Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Reprogramming fate of central memory CD8+T cells by targetig the transcriptional coregulator Tle3

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE213041 | GEO | 2023/10/10

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Reprogramming fate of central memory CD8+T cells by targetig the transcriptional coregulator Tle3 [scRNA-seq]

Project description:The goal of this study is to determine if central memory (Tcm) and effector memory (Tem) CD8 T cells can be reprogrammed to change their fate. We demonstrate that genetic ablation of Tle3 can promote generation of Tcm cells at the expense of Tem cells, and this can occur during the effector phase of the immune response.

2023-10-10 | GSE216633 | GEO

Reprogramming fate of central memory CD8+T cells by targetig the transcriptional coregulator Tle3

Project description:Reprogramming fate of central memory CD8+T cells by targetig the transcriptional coregulator Tle3

| PRJNA878807 | ENA

The transcriptional cofactor Tle3 reciprocally controls effector and central memory CD8<sup>+</sup> T cell fates.

Project description:Antigen-experienced CD8+ T cells form effector and central memory T cells (TEM and TCM cells, respectively); however, the mechanism(s) controlling their lineage plasticity remains incompletely understood. Here we show that the transcription cofactor Tle3 critically regulates TEM and TCM cell fates and lineage stability through dynamic redistribution in antigen-responding CD8+ T cell genome. Genetic ablation of Tle3 promoted CD8+ TCM cell formation at the expense of CD8+ TEM cells. Lineage tracing showed that Tle3-deficient CD8+ TEM cells underwent accelerated conversion into CD8+ TCM cells while retaining robust recall capacity. Tle3 acted as a coactivator for Tbet to increase chromatin opening at CD8+ TEM cell-characteristic sites and to activate CD8+ TEM cell signature gene transcription, while engaging Runx3 and Tcf1 to limit CD8+ TCM cell-characteristic molecular features. Thus, Tle3 integrated functions of multiple transcription factors to guard lineage fidelity of CD8+ TEM cells, and manipulation of Tle3 activity could favor CD8+ TCM cell production.

| S-EPMC10916363 | biostudies-literature

Reprogramming fate of central memory CD8+T cells by targetig the transcriptional coregulator Tle3 [scRNA-seq]

Project description:Reprogramming fate of central memory CD8+T cells by targetig the transcriptional coregulator Tle3 [scRNA-seq]

| PRJNA894535 | ENA

TLE3 is a dual-function transcriptional coregulator of adipogenesis.

Project description:PPAR? and Wnt signaling are central positive and negative regulators of adipogenesis, respectively. Here we identify the groucho family member TLE3 as a transcriptional integrator of the PPAR? and Wnt pathways. TLE3 is a direct target of PPAR? that participates in a feed-forward loop during adipocyte differentiation. TLE3 enhances PPAR? activity and functions synergistically with PPAR? on its target promoters to stimulate adipogenesis. At the same time, induction of TLE3 during differentiation provides a mechanism for termination of Wnt signaling. TLE3 antagonizes TCF4 activation by ?-catenin in preadipocytes, thereby inhibiting Wnt target gene expression and reversing ?-catenin-dependent repression of adipocyte gene expression. Transgenic expression of TLE3 in adipose tissue in vivo mimics the effects of PPAR? agonist and ameliorates high-fat-diet-induced insulin resistance. Our data suggest that TLE3 acts as a dual-function switch, driving the formation of both active and repressive transcriptional complexes that facilitate the adipogenic program.

| S-EPMC3089971 | biostudies-literature

Epigenetic memory of the first cell fate decision prevents complete ES cell reprogramming into trophoblast

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

2014-11-24 | E-GEOD-62150 | biostudies-arrayexpress

Selected microRNAs define cell fate determination of murine central memory CD8 T cells.

Project description:During an immune response T cells enter memory fate determination, a program that divides them into two main populations: effector memory and central memory T cells. Since in many systems protection appears to be preferentially mediated by T cells of the central memory it is important to understand when and how fate determination takes place. To date, cell intrinsic molecular events that determine their differentiation remains unclear. MicroRNAs are a class of small, evolutionarily conserved RNA molecules that negatively regulate gene expression, causing translational repression and/or messenger RNA degradation. Here, using an in vitro system where activated CD8 T cells driven by IL-2 or IL-15 become either effector memory or central memory cells, we assessed the role of microRNAs in memory T cell fate determination. We found that fate determination to central memory T cells is under the balancing effects of a discrete number of microRNAs including miR-150, miR-155 and the let-7 family. Based on miR-150 a new target, KChIP.1 (K (+) channel interacting protein 1), was uncovered, which is specifically upregulated in developing central memory CD8 T cells. Our studies indicate that cell fate determination such as surface phenotype and self-renewal may be decided at the pre-effector stage on the basis of the balancing effects of a discrete number of microRNAs. These results may have implications for the development of T cell vaccines and T cell-based adoptive therapies.

| S-EPMC2889817 | biostudies-literature

Transcriptional Reprogramming during Floral Fate Acquisition

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-06-08 | GSE205299 | GEO

Adipocyte Reprogramming by the Transcriptional Coregulator GPS2 Impacts Beta Cell Insulin Secretion.

Project description:Glucose homeostasis is maintained through organ crosstalk that regulates secretion of insulin to keep blood glucose levels within a physiological range. In type 2 diabetes, this coordinated response is altered, leading to a deregulation of beta cell function and inadequate insulin secretion. Reprogramming of white adipose tissue has a central role in this deregulation, but the critical regulatory components remain unclear. Here, we demonstrate that expression of the transcriptional coregulator GPS2 in white adipose tissue is correlated with insulin secretion rate in humans. The causality of this relationship is confirmed using adipocyte-specific GPS2 knockout mice, in which inappropriate secretion of insulin promotes glucose intolerance. This phenotype is driven by adipose-tissue-secreted factors, which cause increased pancreatic islet inflammation and impaired beta cell function. Thus, our study suggests that, in mice and in humans, GPS2 controls the reprogramming of white adipocytes to influence pancreatic islet function and insulin secretion.

| S-EPMC7495095 | biostudies-literature

Gene expression profiles of CD8+ partial memory T cells (Tpm) compared to naive, effector and memory CD8+ T cells

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

2013-04-30 | E-GEOD-27139 | biostudies-arrayexpress