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Med1 controls effector CD8+ T cell differentiation and survival through mediating the transcriptional regulation of C/EBPβ on T-bet

ABSTRACT: Med1 controls effector CD8+ T cell differentiation and survival through mediating the transcriptional regulation of C/EBPβ on T-bet

PROVIDER: PRJNA796966 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17606970_1.fastq.gz	Fastqsanger.gz
	SRR17606970_2.fastq.gz	Fastqsanger.gz
	SRR17606971_1.fastq.gz	Fastqsanger.gz
	SRR17606971_2.fastq.gz	Fastqsanger.gz
	SRR17606972_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Med1 controls effector CD8+ T cell differentiation and survival through mediating the transcriptional regulation of C/EBPβ on T-bet

Project description:Effector CD8+ T cells are crucial in adaptive immunity for effective protection against infectious pathogens. The regulatory mechanisms underlying CD8+ effector T cell development are incompletely understood. Here, we defined a critical role of mediator complex subunit 1 (Med1) in controlling effector CD8+ T cell differentiation and survival during acute infections. Mice with Med1 deletion in CD8+ T cells exhibited a significantly impaired effector cell expansion with large reduction of KLRG1+ terminally differentiated and Ly6c+ effector cell populations. Med1 deficiency led to enhanced cell apoptosis and expression of exhausted T cell associated inhibitory receptors (PD-1, Tim3, Lag3 and TIGHT). RNA-Seq analysis revealed the defects of T-bet and Zeb2 mediated transcriptional programs in effector differentiation. Overexpression of T-bet could rescue the Med1-deficient CD8+ effector T cell differentiation and survival. Mechanistically, transcription factor C/EBPβ promoted T-bet expression through interacting with Med1 in effector T cells. Collectively, our findings revealed a novel role of Med1 in regulating effector CD8+ T cell differentiation and survival during immune response.

2022-01-17 | GSE193624 | GEO

ChIP-seq analysis of BRD4, MED1 and P65 in SCC1 cells after JQ1 treatment

Project description:To explore genome-wide alteration of BRD4, MED1, p65 and H3K27Ac during BET inhibition, we performed chromatin immunoprecipitation sequencing (ChIP-seq) of SCC1 cells to examine genome-wide recruitment of the MED1, BRD4, p65 and H3K27ac following JQ1 treatment. BET inhibition by JQ1 led to dramatically loss of the recruitment of MED1, BRD4 and p65 at a cohort of key oncogenes associate with tumorigenesis and metastasis. Suggesting BET inhibition is effective strategy to suppress the tumorigenesis and metastasis of head and neck squamous cell carcinoma.

2021-05-05 | GSE131710 | GEO

Genome-wide C/EBPβ traget genes in C/EBPβ-overexpressed HL-60 cells.

Project description:To characterize genome-wide C/EBPβ traget genes in C/EBPβ-overexpressed HL-60 cells by ChIP-seq.

2018-06-13 | GSE100486 | GEO

Med1 overexpression induces cell proliferation

2013-07-18 | GSE48950 | GEO

C/EBPβ deficiency reshapes microglial gene expression

Project description:CCAAT/enhancer binding protein β (C/EBPβ) is a transcription factor that regulates the expression of important pro-inflammatory genes in microglia. Mice deficient for C/EBPβ show protection against excitotoxic and ischemic CNS damage but the involvement of the various C/EBPβ expressing cell types in this neuroprotective effect is not solved. Since C/EBPβ-deficient microglia show attenuated neurotoxicity in culture we hypothesized that specific C/EBPβ deficiency in microglia could be neuroprotective in vivo. In this study we have tested this hypothesis by generating mice with myeloid C/EBPβ deficiency. Mice with myeloid C/EBPβ deficiency were generated by crossing LysMCre and C/EBPβfl/fl mice . Primary microglial cultures from C/EBPβfl/fl (named here as WT) and LysMCre-C/EBPβfl/fl (named here as KO) mice were treated with lipopolysaccharide ± interferon γ (IFNγ) for 6 h and gene expression was analyzed by RNA sequencing. LysMCre-C/EBPβfl/fl mice showed an efficiency of C/EBPβ deletion of 100% in cultured microglia. Transcriptomic analysis of C/EBPβ-deficient primary microglia revealed C/EBPβ-dependent expression of 1068 genes, significantly enriched in inflammatory and innate immune responses GO terms. This study provides new data that support a central role for C/EBPβ in the biology of activated microglia.

2017-06-13 | GSE90046 | GEO

Med1 overexpression induces cell proliferation

Project description:Med1 overexpression leads to induction of a wide spectrum of genes. Adenovirally-driven overexpression of Med1 in mouse liver stimulates hepatocyte DNA synthesis with enhanced expression of DNA replication, cell cycle control and liver specific genes as observed at day 3 and day 5 post injection. Med1 gene is amplified in a number of cancers so in this study we tested the hypothesis that Med1 by itself has the capacity to induce cell proliferation. Analysis of the Med1- induced gene expression showed a robust induction of a wide spectrum of genes involved in hepatocellular proliferation. Med1 floxed mice (Med1fl/fl) were injected with Ad-His-Med1 (adenovirus expressing Med1 gene) via tail vein and killed 3 or 5 days after injection. Ad-LacZ (adenovirus expression beta-galactosidase gene) injected mouse liver served as control. Total RNA were isolated from the liver and subjected to the microarray.

2013-07-18 | E-GEOD-48950 | biostudies-arrayexpress

T-bet and Runx3 orchestrate effector CD8 T cell differentiation and lineage fidelity through cooperative and distinct chromatin regulatory mechanisms

Project description:Effector CD8⁺T cells must rapidly acquire cytotoxic functions while maintaining lineage fidelity and suppressing alternative fates. T-bet and Runx3 are key transcription factors that drive this process, yet their integrated regulatory logic has remained unclear due to the lack of comprehensive binding and chromatin accessibility data. Here, we systematically dissect the cooperative and distinct roles of T-bet and Runx3 in shaping the transcriptional and epigenetic landscape of antiviral CD8⁺ T cells. Using CUT&RUN, ATAC-seq, and RNA-seq across single and double knockout models, we reveal that T-bet and Runx3 coordinate effector differentiation through both chromatin remodeling–dependent and –independent mechanisms. T-bet preferentially binds promoters and restrains Th17-like programs, while Runx3 targets distal elements to suppress Tfh-associated genes and sustain cytotoxic identity. Our findings uncover a cis-regulatory logic wherein these factors act combinatorially to balance activation of effector programs with repression of alternative lineages, ensuring functional precision during antiviral responses. This work establishes a comprehensive framework for understanding lineage enforcement by transcription factors in effector T cells.

2025-07-19 | GSE302525 | GEO

Enterobacteria phage MED1

Project description:Enterobacteria phage MED1 Genome sequencing

| PRJNA252514 | ENA

T-bet regulates the maintenance and ASC differentiation potential of lymph node and lung effector memory B cell subsets

Project description:While human and mouse memory B cells (Bmem) can express T-bet, its role in regulating Bmem function is largely unknown. We characterized multiple transcriptionally distinct clusters of mature, somatically-mutated nucleoprotein (NP)-specific Bmem in LNs and lungs of influenza-infected mice. Although none of the Bmem expressed the plasma cell (PC) lineage commitment factors Blimp1, one cluster was enriched for Tbx21+ cells. Like the previously described human T-bet+ effector Bmem (eBmem) population, Tbx21+ mouse Bmem upregulated gene networks associated with effector metabolism, protein synthesis and the unfolded protein response. Using constitutive and inducible mouse models to ablate T-bet in B cells, we showed that T-bet expression by Bmem was required for persistence of LN and lung eBmem with rapid in vitro and in vivo PC differentiation potential. Thus, T-bet marked NP+ eBmem that were poised to differentiate and was required for maintenance of eBmem that respond in the lung following viral re-exposure.

2025-06-18 | GSE288942 | GEO

RNA-seq profiling of C/EBPβ-overexpressing myoblasts [differentiating myoblasts]

Project description:We previously identified C/EBPβ as an inhibitor of myogenic differentiation and its role in muscle satellite cell’s self-renewal and quiescence. C/EBPβ is regulated during the transition from proliferation to differentiation in myoblasts and that overexpression of C/EBPβ inhibits myocyte differentiation. To identify the molecular mechanism by which C/EBPβ inhibits myogenic differentiation, we performed RNA-seq on C/EBPβ-overexpressing differentiating myoblasts.

2025-06-02 | GSE152053 | GEO

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