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Nuclear matrix associated protein SMAR1 attenuated acute graft-versus-host disease by targeting JAK-STAT signaling in CD4+ T cells

ABSTRACT: Nuclear matrix associated protein SMAR1 attenuated acute graft-versus-host disease by targeting JAK-STAT signaling in CD4+ T cells

PROVIDER: PRJNA956823 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24203200_1.fastq.gz	Fastqsanger.gz
	SRR24203200_2.fastq.gz	Fastqsanger.gz
	SRR24203201_1.fastq.gz	Fastqsanger.gz
	SRR24203201_2.fastq.gz	Fastqsanger.gz
	SRR24203202_1.fastq.gz	Fastqsanger.gz

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Nuclear matrix associated protein SMAR1 attenuated acute graft-versus-host disease by targeting JAK-STAT signaling in CD4+ T cells [ATAC-Seq]

Project description:Nuclear matrix associated protein SMAR1 attenuated acute graft-versus-host disease by targeting JAK-STAT signaling in CD4+ T cells [ATAC-Seq]

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Nuclear matrix associated protein SMAR1 attenuated acute graft-versus-host disease by targeting JAK-STAT signaling in CD4+ T cells [RNA-Seq]

Project description:Nuclear matrix associated protein SMAR1 attenuated acute graft-versus-host disease by targeting JAK-STAT signaling in CD4+ T cells [RNA-Seq]

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Nuclear matrix associated protein SMAR1 attenuated acute graft-versus-host disease by targeting JAK-STAT signaling in CD4+ T cells [RNA-Seq]

Project description:To investigate the function of nuclear matrix associated protein SMAR1 in the CD4+T cell, human primary CD4+ T cells were transfected with the SMAR1 lentivirus vector or empty vector. We performed mRNA gene expression profiling analysis using data obtained from RNA-seq.

2025-04-06 | GSE229930 | GEO

Nuclear matrix associated protein SMAR1 attenuated acute graft-versus-host disease by targeting JAK-STAT signaling in CD4+ T cells [ATAC-Seq]

Project description:As a chromatin remodeling factor, SMAR1 might promote local chromatin changes, leading to the activation or inhibition of specific gene subsets in T cells. We performed high-resolution ATAC-seq on primary CD4+ T cells with SMAR1 overexpression (OE) and control (Ctrl), conducting a genome-wide analysis to map the locations and profile the accessibility of diverse regulatory elements.

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JAK/STAT blockade in cHL

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JAK-STAT pathways maintain homeostasis in immune cells (ATAC-Seq)

Project description:Immune cells need to sustain a state of constant alertness over a lifetime. Yet, little is known about the regulatory processes that control the fluent and fragile balance that is called homeostasis. Here we demonstrate that JAK-STAT signaling, beyond its role in immune responses, is a major regulator of immune cell homeostasis. We investigated JAK-STAT-mediated transcription and chromatin accessibility across 12 mouse models, including knockouts of all STAT transcription factors and of the TYK2 kinase. Baseline JAK-STAT signaling was detected in CD8+ T cells and macrophages of unperturbed mice – but abrogated in the knockouts and in unstimulated immune cells deprived of their normal tissue context. We observed diverse transcription-regulatory programs, including gene regulation by STAT2 and IRF9 independent of STAT1. In summary, our large-scale dataset and integrative analysis of JAK-STAT mutant and wildtype mice uncovered a crucial role of JAK-STAT signaling in unstimulated immune cells, where it contributes to a poised epigenetic and transcription-regulatory state and helps prepare these cells for rapid response to immune stimuli.

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JAK-STAT signaling maintains homeostasis in T cells and macrophages (spatial transcriptomics)

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Expression profiling in the Drosophila eye reveals unexpected repression of Notch signaling by the JAK/STAT pathway

Project description:Although the JAK/STAT pathway regulates numerous processes in vertebrates and invertebrates through modulating transcription, its functionally-relevant transcriptional targets remain largely unknown. With one jak and one stat (stat92E), Drosophila provides a powerful system for finding new JAK/STAT target genes. Genome-wide expression profiling on eye discs in which Stat92E is hyperactivated, revealed 584 differentially-regulated genes, including known targets domeless, socs36E and wingless. Other differentially-regulated genes (chinmo, lama, Mo25, Imp-L2, Serrate, Delta) were validated and may represent new Stat92E targets. Genetic experiments revealed that Stat92E cell-autonomously represses Serrate, which encodes a Notch ligand. Loss of Stat92E led to de-repression of Serrate in the dorsal eye, resulting in ectopic Notch signaling and aberrant eye growth there. Thus, our micro-array documents a new Stat92E target gene and a previously-unidentified inhibitory action of Stat92E on Notch signaling. These data suggest that this study will be a useful resource for the identification of additional Stat92E targets. Identification of the JAK/STAT pathway target genes in the Drosophila eye disc Keywords: Genotype comparison Gene expression profiles from five biological replicates of eye discs with yw (control) and GMR-upd (overexpressing JAK/STAT ligand unpaired) were compared using genome wide mRNA expression profiling by Affymetrix genechip arrays (Drosophila 2.0) and key targets were validated by clonal analysis, in situ hybridization, immunohistochemical staining and quantitative real-time PCR.

2009-08-01 | E-GEOD-15868 | biostudies-arrayexpress

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