Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Assessing the impact of loss of ATF7IP and SETDB1 on the transcriptome

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE86813 | GEO | 2016/10/11

SECONDARY ACCESSION(S): PRJNA342608

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Assessing the impact of loss of ATF7IP and SETDB1 on the global distribution of H3K9me3

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

Assessing the impact of loss of MORC2 and SETDB1 on the global distribution of H3K9me3

Project description:By comparing HeLa cells lacking MORC2 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 MORC2 on the distribution of the repressive H3K9me3 histone modification.

2017-05-29 | GSE95456 | GEO

Targeting the Atf7ip-Setdb1 complex augments anti-tumor immunity by boosting tumor immunogenicity

Project description:Despite substantial progress that has been made in understanding how tumors escape immune surveillance, measures to counteract tumor immune evasion have been limited. Suppression of tumor antigen expression is a common adaptive mechanism that cancers use to evade detection and destruction by the immune system. Epigenetic modifications play a critical role in in various aspects of immune invasion, including the regulation of tumor antigen expression. To identify novel epigenetic regulators of tumor antigen expression, we established a transplantable syngeneic tumor model of immune escape with silenced antigen expression and used this system as a platform for a CRISPR-Cas9 suppressor screen targeting genes encoding epigenetic modifiers. We found that genetic disruption of the chromatin modifiers Atf7ip or its interacting partner Setdb1 in tumor cells restored tumor antigen expression, resulting in augmented tumor immunogenicity concomitant with elevated endogenous retroviral antigens (ERVs), mRNA intron retention. ERVs disinhibition was associated with a robust type I interferon response and increased T cell infiltration, leading to rejection of cells lacking intact Atf7ip or Setdb1. ATF7IP or SETDB1 expression inversely correlated with antigen processing and presentation pathways, interferon signaling, and T cell infiltration and cytotoxicity in human cancers. Our results provide a rationale for targeting Atf7ip or Setdb1 in cancer immunotherapy.

2021-07-23 | GSE179574 | GEO

Assessing the impact of loss of MORC2 on the transcriptome

Project description:By comparing HeLa cells lacking MORC2 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 MORC2 on the transcriptome.

2017-05-29 | GSE95452 | GEO

H3K9me3 ChIP-seq in HeLa cells lacking TASOR, MPP8, periphilin and SETDB1

Project description:We performed ChIP-seq to measure H3K9me3 levels in wild-type HeLa cells and HeLa cells lacking TASOR, MPP8, periphilin and SETDB1 generated through CRISPR/Cas9-mediated gene disruption.

2015-05-28 | GSE63116 | GEO

Assessing the impact of the R252W Charcot-Marie-Tooth disease mutation in MORC2 on HUSH-mediated repression

Project description:HeLa cells lacking MORC2 generated through CRISPR/Cas9-mediated gene disruption were reconstituted with either wild-type or R252W mutant MORC2, and re-repression of HUSH target genes assessed by RNA-seq

2017-05-29 | GSE95455 | GEO

SETDB1 suppresses interferon responses and NK cell-mediated immunosurveillance specifically in monocytic AML: H3K9me3 ChIP-seq of cSAM leukemia cells with Setdb1 depletion [ChIP-seq]

Project description:Monocytic acute myeloid leukemia (AML) responds poorly to current treatments, including venetoclax-based therapy. We conducted in vivo and in vitro CRISPR/Cas9 library screenings using a mouse monocytic AML model, and identified SETDB1 and its binding partners (ATF7IP and TRIM33) as crucial tumor promoters in vivo. The growth-inhibitory effect of Setdb1 depletion in vivo was mainly dependent on NK cell-mediated cytotoxicity. Mechanistically, SETDB1 depletion upregulated interferon-stimulated genes and NKG2D ligands through demethylation of histone H3 Lys9 at the monocyte-specific enhancer regions, thereby enhancing their immunogenicity to NK cells and intrinsic apoptosis. Importantly, these effects were not observed in non-monocytic leukemia cells. We also identified the expression of MNDA and its murine counterpart Ifi203 as biomarkers to predict the sensitivity of each AML to SETDB1 depletion. Our study highlights the critical and selective role of SETDB1 in monocytic AML and underscores its potential as a therapeutic target for current unmet needs.

2024-08-03 | GSE266098 | GEO

SETDB1 suppresses interferon responses and NK cell-mediated immunosurveillance specifically in monocytic AML: Gene expression profiles of cSAM leukemia cells with Setdb1 depletion [RNA-seq]

2024-08-03 | GSE266097 | GEO

Targeting the Atf7ip-Setdb1 complex augments anti-tumor immunity by boosting tumor immunogenicity

Project description:Targeting the Atf7ip-Setdb1 complex augments anti-tumor immunity by boosting tumor immunogenicity

| PRJNA744222 | ENA