Ontology highlight
ABSTRACT:
PROVIDER: PRJNA131661 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:ChIP-on-chip experiment from Ramos cells to analyze genome-wide CRTC2 binding sites in germinal center B cells. The goal was to combine information from our ChIP-on-chip and expression array analyses to compile a list of CRTC2 target genes.
2012-01-01 | GSE23170 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE23169: Transcriptional profiling of Ramos germinal center B cells GSE23170: ChIP-on-chip experiment from Ramos cells to analyze genome-wide CRTC2 binding sites in germinal center B cells Refer to individual Series
2012-01-01 | E-GEOD-23171 | biostudies-arrayexpress
Project description:ChIP-on-chip experiment from Ramos cells to analyze genome-wide CRTC2 binding sites in germinal center B cells. The goal was to combine information from our ChIP-on-chip and expression array analyses to compile a list of CRTC2 target genes. CRTC2 was immunoprecipitated from sheared chromatin isolated from untreated Ramos cells using 2 antibodies which recognize distinct epitopes on the CRTC2 protein. Immunoprecipitates were compared to total input chromatin. 2 biological replicates were performed for each antibody.
2012-01-01 | E-GEOD-23170 | biostudies-arrayexpress
Project description:Transcriptional profiling of Ramos germinal center B cells, comparing untreated cells to cells treated with etoposide, and untreated cells to cells treated with anti-IgM. Both treatments, engagement of the B-cell receptor with anti-IgM and induction of DNA double-strand breaks with etoposide, result in phosphorylation and cytoplasmic sequestration of CRTC2, and cause downregulation of known CRTC2 target gene TCL1. The goal of these experiments was to determine what other genes are downregulated by both of these CRTC2-inactivating treatments, and to compare this list to the list of genes whose promoters were occupied by CRTC2 in our ChIP-on-chip assay. Untreated samples vs. etoposide-treated samples, untreated samples vs. anti-IgM-treated samples. Each comparison was done in biological triplicate plus dye swap.
2012-01-01 | E-GEOD-23169 | biostudies-arrayexpress
Project description:The roles of translational control in the immune system are poorly understood. In this study, we performed CRISPR/Cas9-mediated functional screening of RNA helicases in an in vitro system of plasma cell differentiation and identified Dhx29 as a critical regulator of this process. Mice with B cell-specific deletion of Dhx29 exhibited severely impaired germinal center B cell formation, plasma cell differentiation, and antibody production. Mechanistically, Dhx29 promotes translation of Tcf3 and Tle3 via binding to 5’UTRs of those mRNAs. In the absence of Dhx29, B cells exhibit normal proliferation but fail to undergo class switch to IgG1 and differentiation into plasma cells, resulting in impaired antibody production. Ectopic expression of TCF3 and Tle3 largely restores plasma cell differentiation of Dhx29-deficient B cells. Therefore, this study unravels critical roles of Dhx29 in promoting translation of key transcription factors controlling germinal center response and plasma cell differentiation, discovers a previously unrecognized role of Tle3 in plasma cell differentiation, and illustrates the functional importance of translation control in the immune system.
2026-05-06 | GSE317160 | GEO
Project description:The roles of translational control in the immune system are poorly understood. In this study, we performed CRISPR/Cas9-mediated functional screening of RNA helicases in an in vitro system of plasma cell differentiation and identified Dhx29 as a critical regulator of this process. Mice with B cell-specific deletion of Dhx29 exhibited severely impaired germinal center B cell formation, plasma cell differentiation, and antibody production. Mechanistically, Dhx29 promotes translation of Tcf3 and Tle3 via binding to 5’UTRs of those mRNAs. In the absence of Dhx29, B cells exhibit normal proliferation but fail to undergo class switch to IgG1 and differentiation into plasma cells, resulting in impaired antibody production. Ectopic expression of TCF3 and Tle3 largely restores plasma cell differentiation of Dhx29-deficient B cells. Therefore, this study unravels critical roles of Dhx29 in promoting translation of key transcription factors controlling germinal center response and plasma cell differentiation, discovers a previously unrecognized role of Tle3 in plasma cell differentiation, and illustrates the functional importance of translation control in the immune system.
2026-05-06 | GSE317159 | GEO
Project description:Protective immune responses to many pathogens depend on the development of high affinity antibody-producing plasma cells in germinal centers. Transgenic models suggest that there is a stringent affinity-based barrier to plasma cell development. Whether a similar high affinity barrier regulates plasma cell development under physiologic circumstances, and the nature of the plasma cell fate decision has not been defined precisely. Here we use a fate mapping approach to examine the relationship between germinal center (GC) B cells selected to undergo additional rounds of affinity maturation, germinal center pre-plasma cells and plasma cells. The data show that initial plasma cell selection overlaps with germinal center B cell selection, but that the plasma cell compartment accumulates a less diverse and higher affinity collection of antibodies over time. Thus, whereas the GC continues to diversify over time, affinity-based pre-plasma cell selection sieves the germinal center to enable accumulation of a more restricted group of high affinity antibody secreting plasma cells.
2023-11-02 | GSE246382 | GEO
Project description:Transcriptional profiling of Ramos germinal center B cells, comparing untreated cells to cells treated with etoposide, and untreated cells to cells treated with anti-IgM. Both treatments, engagement of the B-cell receptor with anti-IgM and induction of DNA double-strand breaks with etoposide, result in phosphorylation and cytoplasmic sequestration of CRTC2, and cause downregulation of known CRTC2 target gene TCL1. The goal of these experiments was to determine what other genes are downregulated by both of these CRTC2-inactivating treatments, and to compare this list to the list of genes whose promoters were occupied by CRTC2 in our ChIP-on-chip assay.
2012-01-01 | GSE23169 | GEO
Project description:This study aims to characterize the H3K27me3 modification in wild type and Kdm6b B KO pre-Plasma germinal center B cells, and find the potential mechanism of the Kdm6b B KO pre-Plasma germinal center B cells。
2026-01-12 | GSE270617 | GEO
Project description:The roles of translational control in the immune system are poorly understood. In this study, we performed CRISPR/Cas9-mediated functional screening of RNA helicases in an in vitro system of plasma cell differentiation and identified Dhx29 as a critical regulator of this process. Mice with B cell-specific deletion of Dhx29 exhibited severely impaired germinal center B cell formation, plasma cell differentiation, and antibody production. Mechanistically, Dhx29 promotes translation of Tcf3 and Tle3 via binding to 5’UTRs of those mRNAs. In the absence of Dhx29, B cells exhibit normal proliferation but fail to undergo class switch to IgG1 and differentiation into plasma cells, resulting in impaired antibody production. Ectopic expression of TCF3 and Tle3 largely restores plasma cell differentiation of Dhx29-deficient B cells. Therefore, this study unravels critical roles of Dhx29 in promoting translation of key transcription factors controlling germinal center response and plasma cell differentiation, discovers a previously unrecognized role of Tle3 in plasma cell differentiation, and illustrates the functional importance of translation control in the immune system.
2026-05-06 | GSE317659 | GEO