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RNA-Seq on wild-type and Ezh2 knock-out invariant natural killer T cells and CD44hi CD4+ T cells

ABSTRACT: RNA-Seq on wild-type and Ezh2 knock-out invariant natural killer T cells and CD44hi CD4+ T cells

PROVIDER: PRJNA528411 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8759692.fastq.gz	Fastqsanger.gz
	SRR8759693.fastq.gz	Fastqsanger.gz
	SRR8759694.fastq.gz	Fastqsanger.gz
	SRR8759695.fastq.gz	Fastqsanger.gz

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RNA-Seq on wild-type and Ezh2 knock-out invariant natural killer T cells and CD44hi CD4+ T cells

Project description:Several subsets of NKT cells have been identified, including IFNγ-producing NKT1 cells, IL-4-producing NKT2 cells and IL-17-producing NKT17 cells. We sought to determine to the effect of loss of the polycomb repressive complex 2 protein Ezh2 on gene expression in NKT cells and CD44high CD4+ T cells from mice. Transcriptional profiles of iNKT cells from wild-type (WT) and Ezh2 KO iNKT mice were determined.

2019-03-22 | GSE128652 | GEO

MELK mediates the stability of EZH2 throught site-specific phosphorylation in extranodal natural killer/T-cell lymphoma

Project description:Oncogenic EZH2 is overexpressed and extensively involved in the pathophysiology of different cancers including extranodal natural killer/T-cell lymphoma (NKTL). However, the mechanisms regarding EZH2 upregulation is poorly understood, and it still remains untargetable in NKTL. In this study, we examine EZH2 protein turnover in NKTL and identify MELK kinase as a regulator of EZH2 ubiquitination and turnover. Using quantitative mass spectrometry (MS) analysis, we observed a MELK-mediated increase of EZH2 S220 phosphorylation along with a concomitant loss of EZH2 K222 ubiquitination, suggesting a phosphorylation-dependent regulation of EZH2 ubiquitination. MELK inhibition through both chemical and genetic means led to ubiquitination and destabilization of EZH2 protein. Importantly, we determine that MELK is upregulated in NKTL, and its expression correlates with EZH2 protein expression as determined by tissue microarray derived from NKTL patients. Interestingly, FOXM1, which connected MELK to EZH2 signaling in glioma, was not involved in mediating EZH2 ubiquitination. Furthermore, we identify USP36 as the deubiquitinating enzyme which deubiquitinates EZH2 at K222. These findings uncover an important role of MELK and USP36 in mediating EZH2 stability in NKTL. Moreover, MELK overexpression led to decreased sensitivity to Bortezomib treatment in NKTL based on deprivation of EZH2 ubiquitination. Therefore, modulation of EZH2 ubiquitination status by targeting MELK may be a new therapeutic strategy for NKTL patients with poor Bortezomib response.

2019-08-26 | PXD015008 | Pride

E3 ligase TRIP12 affecting EZH2 ubiquitination in ENKTL

Project description:Effects of potential E3 ligase that mediates polyubiquitination of EZH2 in extranodal natural killer T cell lymphoma

2023-10-14 | PXD046145 |

Gene Regulation by Histone Deacetylase 7 During Invariant Natural Killer T Cell Development

Project description:We have found that the signal-dependent chromatin modulator Histone Deacetylase 7 interacts with and corepresses the signature transcription factor of invariant natural Killer T (iNKT) cells, ZBTB16. This study was designed to determine the global effect on transcription of a gain-of-function mutant of HDAC7 during iNKT cell development and function. Va14/Ja18 T cell receptor transgenic thymocytes and splenocytes, which develop preferentially into iNKT cells, were profiled by RNA-seq with and without expression of a gain-of-functon HDAC7 transgene (HDAC7dP)

2018-05-08 | GSE105026 | GEO

Expression data from Ezh2 epithelial knock-out mouse lungs at E14.5

2015-02-04 | GSE60660 | GEO

Single-cell RNAseq profiling of mouse invariant NKT thymocytes

Project description:Total invariant Natural Killer T cells were purified from mouse thymi (pool of 4 mice) of Fhl2+/+ or Fhl2-/- mice (5 week-old)

2020-09-08 | GSE141895 | GEO

Expression data from Ezh2 epithelial knock-out mouse lungs at E14.5

Project description:Ezh2 epigenetically suppresses developmentally-regulated genes. Ezh2 is highly expressed during development, including in the lung. We knocked out Ezh2 in the developing lung epithelium using a Shh-cre driver which is active in foregut endoderm prior to lung morphogenesis. Many developmentally regulated genes became derepressed in the mutant lungs, leading to defects in lung development. Microarray analysis of genes upregulated in Ezh2 epithelial knock-out mouse lungs compared to Shh-cre controls. We generated Ezh2 epithelial mutant lungs by crossing the Ezh2-floxed line (Su et al., 2003) with the Shh-cre line (Harfe et al., 2004). We isolated RNA from whole mouse lungs at embryonic day 14.5 from 4 Shh-cre:Ezh2-flox/flox embryos (M1-M4) and 4 Shh-cre embryos (C1-C4). Littermates are as follows: C1+C2; C3+C4; M1+M2; M3+M4.

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Dual regulatory role of invariant natural killer T cells in the development and progression of hepatocellular carcinoma

Project description:Our project aims to examine the role of Invariant Natural Killer T cells (iNKT) in Hepatocellular Carcinoma (HCC) which is not known. HCC is a leading cause of death and accounts for ~80% of cases of liver cancer worldwide. Because there are no biomarkers that allow the early diagnosis, HCC is diagnosed at late stages when the tumor is developed enough and is resistant to chemotherapy. The liver is characterized by an immunosuppressive environment and due to this environment, liver is prone to HCC development. Once HCC is developed, the function of immune cells that fight the tumor such as dendritic cells, natural killer cells, helper and cytotoxic T cells is suppressed while the function of regulatory T cells and myeloid- derived suppressor cells is enhanced. However, the role of Natural Killer T cells (NKT) is not known. NKT cells is a population of the immune system which is largely enriched in the liver, which recognize lipid antigens by CD1d molecule and can rapidly produce large amounts of various cytokines to enhance the function of other immune populations. Here, we investgated the role of NKT cell in chemical-induced HCC that recapitulates the development of human HCC usiing genetic models that lack or overproduce NKT cells.

2025-08-11 | GSE279202 | GEO

Mitochondrial Metabolism is Essential for Invariant Natural Killer T Cell Development and Function

Project description:Mitochondrial Metabolism is Essential for Invariant Natural Killer T Cell Development and Function

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Gene Regulation by Histone Deacetylase 7 During Invariant Natural Killer T Cell Development

Project description:Gene Regulation by Histone Deacetylase 7 During Invariant Natural Killer T Cell Development

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