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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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Similar Datasets

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

Control of plasma membrane-associated actin polymerization specifies the pattern of the cell wall in xylem vessels.

Project description:Cell wall patterning is central to determining the shape and function of plant cells. Protoxylem and metaxylem vessel cells deposit banded and pitted cell walls, respectively, which enable their distinctive water transport capabilities, but the mechanisms that specify which cell wall pattern is laid down remain unknown. Here, we show that the pitted cell wall pattern in metaxylem vessels is specified by transcriptional control of actin polymerization. A newly isolated allele of KNOTTED-like homeobox transcription factor 7 (KNAT7) was associated with the formation of banded cell walls in metaxylem vessels. To identify the genes responsible for altering the cell wall pattern in knat7 xylem vessels, we performed an RNA-seq analysis of knat7. We used in vitro cultures of hypocotyls and cotyledons because the population of differentiating xylem cells in intact roots is tiny and these methods efficiently induce ectopic differentiation of xylem vessel elements. Formin Homology Domain-Containing Protein 11 (FH11) was upregulated in knat7 metaxylem, but expressed only in protoxylem vessels in wild-type plants. Loss of FH11 suppressed the knat7 phenotype. Conversely, ectopic overexpression of FH11 in metaxylems mimicked the knat7 phenotype. FH11 function required its plasma membrane anchoring and the actin polymerization activity. Actin polymerization by FH11 at the plasma membrane caused the dispersion of activated ROP GTPases, the determinant of pit formation. These results suggest that decontrol of actin polymerization at the plasma membrane abolishes the pitted cell wall formation and promotes the formation of banded cell walls in metaxylem vessels. This study unveils the importance of the proper control of actin polymerization on cell wall pattern specification.

2025-01-15 | GSE286145 | GEO

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

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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