Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNF5 Regulation of RBBP4 Defines Acute Myeloid Leukemia Growth and Susceptibility to Histone Deacetylase Inhibitors

ABSTRACT: RNF5 Regulation of RBBP4 Defines Acute Myeloid Leukemia Growth and Susceptibility to Histone Deacetylase Inhibitors

PROVIDER: PRJNA656131 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12416700.fastq.gz	Fastqsanger.gz
	SRR12416701.fastq.gz	Fastqsanger.gz
	SRR12416702.fastq.gz	Fastqsanger.gz
	SRR12416703.fastq.gz	Fastqsanger.gz
	SRR12416704.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 15

Similar Datasets

Histone deacetylase inhibitors in alveolar rhabdomyosarcoma

Project description:Histone deacetylase inhibitors in alveolar rhabdomyosarcoma

| PRJNA475783 | ENA

RNF5 Regulation of RBBP4 Defines Acute Myeloid Leukemia Growth and Susceptibility to Histone Deacetylase Inhibitors

Project description:To investigate a potential role for RNF5 in AML, we monitored changes in gene expression profiles in multiple AML cell lines after RNF5 knock-down. PolyA RNA was isolated using the NEBNext Poly(A) mRNA Magnetic Isolation Module, and bar-coded libraries were constructed using the NEBNext Ultra™ Directional RNA Library Prep Kit for Illumina (NEB, Ipswich, MA). Libraries were pooled and single end-sequenced (1×75) on the Illumina NextSeq 500 using the High output V2 kit (Illumina, San Diego, CA). Quality control was performed using Fastqc (v0.11.5, Andrews S. 2010)), reads were trimmed for adapters, low quality 5′ bases, and minimum length of 20 using CUTADAPT (v1.1). The number of reads per sample and the number of aligned reads suggested that read quality and number were good and that the data were valid for analysis. High-quality data were then mapped to human reference genome (hg19) using STAR mapping algorithm (version 2.5.2a). FeatureCounts implemented in Subread (v1.50) was used to count the sequencing reads from mapped BAM files. Analyses of differentially expressed genes (DEGs) were subsequently performed using a negative binomial test method (edgeR) implemented using SARTools R Package. A list of the DEGs was observed and pathway analysis was performed using IPA (http://www.ingenuity.com) based on the following criteria: |log2(fold change)| >0.4 and p value < 0.05.

2021-07-25 | GSE155929 | GEO

Histone deacetylase inhibitors in alveolar rhabdomyosarcoma

Project description:Multiple histone deacetylase inhibitors were tested on multiple alveolar rhabdomyosarcoma cell lines and multiple patient-derived xenograft models of alveolar rhabdomyosarcoma

2018-06-13 | GSE115698 | GEO

Histone deacetylase inhibitors impair glioblastoma cell motility and proliferation

Project description:Histone deacetylase inhibitors impair glioblastoma cell motility and proliferation

| PRJNA789840 | ENA

Transcriptional response to histone deacetylase inhibitors

2015-08-31 | GSE65297 | GEO

Transcriptional response to histone deacetylase inhibitors

Project description:Histone deacetylase inhibitors are a class of drug which rapidly induce hyperacetylation of histone proteins. Here, we aimed to study the association between HDACi-induced histone acetylation and changes in gene expression. To study the early responses to HDACi treatment we treated cells with three different concentrations of two HDACi, sodium valproate (VPA) and suberoylanilide hydroxamic acid over a short timecourse. AH LCL cells were treated with 0.2mM, 1mM or 5mM valproic acid (VPA) or 0.5, 2.5 or 12.5µM suberoylanilide hydroxamic acid (SAHA). GM12878 cells were treated with 1mM VPA. Samples were collected at 0, 30, 60 and 120 minutes. All experiments were carried out in triplicate. One replicate of AH LCL, 0.2mM VPA, 30min and one replicate of AH LCL, 5mM VPA, 30min were eliminated as outliers

2015-08-31 | E-GEOD-65297 | biostudies-arrayexpress

RBBP4 regulates pluripotent-to-2C-like state transition through modulating heterochromatin assembly (Mnase-Seq)

Project description:Cellular totipotency is critical for generating a whole organism, yet how to establish totipotency is still poorly illustrated. Unlike pluripotent stem cells, abundant transposable elements (TEs) are activated in the totipotent cells. Here, we show that histone chaperone RBBP4 but not its homologous RBBP7 is indispensable in maintaining the identity of mouse embryonic stem cells (mESCs). Auxin-induced degradation of RBBP4, but not RBBP7, reprograms pluripotent state to a totipotent-like (also known as 2C-like) state. Mechanistically, RBBP4 could recruit G9a and KAP1 to bind on retrotransposons, especially endogenous retroviruses. RBBP4 degradation reduces the binding of G9a-mediated H3K9me2 on ERVL (particularly MERVL) and KAP1-mediated H3K9me3 on ERV1/ERVK, respectively. Moreover, RBBP4 facilitates nucleosome occupancy through chromatin remodeler CHD4 and RBBP4 depletion leads to attenuation of CHD4 binding and nucleosome occupancy on TEs. Together, our study reveals the important roles of RBBP4 in heterochromatin assembly and its loss activates TEs in mESCs, opening a new way to obtain totipotent cells in vitro.

2023-03-15 | GSE218655 | GEO

RBBP4 regulates pluripotent-to-2C-like state transition through modulating heterochromatin assembly (CUT&Tag)

2023-03-15 | GSE218654 | GEO

RBBP4 regulates pluripotent-to-2C-like state transition through modulating heterochromatin assembly (CUT&RUN)

2023-03-15 | GSE218653 | GEO

RBBP4 regulates pluripotent-to-2C-like state transition through modulating heterochromatin assembly (ChIP-Seq)

2023-03-15 | GSE218652 | GEO