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Innate sensor Dhx9 directly binds to multiple genes related to effector CD8 T cell differentiation [ChIP-Seq]

ABSTRACT: We provide a set of genes that are directly bound by Dhx9 in CD8 T cells from LCMV infected mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE161694 | GEO | 2020/11/19

REPOSITORIES: GEO

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Innate sensor Dhx9 directly binds to multiple genes related to effector CD8 T cell differentiation

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

2020-11-19 | GSE161698 | GEO

Innate sensor Dhx9 directly binds to multiple genes related to effector CD8 T cell differentiation

Project description:Innate sensor Dhx9 directly binds to multiple genes related to effector CD8 T cell differentiation

| PRJNA679186 | ENA

Innate sensor Dhx9 directly binds to multiple genes related to effector CD8 T cell differentiation [ChIP-Seq]

Project description:Innate sensor Dhx9 directly binds to multiple genes related to effector CD8 T cell differentiation [ChIP-Seq]

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Dhx9 controls effector CD8 T cell differetiation program

Project description:We provide differentially gene expression between wt and Dhx9-/- CD8 T cells from LCMV infected mice.

2020-11-15 | GSE161489 | GEO

Innate sensor Dhx9 orchestrates TCR signaling and controls CD8 T cell immunity against viral infection [ATAC-Seq]

Project description:Nuclear sensor molecules of innate cells recognize pathogenic DNA or RNA to activate innate immunity and defense against bacteria and virus infection. Although some sensors exhibit their preliminary functions in T cells, it is still unclear about the underlying mechanism. Here we found a nuclear sensor-Dhx9, was enhanced its expression in effector CD8 T cells. T cell specific deletion of Dhx9 caused an impaired CD8 T cell expansion, memory formation and virus clearance. Mechanically, Dhx9 could directly regulate id2 transcription and in turn control effector CD8 T cell differentiation. Importantly, Dhx9 could bind to Lck protein, mediate Zap70 phosphorylation, and promoting TCR downstream signaling - ERK pathway to protect effector CD8 T cells from apoptosis. The DSRM and DEXDc-Helicase domain is required for Lck binding and Id2 transcription, respectively. Therefore, we revealed a novel regulatory mechanism that innate nuclear sensor regulates T cell fate and function through modulating adaptive pathways.

2020-11-19 | GSE161697 | GEO

Tumor Cell Survival Dependence on the DExH-Box Helicase DHX9

Project description:The ATP-dependent DExH/D-box helicase DHX9 is a key participant in a number of gene regulatory steps, including transcriptional, translational, microRNA-mediated control, DNA replication, and maintenance of genomic stability. DHX9 has also been implicated in maintenance of the tumorigenic process and in drug response. Here, we report that inhibition of DHX9 expression is lethal to multiple human and mouse cancer cell lines. In contrast, using a novel conditional shDHX9 mouse model, we demonstrate that sustained and prolonged suppression of DHX9 is well tolerated at the organismal level. Our results demonstrate a robust tolerance for DHX9 knockdown in non-transformed cells and supports the targeting of DHX9 as an effective and specific chemotherapeutic approach. Comparison of gene expression in large intestine of mice with or without reduced expression of DHX9.

2016-05-19 | E-GEOD-76765 | biostudies-arrayexpress

DHX9 and NPM1 silencing RNA-seq

Project description:In our study, we valided DHX9 and NPM1 interact with KIMAT1, whereas DHX9 also interacts with HIF1A-As2. DHX9 is a highly conserved DEAD-box protein expressed in the nucleus and the cytoplasm, involved in many processes including transcriptional activation, miRNA biogenesis and tumor cell maintenance. NPM1 is predominantly localized in the nucleoplasm, where it associates with active RNA polymerase II and transcriptionally activates genes involved in cancer. We silenced DHX9 and NPM1 and performed RNA-seq to examine the dysregulated genes by DHX9 and NPM1.

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Dhx9 controls effector CD8 T cell differetiation program

Project description:Dhx9 controls effector CD8 T cell differetiation program

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Tumor Cell Survival Dependence on the DExH-Box Helicase DHX9

2016-05-19 | GSE76765 | GEO

RNA damage compartmentalization by DHX9 granules

Project description:Cell division ensures that both genetic information and non-genetic contents are inherited by daughter cells. Whereas considerable detail has been learned about the processing of intact or damaged DNA during the cell cycle (Branzei & Foiani, 2008; Klaasen et al., 2022),(Bakhoum & Cantley, 2018),(Hustedt & Durocher, 2016), how daughter cells deal with other forms of inherited damage is unknown. Here we identified a special kind of cytoplasmic granules responsible for the compartmentalisation of parental RNA damage. We found that ultraviolet (UV)-induced RNA, but not DNA, damage triggered assembly of this unique type of granules characterized by the presence of RNA helicase DHX9. By developing a novel methodology, FANCI, we discovered that DHX9 granules are enriched in damaged intron RNA and pre-mRNA-binding proteins, which is in contrast to other classical stress granules (SGs) that are composed of mature mRNA. Intron damage impeded proper splicing and intron decay, and induced generation of circRNA and dsRNA in the granules. Moreover, we showed that intron damage induced DHX9 granules assembled specifically in postmitotic daughter cells and triggered a cellular dsRNA immune response. Condensation with dsRNA is crucial for DHX9 localization to the granules and the modulation of dsRNA in these granules by DHX9 was crucial for daughter cell survival. Our observations revealed that DHX9 granules constitute a dedicated non-membrane-bound cytoplasmic compartment that protects daughter cells from parental damaged RNA.

2023-11-11 | GSE218180 | GEO

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