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Chip-seq of EZH2 and VAV1 in 24hr differentiated Th1 and Th2 cells with or without EZH2 or Actin polymerization inhibitors

ABSTRACT: Chip-seq of EZH2 and VAV1 in 24hr differentiated Th1 and Th2 cells with or without EZH2 or Actin polymerization inhibitors

PROVIDER: PRJEB40221 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4567770.fastq.gz	Fastqsanger.gz
	ERR4567771.fastq.gz	Fastqsanger.gz
	ERR4567772.fastq.gz	Fastqsanger.gz
	ERR4567773.fastq.gz	Fastqsanger.gz
	ERR4567774.fastq.gz	Fastqsanger.gz

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Chip-seq of EZH2 and VAV1 in 24hr differentiated Th1 and Th2 cells with or without EZH2 or Actin polymerization inhibitors

Project description:CD4 T helper cells can differentiate to several types of cells like Th1, Th2, Th17 and Treg. This process is directed by cytokines and activation of T cells by specific antigens. This process has its own plasticity and it is directed by epigenetic changes allowing cells to develop and differentiate. In this experiment, we wanted to explore the binding pattern of EZH2 in the first 24 hours of Th cells activation and differentiation side by side with VAV1 binding pattern to understand the importance of actin polymerization factors in this process.

2021-08-28 | E-MTAB-9524 | biostudies-arrayexpress

RNA-seq of murine Th1 and Th2 cells differentiated for 24hr with or without the presence of actin and EZH2 inhibitors

Project description:CD4 T helper cells can differentiate to several types of cells like Th1, Th2, Th17 and Treg. This process is directed by cytokines and activation of T cells by specific antigens. This process has its own plasticity and it is directed by epigenetic changes allowing cells to develop and differentiate. In this experiment, we wanted to explore if EZH2 has a transcriptional regulation in the first day of differentiation. To study this we performed RNA-seq with or without UNC1999, an EZH2 inhibitor. Moreover, we wanted to learn the interaction between EZH2 and nuclear Actin, so Cytochalasin B was added to look for similar transcriptional pattern.

2021-08-28 | E-MTAB-9523 | biostudies-arrayexpress

Genome-wide analysis of gene expression in VAV1-/- versus VAV1+/+ bone marrow (BM)-macrophages

Project description:Analysis of differential gene expression profiles in VAV1-/- versus VAV+/+ BM-macrophages , respectively. A distinct expression profile in VAV1-/- versus VAV1+/+ (wild-type) BM-macrophages allows to resolve molecular mechanisms. Total RNA was obtained froms BM-macrophages of VAV1+/+ and VAV1-/- mice

2013-03-08 | E-GEOD-36123 | biostudies-arrayexpress

Genome-wide analysis of gene expression in VAV1-/- versus VAV1+/+ bone marrow (BM)-macrophages

2013-03-08 | GSE36123 | GEO

RNA-seq of murine Th1 and Th2 cells differentiated for 24hr with or without the presence of actin and EZH2 inhibitors

Project description:RNA-seq of murine Th1 and Th2 cells differentiated for 24hr with or without the presence of actin and EZH2 inhibitors

| PRJEB40220 | ENA

EXPRESSION OF VAV1 IN GLIOBLASTOMA MULTIFORME

Project description:Background: Even though much progress has been made in the understanding of the molecular nature of glioma, the survival rates of patients affected of this tumour have not changed significantly during these years. Thus, a deeper understanding of this malignancy is still needed in order to predict its outcome and improve patient treatment. Here, we report that VAV1, a GDP/GTP exchange factor for Rho/Rac proteins with oncogenic potential that is involved in the regulation of cytoskeletal dynamics and cell migration. Methodology/Principal Findings: VAV1 is overexpressed in 32 patients diagnosed with high-grade glioma. Such overexpression is linked to the parallel upregulation of a number of genes coding for proteins also involved in cell invasion- and migration-related processes. Unexpectedly, immunohistochemical experiments revealed that VAV1 is not expressed in glioma cells. Instead, VAV1 is found in non-tumoral astrocyte-like cells that are located either peritumoraly or perivascularly, suggesting that its expression is linked to synergistic signalling cross-talk between cancer and infiltrating cells. Conclusions/Significance: Interestingly, we show that the pattern of expression of VAV1 is a good prognostic factor to unveil populations of high-grade glioma patients with different survival and progression free survival rates.

2010-09-30 | GSE24072 | GEO

Transcription profiling of lymph node T cells isolated from Ezh2fl/fl or Ezh2 deficient mice to study the role of ezh2 on actin polymerization and cell signaling

Project description:Lymph node T cells isolated from Ezh2fl/fl or Ezh2 deficient mice

2007-11-22 | E-GEOD-1566 | biostudies-arrayexpress

Cancer-associated mutations in VAV1 trigger variegated signaling outputs and drive T cell lymphomagenesis

Project description:Mutations in VAV1, a multifunctional signaling protein essential for T lymphocytes, have been recently found in peripheral T cell lymphoma (PTCL) and other tumors. However, their pathobiological significance remains unsettled. Here, we show that these mutations belong to several subclasses according to the spectra of VAV1 signaling branches deregulated by them. These mutations target both known and new regulatory hotspots as well as transitional activation states of the protein. The most frequent VAV1 mutant subclass drives PTCL formation in mice by exacerbating normal VAV1- dependent signaling responses in follicular helper T cells.

2021-09-01 | GSE165006 | GEO

Affinify Purification of EZH2 and phosphodeficient EZH2 identifies phosphorylation dependent interactions of EZH2

Project description:Overexpression of EZH2 in estrogen receptor negative (ER-) breast cancer promotes metastasis. EZH2 has been mainly studied as the catalytic component of the Polycomb Repressive Complex 2 (PRC2) that mediates gene repression by trimethylating histone H3 at lysine 27 (H3K27me3). However, how EZH2 drives metastasis despite the low H3K27me3 levels observed in ER- breast cancer is unknown. We have shown that in human invasive carcinomas and distant metastases, cytoplasmic EZH2 phosphorylated at T367 is significantly associated with ER- disease and low H3K27me3 levels. Here, we explore the interactome of EZH2 and of a phosphodeficient mutant EZH2_T367A. We identified novel interactors of EZH2, and identified interactions that are dependent on the phosphorylation and cellular localization of EZH2 that may play a role in EZH2 dependent metastatic progression.

2018-07-03 | PXD010073 | Pride

Characterization of the spectrum of trivalent VAV1 mutation-driven tumors using a gene-edited mouse model

Project description:VAV1 mutations have been recently found in peripheral T cell lymphoma and non-small cell lung cancer. To understand their pathogenic potential, we generated a gene-edited mouse model that expresses a Vav1 mutant protein that recapitulates the signaling alterations present the VAV1 mutant subclass most frequently found in tumors. We could not detect any overt tumorigenic process in those mice. However, the concurrent elimination of the Trp53 tumor suppressor gene in them drives T cell lymphomagenesis. This process represents an exacerbation of the normal functions that wild-type Vav1 plays in follicular helper T cells. We also found that, in combination with an oncogenic Kras mutation, the Vav1 mutant version favors progression of non-small cell lung cancer. These data indicate that VAV1 mutations play critical, although highly cell typespecific roles in tumorigenesis. They also indicate that such functions are contingent on the mutational landscape of the tumors involved.

2022-10-12 | GSE189221 | GEO

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