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ChIP-chip from lymph node-derived primary lymphocytes with anti-E2F2 and anti-SV40TAg

ABSTRACT: E2F2 is essential for the maintenance of T lymphocyte quiescence. To identify the full set of E2F2 target genes, and to gain further understanding of the role of E2F2 in transcriptional regulation, we have performed ChIP-chip analyses across the genome of lymph node-derived T lymphocytes. Here we show that during quiescence, E2F2 binds the promoters of a large number of genes involved in DNA metabolism and cell cycle regulation, concomitant with their transcriptional silencing.

ORGANISM(S): Mus musculus

PROVIDER: GSE53888 | GEO | 2014/01/09

SECONDARY ACCESSION(S): PRJNA233975

REPOSITORIES: GEO

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ChIP-chip from lymph node-derived primary lymphocytes with anti-E2F2 and anti-SV40TAg

Project description:E2F2 is essential for the maintenance of T lymphocyte quiescence. To identify the full set of E2F2 target genes, and to gain further understanding of the role of E2F2 in transcriptional regulation, we have performed ChIP-chip analyses across the genome of lymph node-derived T lymphocytes. Here we show that during quiescence, E2F2 binds the promoters of a large number of genes involved in DNA metabolism and cell cycle regulation, concomitant with their transcriptional silencing. We performed 3 ChIP-chip experiments with an antibody against E2F2 and another 3 ChIP-chip experiments with an antibody against SV40TAg (irrelevant antibody).

2014-01-09 | E-GEOD-53888 | biostudies-arrayexpress

Analysis of E2F2 interacting proteins

Project description:In an attempt to identify proteins interacting with transcription factor E2F2, proteins extracted from HA-E2F2 overexpressing HEK293T cells were were subjected to immunoprecipitation (IP) with an anti-HA antibody or, as a negative control (NegCt), with an anti-T antibody. Immunoprecipitated proteins were eluted, digested with trypsin, and the resulting peptides were analyzed by LC-MS/MS. The whole procedure was repeated several times in an attempt to gauge reproducibility (nine replicates of the anti-HA IP and six replicates of the control IP).

2013-01-18 | PXD000026 | Pride

Chromatin immunopreciptiation of human BJ-T cells with E2F2 and EwF4 antibodies

Project description:ChIp on chip with E2F2 or E2F4 antibodies on BJ-T cells.

2009-11-16 | E-MEXP-2169 | biostudies-arrayexpress

Increased metastasis with loss of E2F2 in Myc-driven tumors

Project description:In human breast cancer, mortality is associated with metastasis to distant sites. Therefore, it is critical to elucidate the biological mechanisms that underlie tumor progression and metastasis. Using signaling pathway signatures we previously predicted a role for E2F transcription factors in Myc induced tumors. To test this role we interbred MMTV-Myc transgenic mice with E2F knockouts. Surprisingly, we observed that the loss of E2F2 sharply increased the percentage of lung metastasis in MMTV-Myc transgenic mice. Examining the gene expression profile from these tumors, we identified genetic components that were potentially involved in mediating metastasis. These genes were filtered to uncover the genes involved in metastasis that also impacted distant metastasis free survival in human breast cancer. In order to elucidate the mechanism by which E2F2 loss enhanced metastasis we generated knockdowns of E2F2 in MDA-MB-231 cells and observed increased migration in vitro and increased lung colonization in vivo. We then examined genes that were differentially regulated between tumors from MMTV-Myc, MMTV-Myc E2F2-/-, and lung metastases samples and identified PTPRD. To test the role of PTPRD in E2F2-mediated breast cancer metastasis, we generated a knockdown of PTPRD in MDA-MB-231 cells. We noted that decreased levels of PTPRD resulted in decreased migration in vitro and decreased lung colonization in vivo. Taken together, these data indicate that E2F2 loss results in increased metastasis in breast cancer, potentially functioning through a PTPRD dependent mechanism.

2016-08-08 | GSE71815 | GEO

Increased metastasis with loss of E2F2 in Myc-driven tumors

2016-08-08 | E-GEOD-71815 | biostudies-arrayexpress

Recombinant anti-monkey CD3 immunotoxin depletes peripheral lymph node T lymphocytes more effectively than rabbit anti-thymocyte globulin in naive baboons.

Project description: Not available

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Metinel node--the first lymph node draining a metastasis--contains tumor-reactive lymphocytes.

Project description: Not available

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siRNA-mediated E2F1 and E2F2 silencing in growth-stimulated prostate cancer cells

Project description:To study the effect of siRNA-mediated E2F1 and E2F2 silencing in growth-stimulated prostate cancer cells.

2021-10-14 | GSE172094 | GEO

Expression data from lenses triply deficient for E2F1, E2F2, and E2F3 transcription factors

Project description:The E2F family consists of transcriptional repressors and activators that control cell proliferation. In the classic paradigm of cell cycle regulation, the three activators, E2F1, E2F2 and E2F3, are invariably depicted as the final components of a CDK/Rb signaling cascade that executes the transcriptional program necessary to commit cells to enter S phase. Unexpectedly, we find through analysis of Affymetrix expression array data that mature lens epithelial cells deficient for E2F1-3 fail to repress cell cycle-regulated genes (and other targets of E2F) and that this corresponds with subsequent apoptosis and cellular collapse in the lens. Murine lenses were collected at two stages of development for RNA extraction and hybridization on Affymetrix microarrays. Our aim was to determine key events that lead to cellular collapse of lenses triply deficient for E2F1, E2F2, and E2F3 in neonates.

2010-06-23 | E-GEOD-16533 | biostudies-arrayexpress

Analysis of E2F2 interacting proteins

2016-03-09 | MSV000079567 | MassIVE

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