Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Disruption of SUV39H1-mediated H3K9 methylation sustains CAR T cell function [RNA-Seq]

ABSTRACT: Comparing transcriptional profiles (RNAseq) of WT and SUV39H1-edited CAR T cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE245184 | GEO | 2023/10/27

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Disruption of SUV39H1-mediated H3K9 methylation sustains CAR T cell function [ATAC-Seq]

Project description:Comparing genome accessibility profiles (ATACseq) of WT and SUV39H1-edited CAR T cells

2023-10-27 | GSE245186 | GEO

Disruption of SUV39H1-mediated H3K9 methylation sustains CAR T cell function [scRNA/CITE-seq]

Project description:Single cell gene expression profile of WT and SUV39H1-edited CAR T cells at pre-infusion (Day 0), day 9 and day 16 post infusion in tumor (NALM6) bearing NSG mice

2023-11-03 | GSE246960 | GEO

Disruption of SUV39H1-mediated H3K9 methylation sustains CAR T cell function

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

2023-10-26 | GSE245187 | GEO

single cell RNA-sequencing analysis of human SUV39H1-knockout CAR T compared to control CAR T cells (mock) in a xenograft model of lung adenocarcinoma

Project description:We have observed that the inactivation of SUV39H1 enhances 41BBz-CAR T cell long-term persistence, providing protection against tumor relapses and rechallenges in a xenograft mouse model of lung adenocarcinoma. The purpuse of this study is to investigate the transcriptomic differences of lung-infiltrating SUV39H1 knock-out versus mock 41BBz-CAR T cells by single cell RNA sequencing at days 8 and 28 after CAR T cell infusion.

2023-10-31 | GSE244028 | GEO

Nanostring analysis of human SUV39H1-knockout CAR T compared to control CAR T cells (mock) at different timepoint

Project description:Failure of adoptive T cell therapies in cancer patients is linked to limited T cell expansion and persistence, even in memory-prone 41BB-(BBz)-based chimeric antigen receptor (CAR) T cells. In murine CD8+ T cells, SUV39H1 promotes differentiation and expansion of effector CD8+ T cells during acute infection by Listeria monocytogenes by silencing stemness and memory genes (Pace et al. Science, 2018). The purpuse of this study is to investigate the transcriptomic differences of SUV39H1 knock-out versus mock human 41BBz-CAR T cells by Nanostring at different cycles of restimulation.

2023-10-31 | GSE244030 | GEO

Single cell ATAC-sequencing analysis of human SUV39H1-knockout CAR T compared to control CAR T cells (mock) in a xenograft model of lung adenocarcinoma

Project description:We have observed that the inactivation of SUV39H1 enhances 41BBz-CAR T cell long-term persistence, providing protection against tumor relapses and rechallenges in a xenograft mouse model of lung adenocarcinoma. The purpuse of this study was to profile chromatin accessibility of SUV39H1-deficient compared to mock 41BBz-CAR T cells by single-cell assay for transposase accessible chromatin (scATAC-seq) on FACS-sorted T cells eight days after CAR T cell infusion into the mice.

2023-10-31 | GSE244029 | GEO

RNAseq Suv39h1 injected single embryo

Project description:RNAseq Suv39h1 injected single embryo

| PRJNA518908 | ENA

RNA profiling of Suv39h1 overexpressed MLL-AF9 induced acute myeloid leukemia (AML) cells

Project description:Acute myeloid leukemias (AMLs) with rearrangement of the mixed-lineage leukemia (MLL) gene are the most aggressive hematopoietic malignancies. By analyzing the clinical data, we found the expression of SUV39H1 was significantly decreased in AML patients and MLL-AF9 (MA9) induced AML mice, in comparison with controls. Remarkably, when overexpress Suv39h1 in MA9 AML mice, the survival of AML mice was significantly prolonged.To examined the mechanism mediated by Suv39h1 overexpression (SUV-OE), we performed the RNAseq profiling of SUV-OE MA9 AML cells and control cells.

2020-12-22 | GSE115549 | GEO

Effects of SUV39H1 depletion on gene expression in HeLa cells

Project description:HeLa cells were transiently transfected with siRNA against SUV39H1, a histone H3K9 methyltransferase. Several genes were significantly up- or down-regulated. HeLa cells were transiently transfected with siRNA against SUV39H1 or negative control siRNA. Then total RNA was extracted.

2015-08-01 | E-GEOD-59243 | biostudies-arrayexpress

Expression data from Adriamycin-treated Emu-myc; Suv39h1-/- B-cell lymphoma

Project description:Oncogene-induced senescence (OIS), a terminal cell cycle block countering (pre)neoplastic lesions, is characterised on the molecular level by trimethylated histone H3 lysine 9 (h3K9me3), a transcriptionally repressive chromatin mark linked to silencing of S-phase-promoting genes. Whether H3K9-governed chromatin remodelling influences anticancer treatment-induced senescence (TIS) and whether functional control of this mark impacts on treatment outcome is not known. We used global gene expression profiling by microarrays to gain insight into the molecular responses of Emu-myc; Suv39h1-/- B-cell lymphoma cells to senescence-inducing anticancer agent Adriamycin (ADR). Primary lymphoma cells isolated from lymph nodes of Emu-Myc; Suv39h1-/- mice were used. In this model, the c-Myc oncogene is constitutively expressed in the cells of the B-cell lineage, leading to spontaneous development of aggressive B-cell lymphomas. Adriamycin (ADR), a cytostatic drug used as a standard part of several lymphoma treatment regimens, is known to massively induce TIS in Suv39h1-proficient lymphomas, protected from apoptosis by Bcl-2 over expression (Myc;Bcl2). In order to discern the impact of Suv39h1 to TIS induction under these conditions, we analysed here transcriptional profiles of matched pairs of Emu-myc;Suv39h1-/-;Bcl2 lymphomas, untreated or treated for 5 days with ADR.

2013-07-04 | E-GEOD-44355 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data