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A novel spleen-resident immature NK cell subset and its maturation in a T-bet-dependent manner

ABSTRACT: A novel spleen-resident immature NK cell subset and its maturation in a T-bet-dependent manner

PROVIDER: PRJNA553197 | ENA |

REPOSITORIES: ENA

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A novel spleen-resident immature NK cell subset and its maturation in a T-bet-dependent manner

Project description:We identified a unique NK cell subset (DN NK) in the spleen. These cells displayed an immature phenotype and could develop into mature conventional NK (cNK) cells.

2019-07-15 | GSE133950 | GEO

Single-cell transcriptome reveals the novel role of T-bet in suppressing the immature NK gene signature the immature NK gene signature

Project description:Using scRNAseq, we identified five distinct NK cell clusters and define their relative developmental maturity in the murine bone marrow of WT mice. Transcriptome-based machine-learning classifiers revealed that half of the mTORC2-deficient NK cells belongs to the least mature NK cluster. Mechanistically, loss of mTORC2 results in an increased expression of signature genes representing immature NK cells. We further characterized the T-bet-deficient NK cells and found an augmented immature transcriptomic signature. Moreover, deletion of Foxo1 restores the expression of T-bet and corrects the abnormal expression of immature NK genes in Rictor-deficient NK cells.

2020-05-13 | GSE150166 | GEO

Single-cell transcriptome reveals the novel role of T-bet in suppressing the immature NK gene signature the immature NK gene signature

Project description:Single-cell transcriptome reveals the novel role of T-bet in suppressing the immature NK gene signature the immature NK gene signature

| PRJNA631285 | ENA

Identification of a Porcine Liver Eomes<sup>high</sup>T-bet<sup>low</sup> NK Cell Subset That Resembles Human Liver Resident NK Cells.

Project description: Not available

| S-EPMC6836759 | biostudies-literature

BET bromodomain inhibition suppresses TH17-mediated pathology

Project description:IL-17-producing T helper (TH17) cells have been selected through evolution for their ability to control fungal and bacterial infections. It is also firmly established that their aberrant generation and activation results in autoimmune conditions. Using a characterized potent and selective small molecule inhibitor, we show that the bromodomain and extra-terminal domain (BET) family of chromatin adaptors plays fundamental and selective roles in human and murine TH17 differentiation from naM-CM-/ve CD4+ T cells, as well as in the activation of previously differentiated TH17 cells. We provide evidence that BET controls TH17 differentiation in a bromodomain-dependent manner through a mechanism that includes the direct regulation of multiple effector TH17-associated cytokines, including IL17, IL21 and GMCSF. We also demonstrate that BET family members Brd2 and Brd4 associate with the Il17 locus in TH17 cells, and that this association requires bromodomains. We recapitulate the critical role of BET bromodomains in TH17 differentiation in vivo and show that therapeutic dosing of the BET inhibitor is efficacious in mouse models of autoimmunity. Our results identify the BET family of proteins as a fundamental link between chromatin signaling and TH17 biology, and support the notion of BET inhibition as a point of therapeutic intervention in autoimmune conditions. 4 samples were analyzed: two conditions in duplicate. Naive T cells were placed in conditions leading to TH17 differentiation, with and without BET inhibitor. RNA was collected at 48 hours.

2013-09-20 | E-GEOD-37270 | biostudies-arrayexpress

JQ1 promotes invasion in a BET protein independent manner in prostate cancer

Project description:Recent findings have shown that inhibitors targeting BET (bromodomain and extraterminal domain) proteins, such as the small molecule JQ1, are potent growth inhibitors of many cancers and hold promise for cancer therapy. However, some reports also have revealed that JQ1 can activate additional oncogenic pathways and may affect EMT (epithelial mesenchymal transition). Therefore, it is important to address the potential unexpected effect of JQ1 treatment, such as cell invasion and metastasis. Here, we showed that in prostate cancer, JQ1 inhibited cancer cell growth but promoted invasion and metastasis in a BET protein independent manner. Multiple invasion pathways including EMT, BMP (bone morphogenetic protein) signaling, chemokine signaling and focal adhesion pathway were activated by JQ1 to promote invasion. Notably, JQ1 induced upregulation of invasion genes through inhibition of FOXA1, an invasion suppressor in prostate cancer. JQ1 directly interacted with FOXA1, inactivated FOXA1 binding to its interacting repressors, TLE3, HDAC7 and NFIC, thus blocking FOXA1 repressive function and activating the invasion genes. Our finding indicates that JQ1 has an unexpected effect of promoting invasion in prostate cancer. Thus, the ill effect of JQ1 or its derived therapeutic agents could not be ignored during cancer treatment, especially in FOXA1 related cancers.

2022-10-01 | GSE139230 | GEO

RNA-seq of NK-92 cell line upon BET inhibitor treatment (OTX-015)

Project description:Identification of the mechanisms through which BET inhibitor (OTX-015) stimulates natural killer (NK) activation. RNA-seq was performed comparing vehicle- (DMSO) to OTX-015-treated NK-92 cell line.

2024-01-26 | E-MTAB-12853 | biostudies-arrayexpress

Single-cell transcriptome reveals the novel role of T-bet in suppressing the immature NK gene signature.

Project description: Not available

| S-EPMC7255804 | biostudies-literature

ATAC-seq of T-BET and EOMES CRISPR edited Primary human NK cells

Project description:ATAC-seq was performed on peripheral blood NK cells that were CRISPR-edited to knock-out expression of T-BET and EOMES. The following samples were analyzed to elucidate the role of T-BET and EOMES in regulating mature human NK cell chromatin accessibility.

2023-06-06 | GSE227878 | GEO

BET Bromodomains Mediate Transcriptional Pause Release in Heart Failure [ChIP-Seq]

Project description:Heart failure is driven by the interplay between master regulatory transcription factors and dynamic alterations in chromatin structure. Coordinate activation of developmental, inflammatory, fibrotic and growth regulators underlies the hallmark phenotypes of pathologic cardiac hypertrophy and contractile failure. While transactivation in this context is known to be associated with recruitment of histone acetyl-transferase enzymes and local chromatin hyperacetylation, the role of epigenetic reader proteins in cardiac biology is unknown. We therefore undertook a first study of acetyl-lysine reader proteins, or bromodomains, in heart failure. Using a chemical genetic approach, we establish a central role for BET-family bromodomain proteins in gene control during the evolution of heart failure. BET inhibition suppresses cardiomyocyte hypertrophy in a cell-autonomous manner, confirmed by RNA interference in vitro. Following both pressure overload and neurohormonal stimulation, BET inhibition potently attenuates pathologic cardiac remodeling in vivo. Integrative transcriptional and epigenomic analyses reveal that BET proteins function mechanistically as pause-release factors critical to activation of canonical master regulators and effectors that are central to heart failure pathogenesis. Specifically, BET bromodomain inhibition in mice abrogates pathology-associated pause release and transcriptional elongation, thereby preventing activation of cardiac transcriptional pathways relevant to the gene expression profile of failing human hearts. This study implicates epigenetic readers in cardiac biology and identifies BET co-activator proteins as therapeutic targets in heart failure. ChIP-Seq of mouse heart tissues from mice induced with heart failure and treated with JQ1 BET bromodomain inhibitor

2013-08-06 | E-GEOD-46668 | biostudies-arrayexpress

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