Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

DHX9 sustains hematopoietic stem cell function in cooperation with H3 acetylation [RNA-Seq]

ABSTRACT: To elucidate the mechanisms underlying the role of Dhx9 deficiency in hematopoiesis, we performed RNA sequencing on lineage nagative cells from DHX9 hematopoietic cell-specific conditional knockout mice(cKO) and those from WT mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE278362 | GEO | 2026/03/18

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

DHX9 sustains hematopoietic stem cell function in cooperation with H3 acetylation [CUT&Tag]

Project description:We identify DHX9 as critical regulator for HSCs maintenance and it's associated with H3 acetylation, particularly at K27. To elucidate the mechanisms underlying the role of Dhx9 deficiency and H3K27ac in hematopoiesis, we performed CUT&Tag on lineage nagative cells from DHX9 hematopoietic cell-specific conditional knockout mice(cKO) and those from WT mice.

2026-03-18 | GSE278361 | GEO

Tumor Cell Survival Dependence on the DExH-Box Helicase DHX9

Project description:The ATP-dependent DExH/D-box helicase DHX9 is a key participant in a number of gene regulatory steps, including transcriptional, translational, microRNA-mediated control, DNA replication, and maintenance of genomic stability. DHX9 has also been implicated in maintenance of the tumorigenic process and in drug response. Here, we report that inhibition of DHX9 expression is lethal to multiple human and mouse cancer cell lines. In contrast, using a novel conditional shDHX9 mouse model, we demonstrate that sustained and prolonged suppression of DHX9 is well tolerated at the organismal level. Our results demonstrate a robust tolerance for DHX9 knockdown in non-transformed cells and supports the targeting of DHX9 as an effective and specific chemotherapeutic approach. Comparison of gene expression in large intestine of mice with or without reduced expression of DHX9.

2016-05-19 | E-GEOD-76765 | biostudies-arrayexpress

DHX9 and NPM1 silencing RNA-seq

Project description:In our study, we valided DHX9 and NPM1 interact with KIMAT1, whereas DHX9 also interacts with HIF1A-As2. DHX9 is a highly conserved DEAD-box protein expressed in the nucleus and the cytoplasm, involved in many processes including transcriptional activation, miRNA biogenesis and tumor cell maintenance. NPM1 is predominantly localized in the nucleoplasm, where it associates with active RNA polymerase II and transcriptionally activates genes involved in cancer. We silenced DHX9 and NPM1 and performed RNA-seq to examine the dysregulated genes by DHX9 and NPM1.

2020-12-17 | GSE124626 | GEO

Dhx9 controls effector CD8 T cell differetiation program

Project description:We provide differentially gene expression between wt and Dhx9-/- CD8 T cells from LCMV infected mice.

2020-11-15 | GSE161489 | GEO

Engineering ABT-737 Resistance in MYC-driven Lymphomas Identifies DHX9 as a Drug Response Modifier

Project description:Many traditional cytotoxic agents used in the treatment of cancer function by eliciting an apoptotic response in tumor cells. However, evasion of apoptosis by BCL-2 family members is often deregulated prior to therapeutic intervention leading to treatment failure. To address this, ABT-737 was rationally designed to target BCL-2-like family members and has shown promising results against tumor cells dependent on BCL-2 for their survival. One shortcoming is that MCL-1, a member of the BCL-2 family is poorly inhibited by ABT-737 and is a major cause of resistance. To gain insight into biological pathways that could circumvent this resistance, we designed an shRNA screen to identify novel sensitizers to ABT-737 by engineering MYC driven lymphomas that were resistant to ABT-737 due to endogenous MCL-1 expression. Utilizing this model, we performed a shRNA drop-out screen and identified Dhx9 as a target whose suppression sensitizes cells to ABT-737. DHX9 loss lead to replicative stress signaling, which in turn potently induced the BH3-only proteins, NOXA and PUMA, in a p53-dependent manner to curtail MCL-1 activity. Induction of NOXA is essential for ABT-737 sensitization. Our results ascribe a novel role for DHX9 in the replicative stress pathway and link DHX9 activity to p53 function in vivo. Comparison of Arf-/-Eu-myc/Bcl-2 lymphomas expressing either control Rluc.713 or Dhx9 shRNA, Dhx9.1241

2013-04-03 | E-GEOD-36938 | biostudies-arrayexpress

Tumor Cell Survival Dependence on the DExH-Box Helicase DHX9

2016-05-19 | GSE76765 | GEO

RNA damage compartmentalization by DHX9 granules

Project description:Cell division ensures that both genetic information and non-genetic contents are inherited by daughter cells. Whereas considerable detail has been learned about the processing of intact or damaged DNA during the cell cycle (Branzei & Foiani, 2008; Klaasen et al., 2022),(Bakhoum & Cantley, 2018),(Hustedt & Durocher, 2016), how daughter cells deal with other forms of inherited damage is unknown. Here we identified a special kind of cytoplasmic granules responsible for the compartmentalisation of parental RNA damage. We found that ultraviolet (UV)-induced RNA, but not DNA, damage triggered assembly of this unique type of granules characterized by the presence of RNA helicase DHX9. By developing a novel methodology, FANCI, we discovered that DHX9 granules are enriched in damaged intron RNA and pre-mRNA-binding proteins, which is in contrast to other classical stress granules (SGs) that are composed of mature mRNA. Intron damage impeded proper splicing and intron decay, and induced generation of circRNA and dsRNA in the granules. Moreover, we showed that intron damage induced DHX9 granules assembled specifically in postmitotic daughter cells and triggered a cellular dsRNA immune response. Condensation with dsRNA is crucial for DHX9 localization to the granules and the modulation of dsRNA in these granules by DHX9 was crucial for daughter cell survival. Our observations revealed that DHX9 granules constitute a dedicated non-membrane-bound cytoplasmic compartment that protects daughter cells from parental damaged RNA.

2023-11-11 | GSE218180 | GEO

Identificaiton of DHX9 phosphorylation sites after UV

Project description:Immunoprecipitated DHX9 for identification of phosphorylation sites before and after UV irradiation

2023-10-27 | PXD043743 | Pride

H3 acetylation selectively promotes basal progenitor proliferation and neocortex expansion by activating TRNP1 expression

Project description:We performed RNA-Seq and H3K9ac ChIP-Seq from the whole embryonic cortex at E15.5 from BAF155 cKO mice treated either with vehicle or HDAC inhibitor (TSA).

2021-06-05 | GSE176194 | GEO

DHX9 suppresses spurious RNA processing defects originating from the Alu invasion of the human genome [XL9 DHX9 FLASH CLIP-seq]

Project description:Transposable elements increase genetic diversity thus making them an important part of evolution and gene regulation in all organisms that carry these sequences. Bulk of our nascent transcriptome is comprised of transposable elements that have the propensity to form strong secondary structures. It is essential to resolve such strong secondary structures to maintain normal cellular function. Here, we show that the major nuclear RNA helicase DHX9/RHA interacts and remodels embedded Alu retrotransposable elements in the human transcriptome and B1 retrotransposable elements in the mouse transcriptome. To understand the function of DHX9 we used FLASH (Fast cloning of RNA After some Sort of affinity purification for High-throughput sequencing) to identify the in-vivo targets of human DHX9.

2017-03-28 | GSE89598 | GEO

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