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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]

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE229932 | 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

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

2025-04-06 | GSE229933 | GEO

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

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 [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]

| PRJNA956830 | ENA

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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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-κB (NF-κB) 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-κB and Jak-Stat pathways.

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Insights into the role of the JAK/STAT signaling pathway in graft-<i>versus</i>-host disease.

Project description:Allogeneic hematopoietic transplantation (allo-HCT) is a curative therapy for a variety of hematologic malignancies, primarily through immune-mediated clearance of malignant cells. This graft-versus-leukemia (GvL) effect is mediated by alloreactive donor T-cells against recipient malignant cells. Unfortunately, graft versus host disease is a potentially lethal complication of this procedure, also mediated by alloreactive donor T-cells against recipient normal tissues. Graft-versus-host disease (GVHD) remains a key contributor to nonrelapse mortality and long-term morbidity in patients undergoing allo-HCT. Reducing GVHD without interfering with - or ideally while enhancing - GvL, would improve outcomes and increase patient eligibility for allo-HCT. The JAK/STAT signaling pathway acts downstream of over 50 cytokines and is central to a wide variety of inflammatory pathways. These pathways play a role in the development and maintenance of GVHD throughout the disease process and within T-cells, B-cells, macrophages, neutrophils, and natural killer cells. Agents targeting JAK/STAT signaling pathways have shown clinical efficacy and gained US Food and Drug Administration approval for numerous diseases. Here, we review the preclinical and clinical evidence for the role of JAK/STAT signaling in the development and maintenance of GVHD and the utility of blocking agents at preventing and treating GVHD.

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C9ORF72 suppresses JAK-STAT mediated inflammation.

Project description:Hexanucleotide repeat expansion in the gene C9ORF72 is a leading cause of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). C9ORF72 deficiency leads to severe inflammatory phenotypes in mice, but exactly how C9ORF72 regulates inflammation remains to be fully elucidated. Here, we report that loss of C9ORF72 leads to the hyperactivation of the JAK-STAT pathway and an increase in the protein levels of STING, a transmembrane adaptor protein involved in immune signaling in response to cytosolic DNA. Treatment with a JAK inhibitor rescues the enhanced inflammatory phenotypes caused by C9ORF72 deficiency in cell culture and mice. Furthermore, we showed that the ablation of C9ORF72 results in compromised lysosome integrity, which could contribute to the activation of the JAK/STAT-dependent inflammatory responses. In summary, our study identifies a mechanism by which C9ORF72 regulates inflammation, which might facilitate therapeutic development for ALS/FTLD with C9ORF72 mutations.

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