Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide maps of chromatin state for histone modifications and chromatin remodeling factors in WT and PHF6-KO conditions in Jurkat T-ALL cells.

ABSTRACT: We have carried out high-throughput profiling of histone modifications and transcription factors in mammalian cells. First we generated stable PHF6 knock out lines by CRISPR-Cas9 technology in wild type Jurkat cells. We electroporated the RNP complex in Jurkat cells conatining guide RNAs against either non-targeting (EV) or PHF6 (KO) followed by single clone isolation and expansion. We confirmed absolute loss of total protein by WB and indel formation (mutation efficiency) at the PHF6 genomic locus by Sanger sequencing. By obtaining over six to ten billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of well studied histone modifications and transcription factors. This study provides a framework for eluciadting the role of PHF6 in regulating the chromatin landscape encompassing both activating and repressive histone modifications and chromatin remodelers in the context of leukemia.

ORGANISM(S): Homo sapiens

PROVIDER: GSE193713 | GEO | 2025/01/13

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

PHF6 drives satellite DNA chromatin remodeling for resolution of replicative stress-induced DNA damage

Project description:The Plant Homeodomain 6 gene (PHF6) encodes a nucleolar and chromatin-associated factor with proposed roles in chromatin remodeling and transcription regulation. Germline mutations in PHF6 are causative of Börjesson-Forsmann-Lehman syndrome, while somatic loss-of-function genetic alterations support a tumor suppressor role in leukemia. Yet, the specific molecular function and mechanisms of PHF6 remain poorly understood. Here we show that PHF6 associates with chromatin remodeling and DNA repair factors in multiprotein complexes at satellite repeat heterochromatin regions and facilitates double strand break repair in the context of replicative stress-induced DNA damage. Mechanistically, PHF6 localizes to sites of DNA damage and its inactivation impairs the resolution of DNA breaks promoting the accumulation of single and double-stranded DNA lesions. In addition, PHF6 associates with difficult to replicate Histone H3 lysine 9 trimethylation (H3K9me3)-marked heterochromatin at satellite DNA regions, prevents accelerated replication fork dynamics and is required to maintain genomic integrity at fragile sites. In all, these results demonstrate a critical role for PHF6-containing chromatin-remodeling complexes in homologous recombination DNA-repair and in the resolution of satellite DNA-associated replicative stress.

2022-04-05 | GSE152292 | GEO

Chromatin accessibility changes caused by PHF6 knockout in THP1 human AML cell line

Project description:PHF6 is a transcriptional regulator mutated in 3-5% of acute myeloid leukemia. To understand how PHF6 and its functional partner PHIP interact with each other on chromatin, we performed ChIP-Seq for PHF6 (in the presence and absence of PHIP), and for PHIP. We observd that PHF6 and PHIP peaks overlap on chromatin, and PHF6 requires PHIP for its chromatin occupancy. ATAC-Seq and H3K27ac ChIP-Seq showed that PHF6 and PHIP occupy open and active regions of the genome.

2024-11-15 | GSE281626 | GEO

Genome-wide maps of chromatin state for histone modifications and chromatin remodeling factors in WT and PHF6-KO conditions in Jurkat T-ALL cells.

Project description:Genome-wide maps of chromatin state for histone modifications and chromatin remodeling factors in WT and PHF6-KO conditions in Jurkat T-ALL cells.

| PRJNA797372 | ENA

PHF6 OCCUPANCYIN HUMAN T-CELL ACUTE LYMPHOBLASTIC LEUKEMIA

Project description:Here we identify the genome-wide occupancy of PHF6 in T-ALL cells. Human T-ALL cells were cross-linked with formaldehyde for 20 min. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. A sample of whole cell extract (WCE) was sequenced and used as the background to determine enrichment. ChIP was performed using an antibody against total PHF6 (Bethyl A301-451A). This represents the ChIP-seq portion of this dataset.

2014-04-01 | E-GEOD-45864 | biostudies-arrayexpress

Changes in H3K27 acetylation in THP1 human AML cell line on PHF6 knockout, PHF6R274Q mutation, PHIP knockout, and double knockout of PHF6 and PHIP compared to wildtype clones

Project description:PHF6 is a transcriptional regulator mutated in 3-5% of acute myeloid leukemia. To understand how PHF6 and its functional partner PHIP interact with each other on chromatin, we performed ChIP-Seq for PHF6 (in the presence and absence of PHIP), for PHF6R274Q mutant, and for PHIP. We observd that PHF6 and PHIP peaks overlap on chromatin, and PHF6 requires PHIP for its chromatin occupancy. ATAC-Seq and H3K27ac ChIP-Seq showed that PHF6 and PHIP occupy open and active regions of the genome.

2024-11-15 | GSE281627 | GEO

PHF6 occupancy in THP1 human AML cell line in wildtype, PHF6R274Q mutant, and PHIP knockout cells

Project description:PHF6 is a transcriptional regulator mutated in 3-5% of acute myeloid leukemia. To understand how PHF6 and its functional partner PHIP interact with each other on chromatin, we performed ChIP-Seq for PHF6 (in the presence and absence of PHIP), for PHF6R274Q mutant, and for PHIP. We observd that PHF6 and PHIP peaks overlap on chromatin, and PHF6 requires PHIP for its chromatin occupancy. ATAC-Seq and H3K27ac ChIP-Seq showed that PHF6 and PHIP occupy open and active regions of the genome.

2024-11-15 | GSE281628 | GEO

PHF6 and JAK3 mutations cooperate to drive T-cell acute lymphoblastic leukemia progression (ChIP-Seq)

Project description:Chromatin immunoprecipitation sequencing (ChIP-seq) analysis of HA-PHF6-overexpressing (PHF6 OE) K562 cells showed that PHF6 directly bound to the ADGRB1 (BAI1) gene

2022-02-09 | GSE159549 | GEO

The chromatin-binding protein PHF6 functions as an E3 ubiquitin ligase of H2BK120 via H2BK12Ac recognition for activation of trophectodermal genes

Project description:Epigenetic regulation is important for establishing lineage-specific gene expression during early development. Although signaling pathways have been well-studied for regulation of trophectoderm reprogramming, epigenetic regulation of trophectodermal genes with histone modification dynamics have been poorly understood. Here, we identify that plant homeodomain finger protein 6 (PHF6) is a key epigenetic regulator for activation of trophectodermal genes using RNA-sequencing and ChIP assays. PHF6 acts as an E3 ubiquitin ligase for ubiquitination of H2BK120 (H2BK120ub) via its extended plant homeodomain 1 (PHD1), while the extended PHD2 of PHF6 recognizes acetylation of H2BK12 (H2BK12Ac). Intriguingly, the recognition of H2BK12Ac by PHF6 is important for exerting its E3 ubiquitin ligase activity for H2BK120ub. Together, our data provide evidence that PHF6 is crucial for epigenetic regulation of trophectodermal gene expression by linking H2BK12Ac to H2BK120ub modification.

2020-07-13 | GSE144298 | GEO

RNA sequencing of isogenic Phf6 wild type and Phf6 knockout mouse T-ALL cells

Project description:Loss-of-function mutations Phf6 occur frequently in both adult and pediatric T-cell Acute Lymphoblastic Leukemia (T-ALL). Although Phf6 is widely expressed, little is known about its proposed function as epigenetic regulator and tumor suppressor. To address the role of Phf6 in the leukemia development, here we analyze by RNAseq the gene expression profiles of isogenic Phf6 wild type and Phf6 knockout leukemia cells transformed by overexpression of an oncogenic mutant form of the NOTCH1 receptor.

2019-07-31 | GSE117165 | GEO

Chromatin binding protein PHF6 regulates activity-dependent transcription networks to promote hunger response [ChIP-Seq]

Project description:We revealed that PHF6 was bound to the promoters of a subset of neuronal immediate-early genes (IEGs), and this chromatin binding was dynamically regulated by hunger state.

2020-03-16 | GSE133901 | 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