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ChIP-on-chip experiment from Ramos cells to analyze genome-wide CRTC2 binding sites in germinal center B cells

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE23170 | GEO | 2012/01/01

SECONDARY ACCESSION(S): PRJNA133267

REPOSITORIES: GEO

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ChIP-on-chip experiment from Ramos cells to analyze genome-wide CRTC2 binding sites in germinal center B cells

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

CRTC2 couples genotoxic stress and plasma cell differentiation in the germinal center

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

Transcriptional profiling of Ramos germinal center B cells

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

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Project description:The Chromosome 16 Consortium is integrated in the Human Proteome Project that aims to develop an entire map of the proteins encoded by the human genome following a gene-centric strategy (C-HPP) to make progress in the understanding of human biology in health and disease (B/D-HPP). To do this study four human cell lines were selected, MCF7 epithelial cells, CCD18 colon fibroblasts, Ramos and Jurkat B and T lymphocytes respectively. In particular, this subset includes all the data regarding the Ramos cell line. 3 laboratories contributed to compile all the reported data.

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Project description:The goal of this study is to screen the differential genes between Ramos and Rituximab-resistant Ramos cells, then analyze the significant pathways.

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Project description:Populations of circulating immune cells are maintained in equilibrium through signals that enhance the retention or egress of hematopoietic stem cells (HSCs) from bone marrow (BM). Prostaglandin E2 (PGE2) stimulates HSC renewal and engraftment, for example, via induction of the cAMP pathway. Triggering of PGE2 receptors increases HSC survival in part via the PKA-mediated induction of the CREB signaling pathway. PKA stimulates cellular gene expression by phosphorylating CREB at Ser133 and by promoting the dephosphorylation of the cAMP Responsive Transcriptional Coactivators (CRTCs). We show here that disruption of both CRTC2 and CRTC3 causes embryonic lethality, and that a single allele of either CRTC2 or CRTC3 is sufficient for viability. CRTC2 knockout mice that express one CRTC3 allele (CRTC2/3m mice) develop neutrophilia and splenomegaly in adulthood due to the up-regulation of Granulocyte-Colony Stimulating Factor (G-CSF); these effects are reversed following administration of neutralizing anti-G-CSF antiserum. Adoptive transfer of CRTC2/3m BM conferred the splenomegaly/neutrophilia phenotype on WT recipients. Indeed, targeted disruption of both CRTC2 and CRTC3 in stromal cells with a mesenchymal Prx1-Cre transgene also promoted this phenotype. Depletion of CRTC2/3 was found to decrease the expression of Suppressor of Cytokine Signaling 3 (SOCS3), leading to increases in STAT3 phosphorylation and to the induction of CEBPb, a key regulator of the G-CSF gene. As small molecule inhibition of JAK activity disrupted CEBPb induction and reduced G-CSF expression in CRTC2/3m stromal cells, our results demonstrate how cross-coupling between the CREB/CRTC and JAK/STAT pathways contributes to BM homeostasis.

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