RNA-seq of ATF7ip-deficient T cells
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ABSTRACT:
PROVIDER: PRJNA543904 | ENA |
REPOSITORIES: ENA
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Project description:RNA-seq performed in ATF7ip-deficient T cells reveals a defect in Th17 gene induction secondary to increased IL-2 T helper 17 cells (Th17) are critical for fighting infections at mucosal surfaces, however, they have also been found to contribute to the pathogenesis of multiple autoimmune diseases and Th17 cells have been targeted therapeutically. Due to the role of Th17 cells in autoimmune pathogenesis, it is important to understand the factors that control Th17 development. Here we identify the activating transcription factor 7 interacting protein (ATF7ip) as a critical regulator of Th17 differentiation. Mice with T-cell-specific deletion of Atf7ip have impaired Th17 differentiation secondary to the aberrant overproduction of IL-2 with T-cell receptor (TCR) stimulation and are resistant to colitis in vivo. ChIP-seq studies identified ATF7ip as an inhibitor of Il2 gene expression through the deposition of the repressive histone mark H3K9me3 in the Il2-Il21 intergenic region. These results demonstrate a new epigenetic pathway by which IL-2 production is constrained and this may open up new avenues for modulating its production.
2019-05-21 | GSE131533 | GEO
Project description:T helper 17 cells (Th17) are critical for fighting infections at mucosal surfaces, however, they have also been found to contribute to the pathogenesis of multiple autoimmune diseases and Th17 cells have been targeted therapeutically. Due to the role of Th17 cells in autoimmune pathogenesis, it is important to understand the factors that control Th17 development. Here we identify the activating transcription factor 7 interacting protein (ATF7ip) as a critical regulator of Th17 differentiation. Mice with T-cell-specific deletion of Atf7ip have impaired Th17 differentiation secondary to the aberrant overproduction of IL-2 with T-cell receptor (TCR) stimulation and are resistant to colitis in vivo. ChIP-seq studies identified ATF7ip as an inhibitor of Il2 gene expression through the deposition of the repressive histone mark H3K9me3 in the Il2-Il21 intergenic region. These results demonstrate a new epigenetic pathway by which IL-2 production is constrained and this may open up new avenues for modulating its production.
2019-05-21 | GSE131511 | GEO
Project description:Method: To study the effector response of Atf7ip, a) we infected Atf7ip+/fl and Atf7ipfl/fl mice with lcmv . RNAseq was performed using CD8 T cells isolated from Lymph node and Spleen of Het and KO mice. RNA was isolated using Qiagen RNeasy Mini Kit as per manufacturers protocol. The RNA-Seq was performed by UCSF core using Illumina Platform. RNAseq was also carried out using naive CD8 T cells isolated from Atf7ip+/fl and Atf7ipfl/fl mice along with Atf7ip+/fl and Atf7ipfl/fl CD8 T cells stimulated for 72 hrs. This set of samples were sequenced using commercial facility from Genewiz, USA. Results: Our transcriptome analysis (RNA-seq) identified, Il7r, Runx3 etc. to be upregulated in the Atf7ipfl/fl CD8 T cells as compared to the Atf7ip+/fl CD8 T cells.
2021-12-21 | GSE190417 | GEO
Project description:H3K9me3 ChIP-seq in ATF7ip Knockout naïve T cells
| PRJNA543885 | ENA
Project description:RNA-Seq and ChIP-Seq in SIX1 deficient Rhabdomyosarcoma cells
| PRJNA723882 | ENA
Project description:small RNA-Seq of miR-181 deficient Treg cells
| PRJNA512620 | ENA
Project description:By comparing HeLa cells lacking ATF7IP or SETDB1 generated through CRISPR/Cas9-mediated gene disruption to wild-type HeLa cells, the goal of the experiment was to determine the effect of loss of the SETDB1•ATF7IP complex on the transcriptome.
2016-10-11 | GSE86813 | GEO
Project description:By comparing HeLa cells lacking ATF7IP or SETDB1 generated through CRISPR/Cas9-mediated gene disruption to wild-type HeLa cells, the goal of the experiment was to determine the effect of loss of the SETDB1•ATF7IP complex on the distribution of the repress
2016-10-11 | GSE86811 | GEO
Project description:RNA-Seq analysis carried out in three different backcrosses based on Iberian breed with Landrace, Pietrain and Duroc breeds
2017-10-31 | PRJEB23068 | EVA
Project description:CD8+ T cells are critical for the adaptive immune response to infection and tumors. Moreover, CD8+ T cell memory is important for the immune systems response to repeat infections. Here, we identify the activating transcription factor 7 interacting protein as a critical regulator of CD8+ T cell memory and effector responses. Mice with a T cell specific deletion of ATF7ip have a CD8+ T cell intrinsic enhancement of Il7r expression and Il2 expression leading to enhanced memory responses. ChIP-seq studies identified ATF7ip as an inhibitor of Il7r and Il2 gene expression through the deposition of the repressive histone mark H3K9me3 in the Il7r gene loci and Il2-Il21 intergenic region. Interestingly, ATF7ip targeted transposable elements (TE) for H3K9me3 in these regions. These results demonstrate a new epigenetic pathway by which IL7r and IL-2 production are constrained in CD8+ T cells, and this may open up new avenues for modulating their production.
2021-12-21 | GSE190624 | GEO