Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional repressor HIC1 contributes to suppressive function of human induced regulatory T cells

ABSTRACT: Transcriptional repressor HIC1 contributes to suppressive function of human induced regulatory T cells

PROVIDER: PRJNA355073 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

Transcriptional Repressor HIC1 Contributes to Suppressive Function of Human Induced Regulatory T Cells.

Project description:Regulatory T (Treg) cells are critical in regulating the immune response. In vitro induced Treg (iTreg) cells have significant potential in clinical medicine. However, applying iTreg cells as therapeutics is complicated by the poor stability of human iTreg cells and their variable suppressive activity. Therefore, it is important to understand the molecular mechanisms of human iTreg cell specification. We identified hypermethylated in cancer 1 (HIC1) as a transcription factor upregulated early during the differentiation of human iTreg cells. Although FOXP3 expression was unaffected, HIC1 deficiency led to a considerable loss of suppression by iTreg cells with a concomitant increase in the expression of effector T cell associated genes. SNPs linked to several immune-mediated disorders were enriched around HIC1 binding sites, and in vitro binding assays indicated that these SNPs may alter the binding of HIC1. Our results suggest that HIC1 is an important contributor to iTreg cell development and function.

| S-EPMC5842026 | biostudies-literature

HIC1 interacts with FOXP3 multi protein complex: a novel mechanism to regulate human regulatory T cell differentiation and function

Project description:Recent data have shown that Hypermethylated in cancer 1 (HIC1) is an important contributor to iTreg cell development and function. Using affinity-purification and tandem mass spectrometry we systematically characterized the HIC-1 interactome in human iTreg cells. On the basis of these data, we have shown that HIC1 is a part of FOXP3-RUNX1-CBFβ protein complex that regulates Treg signature genes and is indispensable for the suppressive function of FOXP3+ regulatory T cells. SRM was used to validate HIC1 interactors

2023-10-16 | PXD039337 | Pride

Retinoic Acid Induced Transcriptional Repressor HIC1 is Required for Suppressive Function of Human Induced Regulatory T cells [RNA-Seq 1]

Project description:Comparing the gene expression in control siRNA samples and HIC1 siRNA samples

2018-02-21 | GSE90468 | GEO

Transcriptional repressor HIC1 contributes to suppressive function of human induced regulatory T cells

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

2018-02-20 | GSE90570 | GEO

U2OS ad-HIC1 target identification

Project description:The tumor suppressor gene HIC1 (Hypermethylated in Cancer 1) is essential for mammalian development and is epigenetically silenced in many human tumors. Functionally, HIC1 is involved in a complex pathway regulating P53 tumor-suppression activity. HIC1 encodes a sequence-specific transcriptional repressor containing five Krüppel-like C2H2 zinc fingers but only a few genes regulated by HIC1 have been reported, including SIRT1. Keywords: Time Series Design

2007-12-13 | GSE9854 | GEO

Transcription profiling of human U2OS osteosarcoma cell line infected with ad-HIC1 to perform HICI target identification

Project description:The tumor suppressor gene HIC1 (Hypermethylated in Cancer 1) is essential for mammalian development and is epigenetically silenced in many human tumors. Functionally, HIC1 is involved in a complex pathway regulating P53 tumor-suppression activity. HIC1 encodes a sequence-specific transcriptional repressor containing five KrÃ¼ppel-like C2H2 zinc fingers but only a few genes regulated by HIC1 have been reported, including SIRT1. Experiment Overall Design: We performed genome-wide expression profiling analyses to identify new HIC1 target genes, in U2OS human osteosarcoma cells infected with adenoviruses expressing either HIC1 or GFP as control.

2008-06-17 | E-GEOD-9854 | biostudies-arrayexpress

Loss of Hic1 tumor suppressor potentiates Tlr2/NF-kB signaling and promotes tissue damage-associated tumorigenesis in the colon.

Project description:Hypermethylated in cancer 1 (HIC1) represents a prototypic tumor suppressor gene frequently inactivated by DNA methylation in many types of solid tumors. The gene encodes a sequence-specific transcriptional repressor controlling expression of several genes involved in the cycle or stress control. In this study, we employed a conditional Hic1 allele to identify genes influenced by the loss of Hic1.

2016-02-01 | E-MTAB-3486 | biostudies-arrayexpress

RNA-seq profiling of adult skeletal muscle after long term conditional knockout of Hic1 [TA RNA-seq]

Project description:To determine the effects of long term deletion of the transcriptional repressor Hypermethylated in cancer 1 (Hic1) on skeletal muscle, samples were collected of both wild type mice and those conditionally deleted for Hic1 and profiled by RNA sequencing. Aspects of muscle homeostasis were negatively impacted, highlighting cell and non cell autonomous roles for Hic1 in maintaining functional MPs and muscle tissue.

2019-12-05 | GSE133995 | GEO

Analysis of gene expression in control, Hic1 KO and p53 KO mouse embrynoic fibroblast (MEF) cell lines II

Project description:We hypothesised that genetic inactivation of the transcriptional repressor Hic1, would lead to changes in gene expression that may lead to transformation. We assessed changes in gene expression in immortal MEF cell lines in which Hic1 or p53 was inactivated.

2017-10-31 | GSE104393 | GEO

Analysis of gene expression in control, Hic1 KO and p53 KO mouse embrynoic fibroblast (MEF) cell lines I

Project description:We hypothesised that genetic inactivation of the transcriptional repressor Hic1, would lead to changes in gene expression that may lead to transformation. We assessed changes in gene expression in pre-immortal MEF cell lines in which Hic1 was inactivated compared to controls.

2017-10-31 | GSE104392 | 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