Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The gene expression profiles of antigen-primed wildtype and Ddit3-/- CD8 Pmel T cells

ABSTRACT: T cell undergoes ER stress during regular priming which may lead to T cell dysfunction in cancer. ER stress downstream sensor Chop (encoded by Ddit3 gene) negatively regulates CD8 T cell function and cytotoxicity. Because Chop is a C/EBP homologous transcription factor, we sorted antigen-primed wildtype or ddit3-/- Pmel CD8 T cells perform RNA-seq and gene expression profile analysis.

ORGANISM(S): Mus musculus

PROVIDER: GSE112823 | GEO | 2019/04/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

The gene expression profiles of antigen-primed wildtype and Ddit3-/- CD8 Pmel T cells

Project description:The gene expression profiles of antigen-primed wildtype and Ddit3-/- CD8 Pmel T cells

| PRJNA449089 | ENA

Transcription profiling by array of human cell lines expressing high levels of tamoxifen-induced DDIT3

Project description:Identification of genes and functions regulated by DDIT3/GADD153/CHOP by transcriptional profiling of cell lines expressing high levels of tamoxifen induced DDIT3.

2010-09-01 | E-MEXP-2709 | biostudies-arrayexpress

Gene expression analysis in naïve and vaccine (peptide vs. DC) primed pmel-1 CD8 Tcells

Project description:We have shown that DC vaccine is superior to peptide vaccine in terms of priming and expansion of antigen-specific CD8+ T cells. DC vaccine-primed pmel-1 cells displayed better effecter functions than cells by peptide-primed cells in terms of cytokine production and externalization of cytotoxic granules. Furthermore DC vaccine-primed cells were metabolically distinct from peptide-primed cells. To confirm these findings, we performed a microarray analysis using splenic pmel-1 T cells from mice immunized with hgp100 peptide vaccine or DC vaccine. We also used splenic naïve pmel-1 T cells as a control.

2017-08-31 | GSE94538 | GEO

Expression data for naÃ¯ve IL-2 and IL-12 primed Pmel-1 CD8+ T-cells

Project description:The expansion, trafficking and functional effectiveness of adoptively transferred CD8+ T-cells play a critical role in mediating effective anti-tumor immunity. However, the mechanisms which program the highly proliferative and functional state of CD8+ T-cells are not completely understood. We hypothesized that IL-12, a cytokine commonly induced by TLR activation, could enhance T-cell priming by altering responsiveness to antigen and cytokines. Priming of tumor specific CD8+ T-cells in the presence of IL-12 induced the acquisition of a 'polyfunctional' effector response and increased the generation of memory cells. Moreover, IL-12 priming also promoted high levels of the IL-2 receptor alpha-chain (CD25) and robust IL-2 mediated activation of STAT5. This sensitivity to IL-2 translated into enhanced in vivo proliferation of adoptively transferred CD8+ T-cells. Furthermore, real-time, in vivo imaging of T-cell trafficking confirmed the ability of IL-12 priming to drive in vivo proliferation. IL-12 priming enhanced the anti-tumor function of adoptively transferred cells by reducing established subcutaneous tumor burden, and significantly increasing survival in an established intracranial tumor model. Finally, IL-12 priming of human PBMCs generates tumor specific T-cells phenotypically and functionally similar to IL-12 primed Pmel-1 T-cells. These results highlight IL-12 as an important mediator of CD8+ T-cell effector function and anti-tumor immunity. We primed Pmel-1 TCR transgenic CD8+ T-cells with cognate antigen and either IL-2 or IL-12 and compared their gene expression profiles. This was used to identify pathways or genes necessary for anti-tumor activity in vivo. RNA was isolated from Pmel-1 T-cells primed with antigen and cytokine for 6 days and hybridized to Affymetrix arrays.

2010-10-19 | E-GEOD-22443 | biostudies-arrayexpress

Transcription profiling of mouse embryonic fibroblasts (MEF) from wild type vs CHOP-/- genotypes treated with tunicamycin reveals CHOP induces death by promoting protein synthesis and oxidation in the stressed endoplasmic reticulum

Project description:Primary mouse embryonic fibroblasts (pass 3 to 4) were treated with tunicamycin (2 micrograms/ml) for specified times - genotypes were WILDTYPE and CHOP-/-. Each time point n=4. C/EBP homologous protein CHOP is activated by ER stress, and CHOP deletion protects against its lethal consequences.

2007-12-11 | E-GEOD-2082 | biostudies-arrayexpress

Pmel CD8+ stim 1 vs. stim 2

Project description:Repeat experiments of CD8+ pmel effector cells following one and two rounds of restimulation Keywords: repeat sample

2005-03-02 | GSE2348 | GEO

Pmel CD8+ stim 1 vs. stim 2

Project description:Repeat experiments of CD8+ pmel effector cells following one and two rounds of restimulation

2010-06-10 | E-GEOD-2348 | biostudies-arrayexpress

Regulation and role of the pro-apoptotic transcription factor CHOP in Idiopathic Pulmonary Fibrosis

Project description:Idiopathic pulmonary fibrosis (IPF) is a progressive and ultimately fatal interstitial lung disease characterized by alveolar epithelial cell type II (AECII) injury and enhanced fibroblast/myofibroblast proliferation. Recent data show that maladaptive endoplasmic reticulum (ER)-stress leading to AECII apoptosis could play a key role in IPF, although it is still unclear how precisely such response is initiated and signalled. C/EBP homologous protein (CHOP) has been suggested to contribute to a maladaptive ER-stress response in general and has been found to be induced and to be translocated into the nucleus of AECII in IPF in particular. We here show for the first time a novel mechanism for the regulation of CHOP expression during ER-stress in AECII via AP-1 and c-Ets-1. We found these two transcription factors to be up-regulated in AECII under ER-stress conditions and to interact with each other to jointly bind to the CHOP promoter, thereby inducing CHOP gene expression. Moreover, we show for the first time that singular CHOP overexpression in vitro and in vivo is indeed capable of inducing apoptosis of AECII and, consequently, lung fibroblast proliferation and up-regulation of pro-fibrotic markers. We therefore believe that CHOP plays a key role in AEC injury and consecutive fibrosis.

2017-09-23 | GSE87298 | GEO

Real-time quantitative PCR analysis for miRNA in mouse CD8+ pMel-1 T cells

Project description:Mouse CD8+ pMel-1 transgenic T cells were primed by either splenic B cells or LPS-matured bone marrow-derived dendritic cells for 3 days in vitro. CD8+TCRb+ cells were then sorted for miRNA expression profiling by RT-qPCR.

2014-12-01 | GSE60884 | GEO

Coordinated stimulation of axon regenerative and neurodegenerative transcriptional programs by Atf4 following optic nerve injury

Project description:To understand the contributions of the Integrated Stress Response (ISR) to the axon regenerative and neurodegenerative transcriptional programs activated by axon injury in the CNS, we evaluated by RNA-seq the retinal transcriptomes of conditional knockout mouse lines for components of the ISR three days after optic nerve crush injury. Prior to injury, intravitreal injection of AAV2-mTagBFP2-ires-Cre under the control of the human synapsin-1 promoter facilitated neuron-specific knockout of Eif2ak3, the gene that encodes the ER stress-responsive kinase Perk; Atf4, the gene that encodes the ISR mediator Activating transcription factor-4; or Ddit3, the gene that encodes another transcription factor that can mediate the ISR, C/ebp homologous protein, or CHOP. We compared the expression profiles of these transgenic retinas after injury to retinas from wildtype mice with and without injury to identify transcripts whose regulation by axon injury is dependent on ISR signaling.

2023-03-30 | GSE223321 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data