Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Med23 serves as a gatekeeper of the myeloid potential of hematopoietic stem cells

ABSTRACT: Med23 serves as a gatekeeper of the myeloid potential of hematopoietic stem cells

PROVIDER: PRJNA438937 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6856310_1.fastq.gz	Fastqsanger.gz
	SRR6856310_2.fastq.gz	Fastqsanger.gz
	SRR6856311_1.fastq.gz	Fastqsanger.gz
	SRR6856311_2.fastq.gz	Fastqsanger.gz
	SRR6856312_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 16

Similar Datasets

Med23 serves as a gatekeeper of the myeloid potential of hematopoietic stem cells

Project description:In response to myeloablative stresses, HSCs are rapidly activated to replenish myeloid progenitors, while maintaining full potential of self-renewal to ensure life-long hematopoiesis. However, the key factors that orchestrate HSC activities during physiological stresses remain largely unknown. Here we report that Med23 controls the myeloid potential of activated HSCs. Ablation of Med23 in hematopoietic system leads to lymphocytopenia. Med23- deficient HSCs undergo myeloid-biased differentiation and lose the self-renewal capacity. Interestingly, Med23-deficient HSCs are much easier to be activated in response to physio- logical stresses. Mechanistically, Med23 plays essential roles in maintaining stemness genes expression and suppressing myeloid lineage genes expression. Med23 is downregulated in HSCs and Med23 deletion results in better survival under myeloablative stress. Altogether, our findings identify Med23 as a gatekeeper of myeloid potential of HSCs, thus providing unique insights into the relationship among Med23-mediated transcriptional regulations, the myeloid potential of HSCs and HSC activation upon stresses.

2018-07-14 | GSE112008 | GEO

The mediator subunit Med23 serves as a gatekeeper of the myeloid-primed state of hematopoietic stem cells (ATAC-Seq)

Project description:To ensure the rapid response to stimuli, some HSCs are specifically prepared (primed) for tasks involving activation and reconstitution. However, the key factors that regulate the primed state of HSCs are largely unknown. Here we report that Med23 controls the formation of myeloid-primed HSCs. Ablation of Med23 in hematopoietic system leads to lymphocytopenia. Moreover, Med23-deficient HSCs undergo myeloid-biased differentiation and lose the self-renewal capacity. Interestingly, Med23-deficient HSCs are in myeloid-primed state and are much easier to be activated in response to physiological stresses. Mechanistically, Med23 plays essential roles in maintaining stemness genes expression and suppressing myeloid lineage genes expression. Med23 is down-regulated in HSCs and Med23 deletion results in better survival under myeloablative stress. Altogether, our findings identified Med23 as a gatekeeper of the myeloid-primed state of HSCs, thus providing unique insights into the relationship among Med23-mediated transcriptional regulations, the myeloid-primed state of HSCs and HSC activation upon stresses.

2018-07-15 | GSE112357 | GEO

The mediator subunit Med23 serves as a gatekeeper of the myeloid-primed state of hematopoietic stem cells (RNA-Seq)

2018-07-15 | GSE112358 | GEO

The mediator subunit Med23 serves as a gatekeeper of the myeloid-primed state of hematopoietic stem cells

Project description:The mediator subunit Med23 serves as a gatekeeper of the myeloid-primed state of hematopoietic stem cells

| PRJNA445738 | ENA

Med23 serves as a gatekeeper of the myeloid potential of hematopoietic stem cells.

Project description:In response to myeloablative stresses, HSCs are rapidly activated to replenish myeloid progenitors, while maintaining full potential of self-renewal to ensure life-long hematopoiesis. However, the key factors that orchestrate HSC activities during physiological stresses remain largely unknown. Here we report that Med23 controls the myeloid potential of activated HSCs. Ablation of Med23 in hematopoietic system leads to lymphocytopenia. Med23-deficient HSCs undergo myeloid-biased differentiation and lose the self-renewal capacity. Interestingly, Med23-deficient HSCs are much easier to be activated in response to physiological stresses. Mechanistically, Med23 plays essential roles in maintaining stemness genes expression and suppressing myeloid lineage genes expression. Med23 is downregulated in HSCs and Med23 deletion results in better survival under myeloablative stress. Altogether, our findings identify Med23 as a gatekeeper of myeloid potential of HSCs, thus providing unique insights into the relationship among Med23-mediated transcriptional regulations, the myeloid potential of HSCs and HSC activation upon stresses.

| S-EPMC6138688 | biostudies-literature

The mediator subunit Med23 serves as a gatekeeper of the myeloid-primed state of hematopoietic stem cells (ATAC-Seq)

Project description:The mediator subunit Med23 serves as a gatekeeper of the myeloid-primed state of hematopoietic stem cells (ATAC-Seq)

| PRJNA445739 | ENA

The mediator subunit Med23 serves as a gatekeeper of the myeloid-primed state of hematopoietic stem cells (RNA-Seq)

Project description:The mediator subunit Med23 serves as a gatekeeper of the myeloid-primed state of hematopoietic stem cells (RNA-Seq)

| PRJNA445740 | ENA

The mediator subunit Med23 serves as a gatekeeper of the myeloid-primed state of hematopoietic stem cells

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

2018-07-15 | GSE112359 | GEO

MEF wt versus Med23-/- KO after 20% Serum Stimulation

Project description:Affymetrix MOE430A arrays. Mouse embryonic fibroblasts (MEFs) from E11 passaged through crisis. Starved in 0.5% FBS for 16 h then stimulated by 20% serum final concentration for 30 minutes. The purpose was to identify genes affected by the loss of MED23 protein (subunit of the mediator complex). Samples were assayed in duplicate (Set 1 and Set 2) for starved state and serum state cells. Cells starved in low-serum (0.5%) for 16 h then add final conc. 20% FBS for 30 minutes. Harvest total RNA from duplicate samples. One sample set is kept starved and serves as the baseline. The other set is stimulated. This is done for both wild-type cell and the Med23-/- KO cells. We looked for gene expression fold changes greater than 2 (plus or minus) to find genes affected for serum stimulation by the loss of MED23, looking in detail at immediate early genes like Egr1.

2009-04-14 | E-GEOD-15638 | biostudies-arrayexpress

Effect of depletion of Med23 on gene expression during VSV infection of MEF and BMDM cells.

Project description:The detection of cytosolic viral nucleic acids via pattern recognition receptors (PRRs) activates multiple signaling pathways, leading to the production of interferons (IFNs), which are essential for host survival during viral infection. Precise control of PRR gene expression is crucial for maintaining immune homeostasis. Here, we showed that Mediator complex subunit 23 (Med23) is required for the precise production of the innate immune receptor RIG-I in response to RNA virus infection. Med23 deficiency markedly enhances the production of type I IFNs, proinflammatory cytokines and IFN-stimulated genes (ISGs) in both multiple cell lines and primary macrophages infected with RNA viruses or stimulated with poly(I:C). Myeloid-specific Med23 knockout mice were generated to test the critical role of Med23 in host resistance to RNA virus infection in vivo. Mechanistically, Med23 interacts with the transcription factor forkhead box O3 (Foxo3) to negatively regulate RIG-I, thereby modulating IFN-I signaling. Collectively, these findings elucidate a previously unrecognized role of Med23 as a gatekeeper of the RIG-I-mediated antiviral innate immune response and suggest a potential target for controlling viral infection.

2025-06-26 | GSE281340 | 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