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Expression data from WT and E2A-deficient murine DN2 cells

ABSTRACT: The E2A transcription factors promote the development of thymus-seeding cells but it remains unknown whether these proteins play a role in T lymphocyte lineage specification or commitment. By examining E2A-dependent genes in developing T cells, we will address whether these proteins are involved in these processes.

ORGANISM(S): Mus musculus

PROVIDER: GSE43224 | GEO | 2013/02/01

SECONDARY ACCESSION(S): PRJNA185009

REPOSITORIES: GEO

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Expression data from WT and E2A-deficient murine DN2 cells

Project description:The E2A transcription factors promote the development of thymus-seeding cells but it remains unknown whether these proteins play a role in T lymphocyte lineage specification or commitment. By examining E2A-dependent genes in developing T cells, we will address whether these proteins are involved in these processes. DN2 cells from WT and E2A-deficient murine fetal thymi were FACS sorted. Subsequently RNA was extracted, labelled and hybridized to Affymetrix microarrays. The goal of this study is to investigate E2A-dependent genes in developing T cells

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Project description:The transcription factor E2A is essential for lymphocyte development. In this study, we describe a recurrent E2A gene deletion in at least 70% of patients with Sézary syndrome (SS), a subtype of T cell lymphoma. Loss of E2A results in enhanced proliferation and cell cycle progression via derepression of the proto-oncogene MYC and the cell cycle regulator CDK6. Furthermore, by examining the gene expression profile of SS cells following restoration of E2A expression, we identify a number of E2A-regulated genes that interfere with oncogenic signaling pathways including the Ras pathway. Several of these genes are down-regulated or lost in primary SS tumor cells. These data demonstrate a tumor suppressor function of E2A in human lymphoid cells and could help to develop new treatment strategies for human lymphomas with altered E2A activity.

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Project description:We set out to investigate whether overexpression of the bHLH transcription factor, E2A, is sufficient to drive neural differentiation in mouse embryonic stem cells under non-permissive culture conditions. Having identified that overexpression of specifically E2A homodimers, but not E2A monomers, was sufficient to drive neural differentiation, we sought to identify early downstream targets of E2A during the process of neural commitment using RNA-sequencing.

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