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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Lentiviral expression of MiR-31 in CD8 T-cells.

ABSTRACT: Purpose: identify genes regulated by expression of miR-31 in primary mouse CD8 T-cells by exogenously expressing pre-miR-31 from the Plko.3g lentiviral vector. Cells infected with empty Plko.3g vectors were used as controls for infection. Control vector and miR-31 transduced CD8 T-cells with 4 independent biological replicates/condition

ORGANISM(S): Mus musculus

SUBMITTER: Kai Wucherpfennig

PROVIDER: E-GEOD-63549 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Lentiviral expression of MiR-31 in CD8 T-cells.

Project description:Purpose: identify genes regulated by expression of miR-31 in primary mouse CD8 T-cells by exogenously expressing pre-miR-31 from the Plko.3g lentiviral vector. Cells infected with empty Plko.3g vectors were used as controls for infection.

2015-11-01 | GSE63549 | GEO

Comparison of gene expression profiles of naÃ¯ve and in vitro effector CD8+ T cells from wild-type and BATF-/- mice

Project description:The transcription factor BATF is required for Th17 and TFH differentiation. Here, we show that BATF also has a fundamental role in regulating effector CD8+ T cell differentiation. BATF-deficient CD8+ T cells show profound defects in effector expansion and undergo proliferative and metabolic catastrophe early after antigen encounter. BATF, together with IRF4 and Jun proteins, binds to and promotes early expression of genes encoding lineage-specific transcription-factors (T-bet and Blimp-1) and cytokine receptors, while paradoxically repressing genes encoding effector molecules (IFNg and granzyme B). Thus, BATF amplifies TCR-dependent transcription factor expression and augments inflammatory signal propagation but restrains effector gene expression. This checkpoint prevents irreversible commitment to an effector fate until a critical threshold of downstream transcriptional activity has been achieved. P14 TCR transgenic CD8+ T cells from wild-type or BATF-/- mice were examined either as naÃ¯ve cells or after 3 days of in vitro stimulation with antibodies to CD3 and CD28 in the presence of IL-2

2014-03-02 | E-GEOD-54215 | biostudies-arrayexpress

Differential gene expression by NKX2-1 suppression in NCI-H2009 cells

Project description:The NKX2-1 transcription factor, a regulator of normal lung development, is the most significantly amplified gene in human lung adenocarcinoma. To better understand how genomic alterations of NKX2-1 drive tumorigenesis, we generated an expression signature associated with NKX2-1 amplification in human lung adenocarcinoma, and analyzed DNA binding sites of NKX2-1 by genome-wide chromatin immunoprecipitation from NKX2-1-amplified human lung adenocarcinoma cell lines. Combining these expression and cistromic analyses identified LMO3, itself encoding a transcription regulator, as a candidate direct transcriptional target of NKX2-1, in addition to consensus binding motifs including a nuclear hormone receptor signature and a Forkhead box motif in NKX2-1-bound sequences. RNA interference analysis of NKX2-1-amplified cells compared to non-amplified cells demonstrated that LMO3 mediates cell proliferation downstream of NKX2-1; cistromic analysis that NKX2-1 may cooperate with FOXA1. Our findings provide new insight into the transcriptional regulatory network of NKX2-1 and suggest that LMO3 is a transducer of lineage specific cell survival of NKX2-1-amplified lung adenocarcinomas. NCI-H2009 cells with stable expression of either pLKO-Tet-Op-shGFP (n=4) or pLKO-Tet-Op-shNKX2-1 (pooled population; n=3 and a clone; n=3) were treated with 50ng/ml of doxycyline for 48 hours. Total RNA was extracted, gene expression profiling was performed and differential gene expression between shGFP and shNKX2-1 was analyzed to determine the effects by suppression of NKX2-1 in NCI-H2009 cells.

2013-04-15 | E-GEOD-40270 | biostudies-arrayexpress

Genes regulated by has-mir-31 in glioma cell line

Project description:Overexpression of miR-31 inhibits the migration and invasion ability of glioma cell. We sought to obtain the genes regulated by mir-31 in glioma cell line. The gene expression of U251-mir-31 (U251 over expressing mir-31) and U251-control. U251-Control and U251-mir-31 cells were cultured in DMEM cell culture media for RNA extraction and hybridization on Affymetrix.GeneChip.HG-U133_Plus_2.

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Transcription profiling by array of mouse CD8+ naive T cells from mice expressing normal IL-7R or conditional IL-7R alpha switched on or off for different amounts of time

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2010-12-20 | E-TABM-991 | biostudies-arrayexpress

MiR31 increases CD8 T cell sensitivity to type I interferon

Project description:We report that the microRNA (miR)-31 confers CD8 T cell sensitivity to type I interferon (IFN) stimulation following CD3/CD28 engagement. Method: miR31 WT and KO CD8 T cells were stimulated with anti-CD3/CD28 beads for two days, then maintained in 10ng/mL IL-2 for a further 5 days. CD8 T cells were then stimulated with 20ng/mL IFN-beta for 0, 4, or 18h. Total RNA was isolated at each time point and sequenced. Results: Prior to IFN-beta stimulation, miR-31 KO CD8 T cells had a slightly increased effector program (cytotoxic granzymes) and decreased inhibitory program (Mt1/Maf). Stimulation with IFN-beta further enhanced this difference increasing a number of granzymes, Prf1 and Spp1 whilst also decreasing inhibitory genes (Mt1, Mt2, Maf, Ptger2). Conclusion: This study shows that miR-31 may lead to decreased effector function and increased inhibitory programs in CD8 T cells during chronic viral infections, in particular due to continued type I interferon stimulation.

2017-05-07 | GSE98615 | GEO

Brown Adipose YY1 Deficiency Activates Expression of Secreted Proteins Linked to Energy Expenditure and Prevents Diet-Induced Obesity

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-11-10 | E-GEOD-68443 | biostudies-arrayexpress

Expression data from mouse skeletal muscle

Project description:We generated skeletal muscle-specific knockout mice lacking the transcription factor Yin Yang 1 (YY1) and analyzed expression patterns in the skeletal muscle these mice. We used microarrays to detail the global programme of gene expression regulated by YY1. Wild type or knockout mice at 6 months were sacrificed and the soleus was isolated for RNA extraction.

2012-06-29 | E-GEOD-39009 | biostudies-arrayexpress

Developmental stage-specific interplay between GATA1 and IGF signaling in fetal hematopoiesis and leukemogenesis

Project description:This SuperSeries is composed of the following subset Series: GSE16676: Rescue of murine Gata1s mutant M7 leukemic cells by full-length Gata1 GSE16677: Gene expression profiling of Down Syndrome (DS)-AMKL and non-DS AMKL samples GSE16679: Plag1 overexpression cooperates with Evi1 overexpression and Gata1s mutation in leading to M7 leukemia GSE16682: Murine M7 leukemia derived from retroviral insertional mutagenesis of Gata1s fetal progenitors GSE16684: Murine M7 leukemia derived from retroviral insertional mutagenesis of Gata1s fetal progenitors depends on IGF signaling Refer to individual Series

2010-08-01 | E-GEOD-16655 | biostudies-arrayexpress

Transcription profiling of mouse LckCre, CD4Cre-Ctnnbex3 mutants before and after T-cell transformation reveals stabilization of b-catenin induces lymphomas

Project description:Activation of b-catenin has been causatively linked to the etiology of colon cancer. Conditional stabilization of this molecule in pro-T-cells promotes thymocyte development without the requirement for preTCR signaling. We show here that activated b-catenin stalls the developmental transition from the double-positive (DP) to the single-positive (SP) thymocyte stage and predisposes DP thymocytes to transformation. b-Catenin induced thymic lymphomas have a leukemic arrest at the early DP stage. Lymphomagenesis requires Rag activity, which peaks at this developmental stage, as well as additional secondary genetic events. A consistent secondary event is the transcriptional upregulation of c-Myc, whose activity is required for transformation since its conditional ablation abrogates lymphomagenesis. In contrast, the expression of Notch receptors as well as targets is reduced in DP thymocytes with stabilized b-catenin and remains low in the lymphomas indicating that Notch activation is not required or selected for in b-catenin induced lymphomas. Thus, b-catenin activation may provide a mechanism for the induction of T-ALL that does not depend on Notch activation. Experiment Overall Design: This study was used to compare gene expression patterns of LckCre mice, CD4Cre-Ctnnbex3 mice before and after T-cell transformation. 5 independent Lckcre (control), 5 independent CD4Cre-Ctnnbex3 mice and 8 independent mice with lymphomas were used. Thymocytes or tumor masses were collected from Lckcre, CD4Cre-Ctnnbex3 mice. Total RNA isolation and purification followed by synthesis of dscDNA, Biotinylated cRNA and purification of Biotinylated cRNA. Then the hybridization to Affymetrix âMouse Expression Array 430 Genechipsâ was done. Data was analysed by dchip.

2008-06-15 | E-GEOD-7050 | biostudies-arrayexpress

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