Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ENL reads histone β-hydroxybutyrylation to modulate gene transcription (CUT&Tag)

ABSTRACT: ENL reads histone β-hydroxybutyrylation to modulate gene transcription (CUT&Tag)

PROVIDER: PRJNA1106475 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR28852613_1.fastq.gz	Fastqsanger.gz
	SRR28852613_2.fastq.gz	Fastqsanger.gz
	SRR28852614_1.fastq.gz	Fastqsanger.gz
	SRR28852614_2.fastq.gz	Fastqsanger.gz
	SRR28852615_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 10

Similar Datasets

ENL reads histone β-hydroxybutyrylation to modulate gene transcription (CUT&Tag)

Project description:Histone modifications are typically recognized by chromatin-binding protein modules (referred to as “readers”) to mediate fundamental processes such as transcription. Lysine β-hydroxybutyrylation (Kbhb) is a new type of histone mark that couples metabolism to gene expression. However, the readers that prefer histone Kbhb remain elusive. This knowledge gap must be filled in order to reveal the molecular mechanism of this epigenetic regulation. Herein, we developed a chemical proteomic approach, relying upon multivalent photoaffinity probes to capture binders of the mark and identified ENL as a novel target of H3K9bhb. Biochemical studies and CUT&Tag analysis further suggested that ENL favorably binds to H3K9bhb, and co-localizes with it on promoter regions to modulate gene expression. Notably, disrupting the interaction between H3K9bhb and ENL via structure-based mutation leads to the suppressed expression of the gene like MYC that drives cell proliferation.

2024-05-06 | GSE266268 | GEO

ENL reads histone β-hydroxybutyrylation to modulate gene transcription (RNA-Seq)

2024-05-06 | GSE266269 | GEO

ENL reads histone β-hydroxybutyrylation to modulate gene transcription (RNA-Seq)

Project description:ENL reads histone β-hydroxybutyrylation to modulate gene transcription (RNA-Seq)

| PRJNA1106487 | ENA

ENL reads histone β-hydroxybutyrylation to modulate gene transcription.

Project description:Histone modifications are typically recognized by chromatin-binding protein modules (referred to as 'readers') to mediate fundamental processes such as transcription. Lysine β-hydroxybutyrylation (Kbhb) is a new type of histone mark that couples metabolism to gene expression. However, the readers that prefer histone Kbhb remain elusive. This knowledge gap should be filled in order to reveal the molecular mechanism of this epigenetic regulation. Herein, we developed a chemical proteomic approach, relying upon multivalent photoaffinity probes to capture binders of the mark, and identified ENL as a novel target of H3K9bhb. Biochemical studies and CUT&Tag analysis further suggested that ENL favorably binds to H3K9bhb, and co-localizes with it on promoter regions to modulate gene expression. Notably, disrupting the interaction between H3K9bhb and ENL via structure-based mutation led to the suppressed expression of genes such MYC that drive cell proliferation. Together, our work offered a chemoproteomics approach and identified ENL as a novel histone β-hydroxybutyrylation effector that regulates gene transcription, providing new insight into the regulation mechanism and function of histone Kbhb.

| S-EPMC11417371 | biostudies-literature

ENL reads histone β-hydroxybutyrylation to modulate gene transcription

Project description:Identification of hPTM binder through the chemoproteomic approach

2024-06-26 | PXD051689 | Pride

Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling [ChIP-seq and CUT&Tag]

Project description:Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling [ChIP-seq and CUT&Tag]

| PRJNA999348 | ENA

Condensate-promoting ENL mutation induces tumorigenesis via chromatin remodeling [ChIP-seq and CUT&Tag]

Project description:Gain-of-function mutations in the chromatin ‘reader’ ENL, identified in AML and Wilms tumor, have been shown to induce aberrant formation of transcriptional condensates in cellular systems. However, the precise role of these mutations and their condensate forming property in tumorigenesis remains unclear. By creating a conditional knock-in mouse model for the most prevalent ENL mutation, we establish ENL mutant as a bona fide oncogenic driver of acute myeloid leukemia in vivo. Heterozygous expression of ENL mutant perturbs the normal hematopoietic hierarchy and results in the aberrant expansion of myeloid progenitors with increased self-renewal property. Furthermore, the ENL mutant remodels histone modifications to alter differentiation processes and drive oncogenic gene expression during hematopoietic development. Importantly, targeted point mutagenesis to disrupt the condensate formation property completely abolishes ENL mutant’s oncogenic function in hematopoietic stem and progenitor cells (HSPCs). Lastly, short-term treatment with a small molecule inhibitor that blocks the acetyl-binding activity of ENL mutant reverts its impact on chromatin and significantly delays leukemia development in mice. Our studies reveal the crucial biological function of mutation-induced transcriptional condensates in chromatin regulation and cancer in vivo and provide proof-of-concept for targeting of pathogenic condensates as a promising therapy for certain cancers.

2024-04-14 | GSE239468 | GEO

MYC-FACT Interactions Drive Z-DNA Formation to Modulate Transcriptional Dynamics [CUT&TAG]

Project description:MYC-FACT Interactions Drive Z-DNA Formation to Modulate Transcriptional Dynamics [CUT&TAG]

| PRJNA1229492 | ENA

HCT116_SMARCA4 CUT&Tag

Project description:HCT116_SMARCA4 CUT&Tag

| PRJNA875063 | ENA

scNanoSeq-CUT&Tag: a long-read single-cell CUT&Tag sequencing method for efficient chromatin modification profiling within individual cells

Project description:We developed scNanoSeq-CUT&Tag, a streamlined method by adapting a modified CUT&Tag protocol to Oxford Nanopore sequencing platform for efficient chromatin modification profiling at single-cell resolution. We firstly tested the performance of scNanoSeq-CUT&Tag on six human cell lines: K562, 293T, GM12878, HG002, H9, HFF1 and adult mouse blood cells, it showed that scNanoSeq-CUT&Tag can accurately distinguish different cell types in vitro and in vivo. Moreover, scNanoSeq-CUT&Tag enables to effectively map the allele-specific epigenomic modifications in the human genome andallows to analyze co-occupancy of histone modifications. Taking advantage of long-read sequencing,scNanoSeq-CUT&Tag can sensitively detect epigenomic state of repetitive elements. In addition, by applying scNanoSeq-CUT&Tag to testicular cells of adult mouse B6D2F1, we demonstrated that scNanoSeq-CUT&Tag maps dynamic epigenetic state changes during mouse spermatogenesis. Finally, we exploited the epigenetic changes of human leukemia cell line K562 during DNA demethylation, it showed that NanoSeq-CUT&Tag can capture H3K27ac signals changes along DNA demethylation. Overall, we prove that scNanoSeq-CUT&Tag is a valuable tool for efficiently probing chromatin state changes within individual cells.

2024-09-06 | GSE249799 | 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