Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α (RNA-seq)

ABSTRACT: 3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α (RNA-seq)

PROVIDER: PRJNA697860 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13577091_1.fastq.gz	Fastqsanger.gz
	SRR13577091_2.fastq.gz	Fastqsanger.gz
	SRR13577092_1.fastq.gz	Fastqsanger.gz
	SRR13577092_2.fastq.gz	Fastqsanger.gz
	SRR13577093_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α

Project description:3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α

| PRJNA697855 | ENA

3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α (ChIP-seq)

Project description:3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α (ChIP-seq)

| PRJNA697859 | ENA

Reactivation of Zeta-Globin by deletion of BCL11A and LRF in murine cells

Project description:The alpha and beta-globin loci harbour genes that are expressed during development and silenced throughout post-natal life. Learning to reactivate these genes may offer new therapeutic approaches for the hemoglobinopathies, the most common single gene disorders. Here, we address the mechanisms underlying the regulation of the gene encoding zeta-globin, the embryonically expressed alpha-like globin.

2021-05-09 | GSE174110 | GEO

3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α.

Project description:The human ζ-globin gene (HBZ) is transcribed in primitive erythroid cells only during the embryonic stages of development. Reactivation of this embryonic globin synthesis would likely alleviate symptoms both in α-thalassemia and sickle-cell disease. However, the molecular mechanisms controlling ζ-globin expression have remained largely undefined. Moreover, the pharmacologic agent capable of inducing ζ-globin production is currently unavailable. Here, we show that TRIAC, a bioactive thyroid hormone metabolite, significantly induced ζ-globin gene expression during zebrafish embryogenesis. The induction of ζ-globin expression by TRIAC was also observed in human K562 erythroleukemia cell line and primary erythroid cells. Thyroid hormone receptor α (THRA) deficiency abolished the ζ-globin-inducing effect of TRIAC. Furthermore, THRA could directly bind to the distal enhancer regulatory element to regulate ζ-globin expression. Our study provides the first evidence that TRIAC acts as a potent inducer of ζ-globin expression, which might serve as a new potential therapeutic option for patients with severe α-thalassemia or sickle-cell disease.

| S-EPMC8235803 | biostudies-literature

Reactivation of Zeta-Globin by deletion of BCL11A and LRF in HUDEP cells (ChIP-seq)

2021-04-28 | GSE173417 | GEO

Reactivation of Zeta-Globin by deletion of BCL11A and LRF in HUDEP cells (ATAC-seq)

2021-04-28 | GSE173416 | GEO

3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α

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

2024-01-01 | GSE165770 | GEO

A cardiac developmental defect prevents thyroid hormone induced tachycardia in Resistance to Thyroid Hormone alpha

Project description:Purpose: The objective of this study was to determine the cardiac gene expression prifile in the whole heart of mice with mutated thyroid receptor alpha 1 (TRα1R384C+/m) in control condition as well as after treatement with 3,3´,5-triiodo-L-thyronine (T3) for 12 days.

2023-04-23 | GSE206337 | GEO

A cardiac developmental defect prevents thyroid hormone induced tachycardia in the syndrome of resistance to thyroid hormone alpha

Project description:Purpose: the objective of this study was to determine cardiac gene expression profile in the mice heart of mutated thyroid receptor alpha 1 (TRα1R384C+/m) male offspring of control dams as well as of dams treated with 3,3',5-triiodo-L-thyronine (T3) from embryonic day 12.5 to 18.5

2023-04-23 | GSE227847 | GEO

A cardiac developmental defect prevents thyroid hormone induced tachycardia in the syndrome of resistance to thyroid hormone alpha

Project description:Purpose: the objective of this study was to determine the whole DNA methylation profile in the mice heart of mutated thyroid receptor alpha 1 (TRα1R384C+/m) male offspring of control dams as well as of dams treated with 3,3',5-triiodo-L-thyronine (T3) from embryonic day 12.5 to 18.5

2023-04-23 | GSE226701 | GEO

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