Identification of the Early VIP Transriptome and its Associated Interactome in Resting and Activated Murine CD4 T Cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE18526 | GEO | 2010/01/09
SECONDARY ACCESSION(S): PRJNA120199
REPOSITORIES: GEO
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE18524: Identification of the Early VIP Transriptome and its Associated Interactome in Resting Murine CD4 T Cells GSE18525: Identification of the Early VIP Transriptome and its Associated Interactome in Activated Murine CD4 T Cells Refer to individual Series
2010-01-09 | E-GEOD-18526 | biostudies-arrayexpress
Project description:Identification of the Early Vasoactive Intestinal Peptide (VIP) Transriptome and its Associated Interactome in Resting Murine CD4 T Cells In an attempt to understand the biological role of this neuropeptide in the immune system, we choose CD4 T cells as a cellular system for identifying a VIP-induced transcriptome. Murine CD4 T cells were isolated and used to identify changes in gene expression in the absence of PMA/ionomycin (resting) with and without 10-7 M VIP. Balanced-block design, 6 biological replicates. Naïve mouse CD4 T spleenocytes with VIP ligand (sample) vs. naïve mouse CD4 T spleenocytes without VIP ligand (control), dye-swaps.
2010-01-09 | E-GEOD-18524 | biostudies-arrayexpress
Project description:Identification of the Early Vasoactive Intestinal Peptide (VIP) Transriptome and its Associated Interactome in Resting Murine CD4 T Cells In an attempt to understand the biological role of this neuropeptide in the immune system, we choose CD4 T cells as a cellular system for identifying a VIP-induced transcriptome. Murine CD4 T cells were isolated and used to identify changes in gene expression in the absence of PMA/ionomycin (resting) with and without 10-7 M VIP.
2010-01-09 | GSE18524 | GEO
Project description:Identification of the Early Vasoactive Intestinal Peptide (VIP) Transriptome and its Associated Interactome in Activated Murine CD4 T Cells In an attempt to understand the biological role of this neuropeptide in the immune system, we choose CD4 T cells as a cellular system for identifying a VIP-induced transcriptome. Murine CD4 T cells were isolated and used to identify changes in gene expression in the presence of PMA/ionomycin (activated) for five hours with and without 10-7 M VIP. Balanced-block design, 6 biological replicates. PMA/ionomycin (activated) mouse CD4 T spleenocytes with VIP ligand (sample) vs. PMA/ionomycin (activated) mouse CD4 T spleenocytes without VIP ligand (control), dye-swaps.
2010-01-09 | E-GEOD-18525 | biostudies-arrayexpress
Project description:More than 40 years after the discovery of vasoactive intestinal peptide (VIP), its transcriptome in the immune system has still not been completely elucidated. In an attempt to understand the biological role of this neuropeptide in immunity, we chose CD4 T cells as a cellular system. Agilent Mouse Whole Genome microarrays were hybridized with fluorescently labeled total RNA isolated from resting CD4 T cells cultured +/-10(-7)M VIP for 5h or PMA/ionomycin activated CD4 T cells cultured +/-10(-7)M VIP for 5h. These VIP-regulated transcriptomes were analyzed by Significance Analysis of Microarrays (SAM) and Ingenuity Pathway Analysis (IPA) software to identify relevant signaling pathways modulated by VIP in the absence and presence of T cell activation. In resting CD4 T cells, VIP-modulated 368 genes, ranging from 3.49 to -4.78-fold. In the PMA/ionomycin activated CD4 T cells, 326 gene expression levels were changed by VIP, ranging from 2.94 to -1.66-fold. IPA analysis revealed that VIP exposure alters cellular function through EGFR signaling in resting CD4 T cells, and modulates immediate early genes, Fos and CREM/ICER, in activated CD4 T cells. These gene expression changes are suggested to explain at a molecular level how VIP can regulate T cell homing to the gut and induce regulatory T cell generation.
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Project description:Identification of the Early Vasoactive Intestinal Peptide (VIP) Transriptome and its Associated Interactome in Activated Murine CD4 T Cells In an attempt to understand the biological role of this neuropeptide in the immune system, we choose CD4 T cells as a cellular system for identifying a VIP-induced transcriptome. Murine CD4 T cells were isolated and used to identify changes in gene expression in the presence of PMA/ionomycin (activated) for five hours with and without 10-7 M VIP.
2010-01-09 | GSE18525 | GEO
Project description:T cell activation leads to dramatic changes in cellular phenotype. We used activated human CD4 T cells to study how RNA binding proteins define the post-transcriptional landscape. Using RIPseq, we identified the RNA interactome of U2AF2 and show that U2AF2 binds the majority of transcripts that are differentially expressed and/or alternatively spliced during activation. Using RIP mass spectrometry, a unique protein interactome centered on U2AF2 is assembled by activation and comprised of both directly bound central members (RNAse-resistant) and indirectly bound peripheral members (RNAse-sensitive). Knocking down specific U2AF2 interactome members (U2AF1, SYNCRIP, SRRM2, ILF2) selectively affects cytokine secretion and activation markers. The expression and/or alternative splicing of transcripts important for immune cell function are also affected by knocking down these interactome members, both peripheral and central. Furthermore, we show that knockdown of interactome members can affect the proteins and transcripts bound to U2AF2, altering the transcriptome of activated T cells. Our work highlights the importance of understanding the assembly of RNA binding protein complexes as regulators of T cell activation and function.
2016-04-27 | PXD001846 | Pride
Project description:The stability, localization and translation of mammalian mRNAs are largely determined by sequences in the 3' untranslated region (UTR). Here, we describe a conserved program of increased upstream polyadenylation site usage following activation of primary murine CD4+ T lymphocytes. This program, resulting in shorter 3' UTRs, is a characteristic of immune cell activation and strongly correlates with proliferation across diverse cell types and tissues. Enforced expression of full-length 3' UTRs confers differences in protein expression that can in some cases be eliminated by deletion of predicted microRNA target sites in the variably included region. Together, our data indicate that polyadenylation site usage is coordinately regulated such that states of increased proliferation are associated with widespread reduction of 3' UTR-based regulation. Keywords: activation, exon array, time course Two or three biological replicates per time point
2010-05-26 | E-GEOD-10666 | biostudies-arrayexpress
Project description:Highly active antiretroviral therapy (HAART) suppresses human immunodeficiency virus (HIV) replication to undetectable levels but cannot fully eradicate the virus because a small reservoir of CD4+ T cells remains latently infected. Since HIV efficiently infects only activated CD4+ T cells and since latent HIV primarily resides in resting CD4+ T cells, it is generally assumed that latency is established when a productively infected cell recycles to a resting state, trapping the virus in a latent state. In this study, we use a dual reporter virus--HIV Duo-Fluo I, which identifies latently infected cells immediately after infection--to investigate how T cell activation affects the establishment of HIV latency. We show that HIV latency can arise from the direct infection of both resting and activated CD4+ T cells. Importantly, returning productively infected cells to a resting state is not associated with a significant silencing of the integrated HIV. We further show that resting CD4+ T cells from human lymphoid tissue (tonsil, spleen) show increased latency after infection when compared to peripheral blood. Our findings raise significant questions regarding the most commonly accepted model for the establishment of latent HIV and suggest that infection of both resting and activated primary CD4+ T cells produce latency.
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Project description:The stability, localization and translation of mammalian mRNAs are largely determined by sequences in the 3' untranslated region (UTR). Here, we describe a conserved program of increased upstream polyadenylation site usage following activation of primary murine CD4+ T lymphocytes. This program, resulting in shorter 3' UTRs, is a characteristic of immune cell activation and strongly correlates with proliferation across diverse cell types and tissues. Enforced expression of full-length 3' UTRs confers differences in protein expression that can in some cases be eliminated by deletion of predicted microRNA target sites in the variably included region. Together, our data indicate that polyadenylation site usage is coordinately regulated such that states of increased proliferation are associated with widespread reduction of 3' UTR-based regulation. Keywords: activation, exon array, time course
2008-06-20 | GSE10666 | GEO