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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]

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE229930 | GEO | 2025/04/06

REPOSITORIES: GEO

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

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

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

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

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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]

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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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RBPMS in Heart Failure during aging

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Project description:To examine the impact of Cry1 downregulation on gene expression, empty vector (Sh Ctrl) and Sh-RNA targeting Cry1 (Sh Cry1) were used to produce lentiviral vector. Cell were then infected with control and sh-RNA lentivirus and then selected with puromycin. Upon validation of the knockdown with real time PCR. RNA were prepared from cells stably expressing empty vector or sh-RNA against Cry1 and used gene expression profiling by RNA seq. RNA of two biological replicate were prepared from each genotype.

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Lyssavirus matrix protein cooperates with phosphoprotein to modulate the Jak-Stat pathway.

Project description:Phosphoprotein (P) and matrix protein (M) cooperate to undermine the immune response to rabies virus (RABV) infections. While P is involved in the modulation of the Jak-Stat pathway through the cytoplasmic retention of interferon (IFN)-activated STAT1 (pSTAT1), M interacts with the RelAp43-p105-ABIN2-TPL2 complex, to efficiently inhibit the nuclear factor-?B (NF-?B) pathway. Using transfections, protein-complementation assays, reverse genetics and DNA ChIP, we identified a role of M protein in the control of Jak-Stat signaling pathway, in synergy with the P protein. In unstimulated cells, both M and P proteins were found to interact with JAK1. Upon type-I IFN stimulation, the M switches toward pSTAT1 interaction, which results in an enhanced capacity of P protein to interact with pSTAT1 and restrain it in the cytoplasm. Furthermore, the role for M-protein positions 77, 100, 104 and 110 was also demonstrated in interaction with both JAK1 and pY-STAT1, and confirmed in vivo. Together, these data indicate that M protein cooperates with P protein to restrain in parallel, and sequentially, NF-?B and Jak-Stat pathways.

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Activation of the JAK/STAT pathway in Behcet’s Disease

Project description:Th1/Th17-type T-cell responses are upregulated in Behcet’s disease (BD). However, signaling pathways associated with this aberrant immune response are not clarified. Whole-genome microarray profiling was performed with human U133 (Plus 2.0) chips using mRNA of isolated CD14+ monocytes and CD4+ T-cells from PBMC in patients with BD (n=9) and healthy controls (HC) (n=9). Flow cytometric analysis of unstimulated (US) and stimulated (PHA) STAT3 and pSTAT3 expressions of PBMCs were also analysed (BD and HC, both n=26). JAK1 was observed to be upregulated in both CD14+ monocytes (1.94 fold) and CD4+ T-lymphocytes (1.40 fold) of BD patients. Using canonical pathway enrichment analysis, JAK/STAT signaling was identified as activated in both CD14+ monocytes (p=2.95E-06) and in CD4+ lymphocytes (p=8.13E-04) in BD. Interferon (p=1.02E-07) and IL-6 (p=8.91E-03) signaling pathways were also prominent in CD14+ monocytes. Basal unstimulated total STAT3 expression was significantly higher in BD (1.2 vs 3.45, p<0.05). The JAK1/STAT3 signaling pathway is activated in BD, possibly through the activation of Th1/Th17-type cytokines such as IL-2, IFNγ, IL-6, IL-17 and IL-23.

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