Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Persistence of effector memory Th1 cells is regulated by the homeobox only protein Group1 Hopx-/-, Group2 Hopx+/-, Group3 Hopx+/+

ABSTRACT: Hopx appears to be needed for persistence of Th1 effector memory cells. IFN-gamma-producing Th cells are significantly reduced in Hopx-deficient mice compared to Hopx-expressing littermates and Hopx-deficient Th1 cells show a defective persistence upon adoptive transfer. Moreover, Hopx protects Th1 cells from Fas-mediated cell death in vitro. To further dissect the role of Hopx and to identify target genes of Hopx, we have performed transcriptome analysis to compare gene expression in Hopx-deficient versus Hopx-competent Th1 cells. In agreement with the role of Hopx in supporting survival of Th1 effector memory cells, anti-apoptotic cells were up-regulated and pro-apoptotic genes were down-regulated in Hopx-competent compared to Hopx-deficient Th1 cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE24437 | GEO | 2010/09/30

SECONDARY ACCESSION(S): PRJNA132673

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Expression data from DC-induced Hopx-deficient and sufficient regulatory T cells after immunization

Project description:We found that Hopx is required for the function of DC-induced regulatory T cells in vivo. We used microarrays to identify relevant Hopx-targets in such cells after antigenic re-challenge in vivo. CD25/Foxp3 double positive DC-induced Hopx-deficient and sufficient regulatory T cells were FACS sorted to high purity

2010-08-29 | E-GEOD-23167 | biostudies-arrayexpress

HOP homeobox (Hopx) and Histone deacetylase-2 (Hdac2) deficiency effect on the embryonic heart

Project description:Analysis of heart ventricles from Hopx, Hdac2, and both Hopx-Hdac2 deficient embryos at embryonic day E16.5. Results provide insight into the role of Hopx and Hdac2 in cardiac development. We used microarrays to detail the global programme of gene expression underlying cardiac development by Hopx and Hdac2 and identified distinct classes of up-regulated and down-regulated genes during this process. Mouse embryonic ventricles were selected at E16.5 for RNA extraction and hybridization on Affymetrix microarrays. We obtained three independent embryonic ventricles for WT, Hopx-null, Hdac2-null, and Hopx-Hdac2 double null genotypes.

2010-08-19 | E-GEOD-23700 | biostudies-arrayexpress

HOP homeobox (Hopx) and Histone deacetylase-2 (Hdac2) deficiency effect on the embryonic heart

2010-08-19 | GSE23700 | GEO

Next generation sequencing for quantitative transcriptomic analysis of Hopx-wildtype and Hopx-knockout murine bone marrow cells.

Project description:We generated Hopx conditional knockout mouse (Hopx-/-) and studied the biological effects of Hopx knockout on the hematopoietic system, via whole-transcriptome RNA-seq. The findigns of our studies support crucial roles of Hopx in physiological and malignant hematopoiesis.

2023-02-18 | GSE145476 | GEO

Role of Hopx in myogenesis and commitment [HopxKO]

Project description:Progenitor cells require coordinated expression of lineage-specific genes to regulate differentiation into daughter cell types. Hopx labels cardiac progenitors that are commited to the cardiac myocyte lineage. Hopx-deficiency leads to thin myocardium in approximately mid-gestation lethality in approximately 50% of embryos (secondary to thin myocardium and presumed cardiac rupture). Hopx-/- EBs display impaired myogenesis during cardiac differentiation. ChIP-seq and RNA expression analysis suggests that Hopx down regulates Wnt signaling by directly occupying and repressing wnt ligand genes. Analysis of embryoid bodies on day 8 of cardiac differentiation. RNA was made of from 1. Hopx +/- embryoid bodies, 2. Hopx -/- embryoid bodies, Embryonic stem cell lines were derived from littermate mouse blastocysts. Results provide insight into gene programs regulated by Hopx in cardiac development.

2015-06-01 | GSE67253 | GEO

Competitive regulation of HOPX transcription governs cardiomyocyte maturation

Project description:This study establishes the homeodomain only protein, HOPX, as a determinant controlling the molecular switch between cardiomyocyte progenitor and maturation gene programs. This dataset is about time-course CAGE (capped analysis of gene expression) data with genome-wide active transcription footprinting. HOPX CRISPRi cells were differentiated into cardiomyocytes ± DOX and analyzed by CAGE sequencing, among other methods. The study revealed that HOPX interacts with and controls core cardiac networks by regulating the activity of mutually exclusive developmental gene programs.

2022-05-21 | E-MTAB-11719 | biostudies-arrayexpress

Role of Hopx in myogenesis and commitment [HopxKO+Wnt]

Project description:Progenitor cells require coordinated expression of lineage-specific genes to regulate differentiation into daughter cell types. Hopx labels cardiac progenitors that are commited to the cardiac myocyte lineage. Hopx-deficiency leads to thin myocardium in approximately mid-gestation lethality in approximately 50% of embryos (secondary to thin myocardium and presumed cardiac rupture). Hopx-/- EBs display impaired myogenesis during cardiac differentiation. ChIP-seq and RNA expression analysis suggests that Hopx down regulates Wnt signaling by directly occupying and repressing wnt ligand genes. Analysis of embryoid bodies on day 8 of cardiac differentiation. RNA was made of from Hopx +/- embryoid bodies or Hopx -/- embryoid bodies treated with 12.5 uM XAV939. Heterozygous embryoid bodies included 0 uM XAV939, a well-characterized, known Wnt inhibitor. Embryonic stem cell lines were derived from littermate mouse blastocysts. Results provide insight into gene programs regulated by Hopx in cardiac development.

2015-06-01 | GSE67252 | GEO

Next generation sequencing for quantitative transcriptomic analysis of subpopulations of BM cells from young Hopx-wildtype and Hopx-knockout mice.

Project description:Hopx conditional knockout mouse (Hopx-/-) was generated. We then studied the biological effects of Hopx knockout on the hematopoietic system of young mice, via whole-transcriptome RNA-seq.

2023-02-18 | GSE145507 | GEO

Mus musculus

Project description:Persistence of effector memory Th1 cells is regulated by the homeobox only protein Group1 Hopx-/-, Group2 Hopx+/-, Group3 Hopx+/+

| PRJNA132673 | ENA

Homeodomain-only protein (HOPX) negatively regulates CD8+ T cell proliferation and affects differentiation and aging

Project description:HOPX is an atypical homeodomain-containing protein lacking DNA-binding capacity. Via interaction with transcription factors, particularly SRF, it has critical functions in the development of various tissues. Here we unveil an essential regulatory role of HOPX in human T lymphocytes. Human CD8+ T cells expressed all three isoforms (a, b, and c) of HOPX wherein HOPXb was the predominant one. HOPX expression was induced by TCR activation and increased from TN to TEM cells. Overexpression of HOPX constrained the proliferation of TN cells while knockdown of HOPX promoted the proliferation of TEM cells upon TCR activation. Mechanistically, HOPX/SRF bound to the promoters and repressed expression of MYC and NR4A1, the key regulators of T cell proliferation and activation. Importantly, CD8+ T cells from the elderly had elevated levels of HOPX, correlated with their blunted TCR-induced proliferation. Knockdown of HOPX rescued the proliferative capacity of T cells from the elderly. Our results support that HOPX is a molecular switch that balances CD8+ T cell proliferation across subsets and with age.

2024-01-23 | GSE234697 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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