Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Erythroid differentiation regulator-1 is induced by microbiota in early life and drives intestinal stem cell proliferation and regeneration

ABSTRACT: Erythroid differentiation regulator-1 is induced by microbiota in early life and drives intestinal stem cell proliferation and regeneration

PROVIDER: PRJEB35428 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR3665740.fastq.gz	Fastqsanger.gz
	ERR3665741.fastq.gz	Fastqsanger.gz
	ERR3665742.fastq.gz	Fastqsanger.gz
	ERR3665743.fastq.gz	Fastqsanger.gz
	ERR3665744.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Erythroid differentiation regulator-1 induced by microbiota in early life drives intestinal stem cell proliferation and regeneration.

Project description: Not available

| S-EPMC6981263 | biostudies-literature

STAT1 regulates immune-mediated intestinal stem cell proliferation and epithelial regeneration

Project description:STAT1 regulates immune-mediated intestinal stem cell proliferation and epithelial regeneration

| PRJNA1154957 | ENA

STAT1 regulates immune-mediated intestinal stem cell proliferation and epithelial regeneration

Project description:The role of the immune system in regulating tissue stem cells remains poorly understood, as does the relationship between immune-mediated tissue damage and regeneration. Graft vs. host disease (GVHD) occurring after allogeneic bone marrow transplantation (allo-BMT) involves immune-mediated damage to the intestinal epithelium and its stem cell compartment. To assess impacts of T-cell-driven injury on distinct epithelial constituents, we performed single cell RNA sequencing on intestinal crypts following experimental BMT. Intestinal stem cells (ISCs) from GVHD mice exhibited global transcriptomic changes associated with a substantial Interferon-γ response and upregulation of STAT1. To determine its role in crypt function, STAT1 was deleted within murine intestinal epithelium. Following allo-BMT, STAT1 deficiency resulted in reduced epithelial proliferation and impaired ISC recovery. Similarly, epithelial Interferon-γ receptor deletion also attenuated proliferation and ISC recovery post-transplant. Investigating the mechanistic basis underlying this epithelial response, ISC STAT1 expression in GVHD was found to correlate with upregulation of ISC c-Myc. Furthermore, activated T cells stimulated Interferon-γ- dependent epithelial regeneration in co-cultured organoids, and Interferon-γ directly induced STAT1-dependent c-Myc expression and ISC proliferation. These findings illustrate immunologic regulation of a core tissue stem cell program after damage and support a role for Interferon-γ as a direct contributor to epithelial regeneration.

2024-09-09 | GSE276126 | GEO

FOXK1 and FOXK2 Promote Cardiomyocyte Proliferation and Heart Regeneration

Project description:Promoting the proliferation of endogenous cardiomyocytes represents a promising strategy for treating cardiac injuries. Identifying key factors that regulate cardiomyocyte proliferation can advance the development of novel therapies for heart regeneration. Here we identify that FOXK1 and FOXK2 act as master regulators of cardiomyocyte proliferation and metabolism. The expression of FOXK1 and FOXK2 decreased with postnatal heart development. Cardiomyocyte-specific knockout of Foxk1 or Foxk2 inhibited neonatal heart regeneration after myocardial infarction (MI) injury. Conversely, AAV9-mediated cardiomyocyte-specific overexpression of FOXK1 or FOXK2 prolonged the postnatal proliferative window of cardiomyocytes and enhanced cardiac repair in adult mice by promoting endogenous cardiomyocyte proliferation after MI. Mechanistically, FOXK1 and FOXK2 induce Ccnb1 and Cdk1 transcription and cardiomyocyte cell cycle progression, respectively. Ccnb1 knockdown hindered FOXK1 overexpression-induced cardiomyocyte proliferation, and the same effect was observed when Cdk1 was knocked down in FOXK2 overexpressing cardiomyocytes. Additionally, we further revealed that FOXK1 and FOXK2 induced a metabolic shift toward glycolysis by promoting HIF1α expression in cardiomyocytes, which favors cardiomyocyte proliferation. Our findings identify FOXK1 and FOXK2 as critical triggers of cardiomyocyte proliferation and define these two transcription factors as novel therapeutic targets for myocardial infarction.

2025-02-13 | MTBLS12191 | MetaboLights

Yap1 promotes proliferation of transiently amplifying stress erythroid progenitors during erythroid regeneration.

Project description: Not available

| S-EPMC6952558 | biostudies-literature

HMGB2 Promotes Cardiomyocyte Proliferation and Heart Regeneration Through MTA2-driven Metabolic Reprogramming

Project description:Neonatal heart possesses the unique ability to regenerate post-injury. Underlying related mechanisms and reactivation of this process are crucial for regeneration medicine. Using quantitative proteomics with tandem mass tag labeling, RNA-sequencing (RNA-seq) and single-nucleus RNA-seq dataset analyses, high mobility group box 2 (HMGB2) was identified as a key regulator of cardiomyocyte proliferation, whose expression declines during postnatal heart development and increases in the high regenerative potential cardiomyocyte populations in hearts post-injury. Cardiomyocyte-specific HMGB2 knockdown curtails cardiomyocyte proliferation and impairs heart regeneration following apical resection (AR) in neonatal mice, while cardiomyocyte-specific HMGB2 overexpression enhances cardiomyocyte proliferation and facilitates cardiac regeneration and repair in adult mice post-myocardial infarction (MI). Mechanistically, RNA-seq analysis revealed that HMGB2 promotes cardiomyocyte proliferation via activating hypoxia inducible factor 1ɑ (HIF-1α)-mediated glycolysis. This study further found HMGB2 can directly interact with metastasis-associated protein 2 (MTA2) and inhibit its ubiquitination degradation to stabilize HIF-1α protein through immunoprecipitation-mass spectrometry (IP-MS) analysis. Finally, activating HIF-1α or MTA2 could also promote cardiomyocyte proliferation and cardiac repair in adult mice following MI. Taken together, these findings highlight HMGB2 plays a crucial role in promoting heart regeneration through regulating glycolysis. Activating the HMGB2-MTA2-HIF-1α axis might serve as potential therapeutic options for regenerative therapies post-myocardial injury.

2026-05-01 | GSE302427 | GEO

Regeneration Alters Open Chromatin and Cis-Regulatory Landscape of Erythroid Precursors

Project description:Regeneration Alters Open Chromatin and Cis-Regulatory Landscape of Erythroid Precursors

| PRJNA1150669 | ENA

Tp53 suppression promotes cardiomyocyte proliferation during zebrafish heart regeneration

Project description:Tp53 suppression promotes cardiomyocyte proliferation during zebrafish heart regeneration

| PRJNA612190 | ENA

Amplified EPOR/JAK2 genes define a unique subtype of acute erythroid leukemia

Project description:Acute erythroid leukemia (AEL) is a unique subtype of acute myeloid leukemia characterized by prominent erythroid proliferation, whose molecular basis is poorly understood. To elucidate the underlying mechanism of erythroid proliferation, we performed comprehensive genomic study. The aim of this study is to unveil genotype phenotype correlations and the feasible molecular targets for therapy of AEL.

| EGAS00001005810 | EGA

ASCL2 is a key regulator of the proliferation-differentiation equilibrium in the esophageal epithelium

Project description:The esophagus is protected from the hostile environment by a stratified epithelium, which renews rapidly. Homeostasis of this epithelium is ensured by a rare population of stem cells in the basal layer: Keratin 15+ (Krt15+) cells. However, little is known about the molecular mechanisms regulating their distinct features, namely self-renewal, potency, and epithelial regeneration. Achaete-Scute Family BHLH Transcription Factor 2 (ASCL2) is strongly upregulated in Krt15+ stem cells and is known to contribute to stem cell maintenance in other tissues. Herein, we investigated the role of ASCL2 in maintaining homeostasis under normal and stress conditions in the esophageal epithelium. ASCL2 overexpression severely dysregulated cell differentiation and cell fate. Proliferation was also reduced due potentially to a blockage in the G1 phase of the cell cycle or an induction of quiescence. Mass spectrometry analysis confirmed alterations in several proteins associated with differentiation and cell cycle. In addition, overexpression of ASCL2 enhanced resistance to radiation and chemotherapeutic drugs. Overall, these results denoted the role of ASCL2 as a key regulator of the proliferation-differentiation equilibrium in the esophageal epithelium.

2024-05-24 | PXD039477 | Pride

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