Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Concerted action of Helios and Ikaros balances the strength of B cell receptor signaling and controls the expression of inositol 5-phosphatase SHIP

ABSTRACT: Inositol 5-phosphatase SHIP is differentially expressed in Ikaros and Helios deficient cells. In the absense of Ikaros SHIP is upregulated where as in the absense of Helios it is downregulated. Ikaros binds to the promoter of the SHIP gene. Article provides insight into the mechanisms of action Ikaros employs to regulate BCR signaling. Two replicates of Ikaros deficient and wild type DT40 avian B cells.

ORGANISM(S): Gallus gallus

SUBMITTER: Pekka Kohonen

PROVIDER: E-GEOD-20946 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Concerted action of Helios and Ikaros controls the expression of the inositol 5-phosphatase SHIP.

Alinikula Jukka J Kohonen Pekka P Nera Kalle-Pekka KP Lassila Olli O

European journal of immunology 20100901 9

Ikaros family transcription factors have a key role in lymphoid development, and their aberrant function contributes to a multitude of lymphoid malignancies. Ikaros and Helios bind to similar DNA sequences, and Helios associates with Ikaros-containing chromatin remodeling complexes. Previously, we have shown that loss of Ikaros leads to diminished BCR-signaling strength. In this study, we describe a Helios-deficient chicken DT40 B-cell line with a BCR signaling phenotype that is the opposite to ...[more]

PMID: 20602434

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Project description:"The main goal of the project is to develop a new generation of bioinformatics resources for the integrative analysis of multiple types of omics data. These resources include both novel statistical methodologies as well as user-friendly software implementations. STATegra methods address many aspects of the omics data integration problem such as the design of multiomics experiments, integrative transcriptional and regulatory networks, integrative variable selection, data fusion, integration of public domain data, and integrative pathway analysis. To support method development STATegra uses a model biological system, namely the differentiation process of mouse pre-B-cells. The STATegra consortium generated data focused on a critical step in the differentiation of B lymphocytes, which are key components of the adaptive immune system. Transcription factors of the Ikaros family are central to the normal differentiation of B cell progenitors and their expression increases in response to developmental stage-specific signals to terminate the proliferation of B cell progenitors and to initiate their differentiation. In particular, a novel biological system that models the transition from the pre-BI stage to the pre-BII subsequent stage, where B cell progenitors undergo growth arrest and differentiation, was used. The approach involves a pre-B cell line, B3 , and an inducible version of the Ikaros transcription factor, Ikaros-ERt2. Ikaros factors act to down-regulate genes that drive proliferation and to simultaneously up-regulate the expression of genes that promote the differentiation of B cell progenitors. Hence, in the B3 system, before induction of Ikaros, cells proliferate and their gene expression pattern is similar to proliferating B cell progenitors in vivo. Following Ikaros induction, B3 cells undergo gene expression changes that resemble those that occur in vivo during the transition from cycling to resting pre-B cells, followed by a marked reduction in cellular proliferation and by G1 arrest. On this system the consortium has created a high-quality data collection consisting of a replicated time course using seven different omics platforms: RNA-seq, miRNA-seq, ChIP-seq, DNase-seq, Methyl-seq, proteomics and metabolomics, which is used to assess and to validate STATegra methods."

Dataset Information

Concerted action of Helios and Ikaros balances the strength of B cell receptor signaling and controls the expression of inositol 5-phosphatase SHIP

Publications

Concerted action of Helios and Ikaros controls the expression of the inositol 5-phosphatase SHIP.

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