Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptomic profiling of HBG gene expression in HEK293T cell line

ABSTRACT: Transcriptomic profiling of HBG gene expression in HEK293T cell line

PROVIDER: PRJNA1085296 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR28260621_1.fastq.gz	Fastqsanger.gz
	SRR28260621_2.fastq.gz	Fastqsanger.gz
	SRR28260622_1.fastq.gz	Fastqsanger.gz
	SRR28260622_2.fastq.gz	Fastqsanger.gz
	SRR28260623_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 24

Similar Datasets

Transcriptomic profiling of HBG gene expression in HEK293T cell line

Project description:Efficiency of HBG gene activation by the Cas12f/cgRNA system. In a doxycycline-inducible dCas12f-VPR knock-in (KI) HEK293T cell line, transiently transfected plasmids encoding U6, linear, and circular gRNAs targeting HBG1, and cgRNAs targeting mNeonGreen (negative control, NC) to activate HBG gene expression. RNA-seq analysis showed that cgRNAs exhibited increased efficiency in the target gene HBG1 and slight lower specificity when compared with U6 and linear gRNAs.

2024-03-12 | GSE261105 | GEO

An Intergenic Silencer Region Regulates HBG Expression

Project description:The most common genetic disorders worldwide are the β-hemoglobinopathies, including sickle cell disease and β-thalassemia caused by HBB gene mutations. Five functional β-like globin genes on chromosome 11 are expressed during development in a tissue and stage-specific manner. The HBG genes encoding g-globin polypeptide chains to form fetal hemoglobin (HbF), undergo gene silencing during the first year of life. Our study aimed to characterize an upstream DNA regulatory region that can be targeted for HBG reactivation during adult development. We investigated the intergenic region between HBE1 and HBG2 which we termed the fetal chromatin domain (FCD) to define its role in globin gene regulation. Using normal human CD34+ stem cells to establish erythroid progenitors, we characterized the binding of different transcription factors to the FCD, which facilitated long-range chromatin looping between the FCD and locus control region and HBG. Using CRISPR/Cas9 genome editing technology, the FCD was knocked out in KU812 and CD34+ stem cells. We observed enhanced HBG transcription and HbF expression in both lines. For FCD knockout CD34+ stem cells, flow cytometry showed increased HbF positive cells and HbF expression and enhanced long-range interactions between the locus control and HBG region. Single cell RNA-sequencing revealed normal erythropoiesis in the FCD-KO line and partial reversal of HBG silencing. These results support a putative silencer role of the FCD in regulating HBG transcription and HbF expression.

2025-11-26 | GSE311528 | GEO

ATAC-seq of HEK293T cell line

Project description:ATAC-seq of HEK293T cell line

| PRJEB20596 | ENA

RNA-seq of HEK293T cell line

Project description:RNA-seq of HEK293T cell line

| PRJEB20597 | ENA

Removal of promoter DNA methylation by epigenome editing reverses HBG silencing [CUT&RUN]

Project description:Beta-hemoglobinopathies caused by mutations in adult-expressed HBB can be treated by re-activating the adjacent paralogous genes HBG1 and HBG2 (HBG), which are normally silenced perinatally. Although HBG expression is induced by global demethylating drugs, their mechanism is poorly understood and toxicity limits their use. We identified the DNMT1-associated maintenance methylation protein UHRF1 as a mediator of HBG repression in a genome-wide screen. Loss of UHRF1 in the adult-type erythroid cell line HUDEP2 caused global demethylation and HBG activation that was reversed upon localized promoter re-methylation. Conversely, targeted demethylation of the HBG promoters activated their genes in HUDEP2 or primary CD34+ cell-derived erythroblasts. Mutation of MBD2, a CpG-methylation reading component of the NuRD complex, to impair methylation sensitivity recapitulated the effects of promoter demethylation. Our studies demonstrate that localized CpG-methylation at the HBG promoters facilitates developmental silencing and identify a targeted therapeutic approach for b-hemoglobinopathies via epigenomic editing.

2025-06-24 | GSE284291 | GEO

Removal of promoter DNA methylation by epigenome editing reverses HBG silencing [ATAC-seq]

2025-06-24 | GSE284290 | GEO

Removal of promoter DNA methylation by epigenome editing reverses HBG silencing [RNA-seq]

2025-06-24 | GSE284289 | GEO

GLUTag cell line transcriptomic profiling

Project description:GLUTag cell line transcriptomic profiling

| PRJNA798250 | ENA

Effect of SRPK1 knockdown on gene expression of HEK293T cell line

Project description:Effect of SRPK1 knockdown on gene expression of HEK293T cell line

| PRJNA1193674 | ENA

Gene expression analysis of HEK293T cells after CHMP5 gene modulation

Project description:Microarray-based gene expression analysis identified genes differentially expressed in HEK293T cells after CHMP5 gene modulation. In this study, HEK293T cells, silenced for CHMP5 using sh-CHMP5 was compared to genome wide expression changes when compared to cellular transfections with a sh-luciferase control by Significance Analysis of Microarray data. Further, overexpression of CHMP5 using the vector pCMV_CHMP5 was compared to cellular transfections with an empty vector pCMV in the cell line HEK293T

2010-07-08 | E-GEOD-17003 | 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