Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2985260.fastq.gz | Fastqsanger.gz | |||
| ERR2985270.fastq.gz | Fastqsanger.gz | |||
| ERR2985261.fastq.gz | Fastqsanger.gz | |||
| ERR2985271.fastq.gz | Fastqsanger.gz | |||
| ERR2985262.fastq.gz | Fastqsanger.gz |
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Project description:The generation of CD8+ T-cell memory is an important aim of immunization. While several distinct subsets of CD8+ T-cell memory have been described, the lineage relationships between effector (EFF), effector memory (EM) and central memory (CM) T cells remain contentious. Specifically, there is contradictory experimental evidence to support both the linear (Naive>EFF>EM>CM) and progressive differentiation (Naive>CM>EM>EFF) models. In this study, we applied a systems biology approach to examine global transcriptional relationships between the three major CD8+ T cell subsets arising endogenously as a result of vaccination with three different prime-boost vaccine regimens. Differential gene expression analysis and principle component analysis revealed that central memory cells were more closely related to naive T cells than both effector memory and effector cells. When the transcriptional relationships between subsets were enriched in an unbiased fashion with known global transcriptional changes that result when T-cells repeatedly encounter antigen, our analysis favored a model whereby cumulative antigenic stimulation drives differentiation specifically from Naive > CM > EM > EFF. These findings provide an insight into the lineage relationship between mature CD8+ T-cell subsets and will help in the rational design of vaccines aimed at generating effective immune responses against infections and cancer. Effector (EFF), effector memory (EM), central memory (CM) and naive CD8+ T cells from mice spleen. Memory subset arise endogenously as a result of vaccination with three different prime-boost vaccine regimens: DNA-rAd5, rAd5-rAd5 and rAd5-rLCMV.
2013-08-01 | E-GEOD-42459 | biostudies-arrayexpress
Project description:Chromatin insulators demarcate the genome into distinct transcriptional domains and contribute to higher-order genome organization. In Drosophila, Su(Hw), CP190, and Mod(mdg4)67.2 are core protein components of the gypsy insulator complex. Multimerization of these core components contributes to formation of large structures within the nucleus termed insulator bodies. Post-translational modifications of insulator proteins appear to affect insulator body localization and be required for full insulator activity, but few factors involved in these processes have been identified. To address this gap in understanding, we performed a high-throughput visual screen for Mod(mdg4)67.2-GFP localization using a ubiquitination-related RNAi library. We identified ubiquitination pathway proteins Effete (Eff) and Cullin 4 (Cul4), as novel regulators of CP190 localization and function. Both Eff and Cul4 physically associate with gypsy insulator proteins and promote gypsy-dependent insulator barrier activity. Moreover, Cul4 extensively colocalizes with CP190 on chromatin and assists in the recruitment of CP190 to gypsy sites. Both Eff and Cul4 affect transcription near topologically associating domain (TAD) borders, with Eff specifically altering the 3D nuclear positioning of gypsy insulator sites. Overall, our findings reveal a novel role for ubiquitination pathway-related enzymes in chromatin insulator activity, 3D genome organization, and gene expression.
2026-02-27 | GSE243452 | GEO
Project description:Tissue nanotransfection (TNT) based topical electrophoretic delivery of Etv2, Foxc2, and Fli1 (EFF) plasmids achieve induced vasculogenesis (iV) in the skin by inducing vasculogenic fibroblasts (VF). scRNA-seq analysis revealed TET-dependent gain of VF in dermal fibroblasts in response to EFF. Emergence of VF required TET-dependent demethylation of fibroblast-borne endothelial genes in vivo. Fibroblast-specific inducible overexpression of EFF in TARGATT mice caused induction of TET1/2/3, followed by transition of fibroblast to VF in vivo. TET induction was associated with elevated 5-hmC abundance in VF. TET-dependent demethylation of fibroblast-borne endothelial genes caused the formation of VF and rescued perfusion in diabetic ischemic limbs. TNTEFF rescued perfusion and closure of diabetic wounds. TET enzymes, suppressed in diabetics, play a pivotal role in causing endogenous EFF-induced VF state change of skin fibroblasts. TNT delivery of EFF transcription factors upregulate TET expression. This work is the first to recognize the significance of TET in the inducible formation of blood vessels to rescue diabetic ischemic tissue.
2024-12-05 | GSE268094 | GEO
Project description:This study aims to define how Id2 and Id3 regulate exhausted CD8+ T cell fate. We found that Id2 deletion reduced the Tex-eff population, whereas Id3 ablation in CD4-Cre mice diminished Tpex cells, indicating subset-specific roles for Id2 and Id3. Mechanistically, E2A is a major target of Id2/3, and Runx3 interacts with E2A. Pulldown of Id2/3 recovered both E2A and Runx3, supporting an Id2/3?E2A?Runx3 regulatory complex. To map the genomic occupancy of Id2 and Id3, we expressed 3×T7-tagged Id2 or Id3 in in vitro-primed CD45.2+ P14 cells, adoptively transferred these cells into CD45.1 recipient mice, and infected the recipients with LCMV Clone 13. On day 6 post-infection, Tex-eff and Tpex cells were isolated for T7 CUT&RUN to define Id2 binding in Tex-eff cells and Id3 binding in Tpex cells, with the empty T7 vector backbone used as a negative control.
2026-04-20 | GSE310322 | GEO