Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

47 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNAseq of naive CD4 T cells deficient for Elp3 activated for 18h against WT control

ABSTRACT: CD4 T cell deficient for the Elp3 gene have a delayed cell cycle entry. We explored by RNAseq by which molecular pathway the absence of Elp3 delayed the cell cycle entry. Naive T cell from CD4-cre Elp3 fl/fl mice and WT littermate were purified and activated in vitro with CD3 and CD28 antibodies for 18h.

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Mus musculus

SUBMITTER: Pierre Lemaitre

PROVIDER: E-MTAB-9057 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

RNAseq of follicular helper T cell from Elp3 deficient mice after Complete Freund Adjuvant immunisation

Project description:Loss of Elp3 in CD4 T cells hindered the development of an optimal T follicular helper T cell (TFH) response. To understand the molecular pathway by which Elp3 is necessary for TFH responses, mice deficient for Elp3 in T cells and WT littermate were immunized with ovalbumin emulsified with complete Freund Adjuvant. 8 days later, TFH were sorted from the draining lymph nodes and submitted for RNAseq

2020-07-31 | E-MTAB-9059 | biostudies-arrayexpress

RNA-seq of long-term hematopoietic stem cells and myeloid progenitors of control mice or mice conditionally deficient for Trp53 or Elp3 or both genes in the hematopoietic system

Project description:Aim of the experiment was to compare the gene expression responses of long-term hematopoietic stem cells (HSCs) and myeloid-restricted progenitors (MyPs) to the hematopoietic cell-restricted deletion of the catalytic subunit Elp3 of the Elongator complex. Since Elp3 deletion resulted in activation of the p53 pathway, we also studied the transcriptome of MyPs deficient for Trp53 or for both Elp3 and Trp53. The Elp3fl/fl strain was generated in house and first described in (DOI: 10.1084/jem.20142288). The Trp53 strain was first described in (DOI: 10.1101/gad.14.8.994) and was purchased from the Jackson Laboratory. Littermates of 8-12 weeks old were used in all experiments.

2020-12-10 | E-MTAB-6992 | biostudies-arrayexpress

Polysome profiling analysis of myeloid progenitors of control mice or mice conditionally deficient for Elp3 in the hematopoietic system

Project description:Aim of the experiment was to compare the genes enriched in the heavy polysome fraction of myeloid progenitors originating from control Elp3fl/fl mice, and in myeloid progenitors originating from mice that underwent hematopoietic cell-restricted deletion of the catalytic subunit Elp3 of the Elongator complex (Elp3HscKO mice). The Elp3fl/fl strain was generated in house and first described in (DOI: 10.1084/jem.20142288). Littermates of 8-12 weeks old were used in all experiments.

2020-12-10 | E-MTAB-9628 | biostudies-arrayexpress

Control vs Elp3-deficient mouse myeloid progenitors 6-plex TMT LC-MSMS

Project description:6-plex TMT LC-MSMS quantification of proteins in myeloid progenitors (Lineage- Sca1- Kit+ cells) isolated from the bone marrow of 8-12 week old male and female control and Elp3-deficient (Elp3fl/fl vav-iCreT/+) mice. Biological triplicates of each genotype were analyzed, each consisting of 1.10e6 cells from pools of 12-14 control (Elp3fl/fl) or 26-38 (Elp3-deficient) male and female mice.

2021-01-26 | PXD010486 | Pride

Raptor/mTORC1-dependent metabolic programming of exit from quiescence underlies T cell activation and fate decisions

Project description:Naïve T cells respond to antigen stimulation by exiting from quiescence into clonal expansion and functional differentiation, but the control mechanism is elusive. Here we describe that Raptor/mTORC1-dependent metabolic reprogramming is a central determinant of this transitional process. Loss of Raptor abrogates T cell priming and Th2 cell differentiation, although Raptor function is less important for continuous proliferation of actively cycling cells. mTORC1 coordinates multiple metabolic programs in T cells including glycolysis, lipid synthesis and oxidative phosphorylation to mediate antigen-triggered exit from quiescence. mTORC1 further links glucose metabolism to the initiation of Th2 differentiation by orchestrating cytokine receptor expression and cytokine responsiveness. Activation of Raptor/mTORC1 integrates T cell receptor (TCR) and CD28 co-stimulatory signals in antigen-stimulated T cells. Our studies identify a Raptor/mTORC1-dependent pathway linking signal-dependent metabolic reprogramming to quiescence exit, and this in turn coordinates lymphocyte activation and fate decisions in adaptive immunity. We used microarrays to explore the gene expression profiles differentially expressed in CD4+ T-cells from wild-type (WT) and CD4(cre) x Raptor(fl/fl) mice before and after stimulation with anti CD3/CD28 antibodies.

2014-01-27 | E-GEOD-51668 | biostudies-arrayexpress

Reference proteome of highly purified human Th1 cells reveals strong effects on metabolism and protein ubiquitination upon differentiation

Project description:The differentiation of human CD4+ T cells into different subtypes of T helper cells and regulatory T cells is crucial for an appropriate immunological response. Among all subtypes Th1 cells are the most prominent specific cell type, representing about 50% of all lymphocytes. So far most global proteomic studies have used either only partially purified T helper cell subpopulations and/or have employed artificial protocols for inducing specific T helper cell subtypes and/or applied gel based approaches. These studies have shed light on molecular details of certain aspects of the proteome. Nevertheless a more global analysis of highly pure primary naïve and Th1 cells by LC-MS/MS is needed in order to contribute to the proteome based T cell subtype characterization. We were able to identify 1757 proteins in total, out of which 49 were significantly regulated. The utilization of highly purified Th1 cells for a global proteome assessment and the bioinformatical comparison to naïve cells reveals the relevance of changes in the metabolism and the ubiquitination pathways upon T cell differentiation.

2015-10-13 | PXD001066 | Pride

Ribosome profiling experiment in control or Elp3 depleted B16 melanoma cells

Project description:We report the application of ribosome profiling using high-throughput sequencing and total mRNA used for normalisation upon depletion of ELP3 protein in B16 melanoma cells.

2018-06-26 | GSE111891 | GEO

Comparative analysis of the proteome of Th2 lymphocytes from WT or ASB2 KO mice

Project description:ASB2α is an E3 ubiquitin ligase which is upregulated during Th2 differentiation of naive CD4+ T lymphocyte, and which is known to trigger ubiquitylation and proteasomal degradation of filamins (FLN) a and b. Because E3 ubiquitin ligases often ubiquitylate several substrates, we used an unbiased and broad mass spectrometry approach to identify ASB2α substrates in Th2 lymphocytes generated from naïve CD4+ T lymphocytes of control or ASB2 KO mice.

2024-09-24 | PXD044062 | Pride

Elp3 links tRNA modification to IRES-dependent translation of LEF1 to sustain metastasis in breast cancer

Project description:Quantitative and qualitative changes in mRNA translation occur in tumor cells and support cancer progression and metastasis. Post-transcriptional nucleoside modifications of transfer RNAs (tRNAs) at the wobble U34 base are highly conserved and contribute to translation fidelity. Here, we show that ELP3 and CTU1/2, partner enzymes in U34 mcm5s2-tRNA modification, are upregulated in human breast cancers and sustain metastasis. Elp3 genetic ablation strongly impaired invasion and metastasis formation in the PyMT model of invasive breast cancer. Mechanistically, ELP3 and CTU1/2 support cellular invasion through the translation of the oncoprotein DEK. As a result, DEK promotes the IRES-dependent translation of the pro-invasive transcription factor LEF1. Consistently, a DEK mutant, whose codon composition is independent of U34 mcm5s2-tRNA modification, escapes the ELP3- and CTU1-dependent regulation and restores the IRES-dependent LEF1 expression. Our results demonstrate the key role of U34 tRNA modification to support specific translation during breast cancer progression and highlight a functional link between tRNA modification- and IRES-dependent translation during tumor cell invasion and metastasis.analysis of transcriptomic changes due to Elp3genetic deletion in cells extracted from PyMT mammary tumors.

2016-09-29 | GSE85810 | GEO

RNA sequencing of short time IL-4 stimulated bone marrow derived cells with or without Elp3

Project description:Comparison of transcriptome of 2 hours IL-4 treated bone marrow derived cells (BMDMs) from WT and Elp3 KO mice

2022-07-04 | GSE166169 | GEO