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Ankrd11 deficiency reverses the dysfunction of chronic HBV-specific T-cell [Cut&Tag]

ABSTRACT: To investigate the impact of Ankrd11 deficiency on H3K27ac modification in CD8 T cells, we performed H3K27ac CUT&Tag assays comparing H3K27ac modification levels between Ankrd11-knockout and wild-type CD8 T cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE299521 | GEO | 2026/07/25

REPOSITORIES: GEO

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Ankrd11 deficiency reverses the dysfunction of chronic HBV-specific T-cell [ATAC-seq]

Project description:To investigate the impact of Ankrd11 deficiency on chromatin accessibility in CD8 T cells, we performed ATAC-seq to analyze differences in chromatin openness between Ankrd11-knockout CD8 T cells and wild-type CD8 T cells.

2026-07-25 | GSE299519 | GEO

Ankrd11 deficiency reverses the dysfunction of chronic HBV-specific T-cell [RNA-seq]

Project description:To investigate the transcriptomic changes in CD8 T cells upon Ankrd11 deficiency, we performed RNA-seq to analyze alterations in the transcriptome between Ankrd11-knockout and wild-type CD8 T cells.

2026-07-25 | GSE299520 | GEO

Ankrd11 deficiency reverses the dysfunction of chronic HBV-specific T-cell [Cut&Tag]

Project description:Ankrd11 deficiency reverses the dysfunction of chronic HBV-specific T-cell [Cut&Tag]

| PRJNA1274902 | ENA

Ankrd11 deficiency reverses the dysfunction of chronic HBV-specific T-cell [RNA-seq]

Project description:Ankrd11 deficiency reverses the dysfunction of chronic HBV-specific T-cell [RNA-seq]

| PRJNA1274899 | ENA

Ankrd11 deficiency reverses the dysfunction of chronic HBV-specific T-cell [ATAC-seq]

Project description:Ankrd11 deficiency reverses the dysfunction of chronic HBV-specific T-cell [ATAC-seq]

| PRJNA1274907 | ENA

CUT-tag analysis of C1qbp sufficient and deficient CD8+ T cells

Project description:This study is aimed to Investigate whether C1qbp deficiency affects the histone modification during the differentiation stage of CD8+ T cells. Transferred WT and C1qbp KO P14 cells sorted from the spleen of donor mice on day 5 post-infection with LCMV Armstrong were collected and treated for CUT-tag. CUT-tag-Seq analysis provided evidence of histone modification changes between WT and C1qbp KO CD8+ T cells. Our study shows that on day 5 post-infection with LCMV Armstrong, along with mRNA expressing profiling, the CUT-tag-seq exhibits obvious changes in H3K27me3 and H3K27Ac modification of indicated genes of WT and C1qbp KO CD8+ T cells.

2021-06-09 | GSE176368 | GEO

Minor splicing factor 65K/RNPC3 interacts with ANKRD11 and mediates HDAC3-regulated histone deacetylation and transcription

Project description:Pre-mRNA splicing is coupled with DNA- and other RNA-processing machineries in the nucleus to form multilayer networks for accurate regulation of gene expression. However, those established couplings are major spliceosome-related, whether the minor spliceosome is involved remains unclear. Here, we first identified a direct interaction between a minor-specific protein 65K/RNPC3 and the histone deacetylase HDAC3 cofactor ANKRD11 through affinity co-purification using Drosophila lysate. In vivo assays revealed that the head of both DmAnkrd11Δ/Δ and Dm65KΔ/Δ mutants exhibited increased histone acetylation at H3K9 and H4K5, consistent with the high level of ANKRD11 in the central nervous systems. We then found that the 65K-ANKRD11 interaction is conserved in human, in which the HsANKRD11 middle-stretched domain mediates Hs65K association with HDAC3. CUT&Tag assays demonstrated that HDAC3 and Hs65K synergistically bind on chromatin, and the knockdown of ANKRD11 simultaneously decreased their bindings at the same chromatin locations and also increased nearby acetylation of H3K9. Sequencing of mRNAs revealed that the deficiency of HsANKRD11 or Hs65K caused changes in gene expression correlated with their chromatin-binding changes of HDAC3 and Hs65K and the levels of H3K9ac. This study provides a novel strategy for the regulation of histone deacetylation and gene expression through a minor spliceosome-specific component.

2024-03-31 | GSE243715 | GEO

RNA-Seq of SETD5 W834C and ANKRD11 E2522K homozygous mESCs with matched controls

Project description:Setd5 and Ankrd11 are components of the mammalian SET3C complex which are mutated in neuro developmental disorders. We have generated independent clones of mESCs with a missense mutation equivalent to the KBG syndrome mutation E2522K in Ankrd11. We have also generated independent clones of mESCs with W834C and ΔKWK (where K833 to K835 are missing) in Setd5.

2026-04-27 | E-MTAB-15318 | biostudies-arrayexpress

ANKRD11 Binds to Cohesin to Regulate Neural and Craniofacial Development

Project description:In this study, we analyzed gene expression changes in the E14 mESC wild-type cell line and the ANKRD11 Y347A mutant cell line using RNA-seq.

2025-01-24 | GSE273955 | GEO

Ankrd11, a chromatin regulator and a KBG syndrome risk gene, is a critical regulator of cardiac neural crest cell biology and heart development [MERSCOPE]

Project description:ANKRD11 (Ankyrin Repeat Domain 11) is a chromatin regulator and a risk gene for KBG syndrome, a rare developmental disorder characterized by multiple organ abnormalities, including cardiac defects. However, the role of ANKRD11 in heart development is unknown. The neural crest plays a leading role in embryonic heart development, and its dysfunction is implicated in congenital heart defects. We demonstrate conditional knockout of Ankrd11 in the murine embryonic neural crest results in persistent truncus arteriosus, ventricular dilation, and impaired ventricular contractility. We further show these defects occur due to aberrant cardiac neural crest cell organization leading to outflow tract septation failure. Finally, knockout of Ankrd11 in the neural crest leads to impaired expression of various transcription factors, chromatin remodelers and signaling pathways, including mTOR, BMP and TGF-β in the cardiac neural crest cells. In this work, we identify Ankrd11 as a novel regulator of neural crest-mediated heart development and function.

2024-02-25 | GSE258835 | GEO

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