Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single cell RNA-seq analysis of normal, premalignant state and tumor mouse models of VAV1-MYOF gene fusion in Peripheral T-Cell Lymphoma

ABSTRACT: Single cell RNA-seq analysis of normal, premalignant state and tumor mouse models of VAV1-MYOF gene fusion in Peripheral T-Cell Lymphoma

PROVIDER: PRJNA701571 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Bulk transcriptomic analysis of normal, premalignant state and tumor mouse models of VAV1-MYOF gene fusion in Peripheral T-Cell Lymphoma

Project description:The goal of this study is to identify transcriptomic effects of VAV1-MYOF expression in mouse CD4+ T lymphocytes in tumor development as well as changes in the microenvironment. To this end, mice conditionally expressing VAV1-MYOF were crossed with the CD4CreERT2 line or CD4-Cre, under the control of the mouse Cd4 promoter to generate CD4 specific VAV1-MYOF models. In inducible models, mice were treated with vehicle only or Tamoxifen to induce expression of VAV1-MYOF1 in CD4+ T cells. CD4CreERT2 mice were included as a negative control. Total RNA was extracted from whole spleen samples or CD4+ T cells isolated by single cell suspensions of spleen by negative selection using the mouse naive CD4+ T Cell Isolation Kit (Milteny#130-104-453) according to the manufacturer’s protocol. Standard Illumina poly-A RNA seq was performed.

2021-05-12 | GSE166671 | GEO

Single cell RNA-seq analysis of normal, premalignant state and tumor mouse models of VAV1-MYOF gene fusion in Peripheral T-Cell Lymphoma

Project description:The goal of this study is to identify transcriptomic effects of VAV1-MYOF expression in mouse CD4+ T lymphocytes and tumor progression in TET2KO and TET2WT backgrounds. To this end, mice conditionally expressing VAV1-MYOF were crossed with the CD4CreERT2 line or CD4-Cre, under the control of the mouse Cd4 promoter to generate CD4 specific VAV1-MYOF models. In inducible models, mice were treated with vehicle only or Tamoxifen to induce expression of VAV1-MYOF1 in CD4+ T cells. Mice were crossed with CD4-CreERT2 Tet2f/f to obtain the experimental phenotypes. Whole spleen samples were processed and single cell suspensions were analyzed using scRNA-seq technologies.

2021-05-12 | GSE166672 | GEO

Bulk transcriptomic analysis of normal, premalignant state and tumor mouse models of VAV1-MYOF gene fusion in Peripheral T-Cell Lymphoma

Project description:Bulk transcriptomic analysis of normal, premalignant state and tumor mouse models of VAV1-MYOF gene fusion in Peripheral T-Cell Lymphoma

| PRJNA701570 | ENA

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

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

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

Vav1 regulates T cell activation through a feedback mechanism and crosstalk between the T cell receptor and CD28 in CD3-stimulated T cells

Project description:Vav1, a Rac/Rho guanine nucleotide exchange factor and a critical component of the T cell receptor (TCR) signaling cascade, is rapidly tyrosine phosphorylated in response to T cell activation. Previous studies using Vav1 knockout models have demonstrated its importance in TCR signaling. Although Vav1 has established roles in proliferation, cytokine secretion, Ca2+ responses, and cytoskeletal regulation, its function in the regulation of phosphorylation of TCR components, including the ζ chain, the CD3 δ, ε, γ chains, and the associated kinases Lck, and ZAP-70 is not well established. To obtain a more comprehensive picture of the role of Vav1 in receptor proximal signaling, we performed a wide-scale characterization of Vav1-dependent tyrosine phosphorylation events using quantitative phosphoproteomic analysis of Vav1-deficient T cells across a time course of TCR stimulation. Among the 642 tyrosine phosphorylation sites identified and quantified in cells with or without Vav1, we observed statistically significant alterations in phosphorylation on proteins implicated in canonical actin cytoskeletal rearrangement and cell cycle progression, supporting the previously established role of Vav1 in these functions of TCR signaling. Critically, this study revealed a new role for Vav1 in negative feedback regulation of the phosphorylation of immunoreceptor tyrosine-based activation motifs within the ζ chains, CD3 δ, ε, γ chains, as well as activation sites on the critical T cell tyrosine kinases Itk, Lck, and ZAP-70. Our study also uncovered a previously unappreciated role for Vav1 in crosstalk between the CD28 and TCR signaling pathways.

2016-05-31 | PXD002022 | Pride

Transcriptomic analysis of normal, premalignant and malignant lymphocytes from mouse models of Peripheral T-Cell Lymphoma

Project description:Transcriptomic analysis of normal, premalignant and malignant lymphocytes from mouse models of Peripheral T-Cell Lymphoma

| PRJNA701567 | ENA