016-08-01 | E-GEOD-59308 | biostudies-arrayexpress

Halobacterium growth

Project description:We report detailed characterization of physiological changes encoded by 63% of all genes within the archaeon Halobacterium salinarum subsp. NRC-1 during routine laboratory growth. While the majority of these changes occur during the transition from rapid exponential growth to the stationary phase, we were also able to detect transient changes in gene expression. This demonstrated the presence of several additional albeit subtle physiological states that exist beyond what might be anticipated from a direct interpretation of the growth profile. Changes in the abundance of several key intracellular metabolites over the growth curve corroborated observations of changes in gene expression of enzymes that catalyze their synthesis. Next, we investigated the roles of general transcription factors (GTFs) in mediating these global growth-associated gene expression changes. This revealed numerous phenotypic perturbations including slowed growth, gas vesicle biogenesis deficiency and morphologic abnormalities upon the overexpression of a single GTF - TBPd. These phenotypes were quantified and were attributed to a perturbation in the regulation of aconitase. Importantly, our results demonstrate why an experiment design as simple as a simple batch culture can be enormously informative of activities and interrelationships of a large fraction of all genes in a microbe. This SuperSeries is composed of the following subset Series: GSE14832: Halobacterium growth in standard growth media: time course GSE14835: Halobacterium growth with added uracil: time course GSE14836: Halobacterium delta-ura3 growth with added uracil: time course Refer to individual Series

2010-02-10 | E-GEOD-14976 | biostudies-arrayexpress

Murine spleen B cells miR181b vs control (G4122A)

Project description:Transcriptional profile of mouse primary spleen B cells overexpresing miR181b-GFP vectors compared to B cells overexpressing control-GFP vectors Keywords: Genetic modification Two-condition experiment: B-miR181b vs. B-control. Biological replicates: 1 control, 1 miR181b.

2008-08-20 | E-GEOD-12156 | biostudies-arrayexpress

The Aurora B kinase and the polycomb protein Ring1B combine to regulate active promoters in quiescent lymphocytes [RNA-Seq]

Project description:Expression profiling of resting B cells to classify active and silent genes based on expression levels 4 biological replicates of mRNA extracted from freshly purified mouse CD43 negative resting B cells

2013-09-27 | E-GEOD-42704 | biostudies-arrayexpress

Effects of EDAG knockdown on gene expression profiles in human erythroid cells

Project description:To investigate the effects of EDAG knockdown on gene exrpession profile in human cord blood CD34+ cells with EPO treatment with microarray assay. Freshly isolated human cord blood CD34+ cells were pre-activated for 24 hours and then infected with EDAG RNAi lentivirus or control lentivirus for 3 times within 24 hours. Then the cells were cultured in the presence of EPO to induce erythroid differentiation. Four days later, the cells were harvested for microarray test. The microarray showed that 3149 differentially expressed genes in siEDAG group compared to control group.The altered genes were associated with gene exrpression, cell cycle and hematopoietic differentiation. These data show that EDAG knckdown led to down-regulation of erythroid genes which are activated by GATA1. Human CD34+ cells infected with EDAG RNAi or control lentivirus were treated with EPO (5U/ml) for 4 days and gene expression were measured using Agilent human whole Genome 8*60K array. Two replicates.

2013-11-06 | E-GEOD-46720 | biostudies-arrayexpress

Expression data from untreated vs. BMP4-treated cultured wild-type and MuSK null muscle cells (myoblasts and myotubes)

Project description:Bone morphogenic proteins (BMPs) function in virtually all tissues with cell-type specific outcomes. Since there are a relatively small number of BMP receptors this exquisite signaling specificity requires additional molecules to regulate the output of this pathway. We demonstrated that the receptor tyrosine kinase MuSK that is selectively expressed in muscle and plays a critical role in synapse formation and maintenance binds to BMP4 and related BMPs. Since BMPs regulate the transcription of a set of genes, we performed microarrays for wild-type and MuSK null muscle cells to test if MuSK regulates BMP responses in muscle cells. We shought to determine if MuSK regulates BMP responses in muscle cells and if the cell context made any difference in MuSK regulation of BMP pathway. To test this, expression profiles of untreated vs. BMP4-treated undifferentiated myoblast and differentiated myotube cultures were generated for both wild-type and MuSK-null genotypes. All conditions were done in triplicates. In total 24 arrays were analyzed.

2015-08-03 | E-GEOD-59567 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data