Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ZFP148 is a transcriptional regulator of effector CD8+ T cell differentiation [single-cell_multiome]

ABSTRACT: Chronic antigen exposure, as seen in persistent viral infections and cancer, drives CD8⁺ T cells to differentiate into diverse subsets: progenitor/stem-like, effector, and exhausted/dysfunctional cells. While genetic and epigenetic factors influencing these subsets are known, the mechanisms regulating their dynamic balance remain unclear. We identified Zinc-Finger Protein 148 (ZFP148) as a novel transcriptional checkpoint in CD8⁺ T cell effector differentiation. Using a genetic approach that deletes ZFP148 specifically in CD8+ T cells, we performed matched single cell RNA-seq and ATAC-seq on antigen-specific CD8+ T cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE297040 | GEO | 2026/02/02

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

ZFP148 is a transcriptional regulator of effector CD8+ T cell differentiation

Project description:In the setting of chronic antigen stimulation, such as chronic viral infection and cancer, antigen-specific CD8+ T cells differentiate into a heterogeneous pool of progenitor/stem-like, effector, and exhausted/dysfunctional subsets. Though genetic and epigenetic programs that contribute to the generation of each subset have been reported, how these subsets are dynamically regulated and how their balance can be shifted from exhausted toward cytolytic effector cells remain as outstanding questions. Here, we identified Zinc-Finger Protein 148 (ZFP148) as a novel transcriptional checkpoint for CD8+ T cell effector differentiation. We performed CUT&Tag followed by seuqencing (CUT&Tag-seq) of ZFP148 in activated CD8+ T cells from healthy C57BL/6J mice to identify direct DNA-binding activity of ZFP148.

2026-02-02 | GSE296311 | GEO

Expression data from small intestine crypts of Zfp148gt/+APCMin/+ and Zfp148+/+APCMin/+ mice

Project description:The transcription factor Zinc finger protein 148 (Zfp148) interacts physically with the tumor suppressor p53, but the siginficance of this interaction is not known. We recently showed that knockout of Zfp148 in mice leads to ectopic activation of p53 in tissues and cultured fibroblasts, suggesting that Zfp148 represses p53 activity. Here we hypothesized that targeting Zfp148 would unleash p53 activity and protect against cancer development, and test this idea in the APCMin/+ mouse model of intestinal adenomas. Crypt-enriched tissues were isolated by laser microdissection (PALM) from the small intestines (proximal) of Zfp148gt/+APCMin/+ and Zfp148+/+APCMin/+ mice for RNA extraction and hybridization to Affymetrix microarrays.

2016-02-10 | E-GEOD-77773 | biostudies-arrayexpress

Expression data from small intestine crypts of Zfp148gt/+APCMin/+ and Zfp148+/+APCMin/+ mice

2016-02-10 | GSE77773 | GEO

Zfp281 and Zfp148 control CD4+ T cell thymic development and Th2 functions. (ChIP-seq)

Project description:How CD4+-lineage gene expression is initiated in differentiating thymocytes remains poorly understood. Here, we show that the paralog transcription factors Zfp281 and Zfp148 control both this process and cytokine expression by Th2 effector cells. Genetic, single-cell, and spatial transcriptomic analyses show that these factors promote the intrathymic CD4+ T cell differentiation of MHC II-restricted thymocytes, including expression of the CD4+ lineage-committing factor Thpok. In peripheral T cells, Zfp281 and Zfp148 promote chromatin opening at and expression of Th2 cytokine genes, but not of the Th2 lineage determining transcription factor Gata3. Zfp281 interacts with Gata3, and binds Gata3 genomic binding sites at loci encoding Thpok and Th2 cytokines. Thus, Zfp148 and Zfp281 collaborate with Gata3 to promote CD4+ T cell development and Th2 cell responses.

2023-11-13 | GSE207469 | GEO

Zfp281 and Zfp148 control CD4+ T cell thymic development and Th2 functions

Project description:How CD4+ lineage gene expression is initiated in differentiating thymocytes remains poorly understood. Here, we show that the paralog transcription factors Zfp281 and Zfp148 control both this process and cytokine expression by T helper cell type 2 (TH2) effector cells. Genetic, single-cell, and spatial transcriptomic analyses showed that these factors promote the intrathymic CD4+ T cell differentiation of class II major histocompatibility complex (MHC II)–restricted thymocytes, including expression of the CD4+ lineage–committing factor Thpok. In peripheral T cells, Zfp281 and Zfp148 promoted chromatin opening at and expression of TH2 cytokine genes but not of the TH2 lineage–determining transcription factor Gata3. We found that Zfp281 interacts with Gata3 and is recruited to Gata3 genomic binding sites at loci encoding Thpok and TH2 cytokines. Thus, Zfp148 and Zfp281 collaborate with Gata3 to promote CD4+ T cell development and TH2 cell responses. This SuperSeries is composed of the SubSeries listed below.

2023-11-10 | GSE207572 | GEO

ZFP148 is a transcriptional regulator of effector CD8+ T cell differentiation

Project description:ZFP148 is a transcriptional regulator of effector CD8+ T cell differentiation

| PRJNA1258888 | ENA

Expression of miRNAs in human ex-vivo CD8+ T cell subsets

Project description:The aim was to assess miRNA expression in 3 human ex-vivo CD8+ T cell subsets which span from antigen inexperienced cells (NaM-CM-/ve) to early memory cells (central memory, Tcm) and later stage memory cells (effector memory, Tem) CD8+ T cells were sorted on a FACS Aria II machine. N = naM-CM-/ve = CD8+, CCR7+, CD45RA+, CD45RO-, Tcm = central memory = CD8+, CCR7+, CD45RA-, CD45RO-,Tem= effector memory = CD8+, CCR7-, CD45RA-, CD45RO+ PBMC were isolated from 3 healthy human donors and sorted by FACS into 3 CD8+ T cell subsets. Total RNA was purified using the miRVANA kit (Ambion)

2014-10-24 | E-GEOD-54867 | biostudies-arrayexpress

ZFP148 is a transcriptional regulator of effector CD8+ T cell differentiation [single-cell_multiome]

Project description:ZFP148 is a transcriptional regulator of effector CD8+ T cell differentiation [single-cell_multiome]

| PRJNA1262431 | ENA

Transcription profiling of mouse CD8 T cells reveals prolonged IL-2R alpha expression on virus-specific CD8+ T cells favors terminal effector differentiation in vivo

Project description:CD25, the high affinity interleukin-2 (IL-2) receptor alpha-chain, is rapidly upregulated by antigen-specific CD8+ T cells after T cell receptor stimulation. We demonstrated that during an acute viral infection, CD25 expression was dynamic, and a subset of virus-specific CD8+ T cells sustained CD25 expression longer than the rest. Examination of the in vivo fate of effector CD8+ T cells exhibiting differential responsiveness to IL-2 revealed that CD25lo cells, which were relatively less sensitive to IL-2, preferentially upregulated CD127 and CD62L and gave rise to the functional long-lived memory pool. In contrast, CD25hi cells that accumulate enhanced IL-2 signals, proliferated more rapidly, were prone to apoptosis, exhibited a more pronounced effector phenotype, and appeared to be terminally differentiated. Sustained IL-2 receptor signaling resulted in increased CD8+ T cell proliferation, higher granzyme B expression and exaggerated contraction after antigen clearance. These data support the hypothesis that prolonged IL-2 signals during priming promote terminal effector differentiation of CD8+ T cells. Experiment Overall Design: An important question in memory development is understanding the differences between effector CD8 T cells that die versus effector cells that survive and give rise to memory cells. In this study we have performed genomic profiling of terminal effectors and memory precursors as defined by CD25 heterogeneity, towards better understanding the generation of these subsets. The two effector subsets were FACS purified based on the amount of cell surface CD25 expression into CD25lo and CD25hi subsets during the early expansion phase (Days 3-4 post-infection) and analyzed for their gene expression profiles (by genome-wide microarray analyses).

2010-02-17 | E-GEOD-19825 | biostudies-arrayexpress

CD8+ T-cell memory bears the transcriptional imprint of progressive differentiation

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

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