Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ChIP-seq analysis of ENL following KAT6A CRISPR targeting

ABSTRACT: ChIP-seq analysis of ENL following KAT6A CRISPR targeting

PROVIDER: PRJNA693198 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13482465.fastq.gz	Fastqsanger.gz
	SRR13482466.fastq.gz	Fastqsanger.gz
	SRR13482467.fastq.gz	Fastqsanger.gz
	SRR13482468.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

ChIP-seq analysis of ENL following KAT6A CRISPR targeting

Project description:ChIP-seq analysis of ENL in MOLM-13 human leukemia cells transduced with lentivirus containing CRISPR-Cas9 EV or sgKAT6A for 5 days

2021-10-20 | GSE165076 | GEO

Epigenetic profiling of cells following KAT6A CRISPR targeting

Project description:Epigenetic profiling of cells following KAT6A CRISPR targeting

| PRJNA659930 | ENA

Transcriptional profiling of MOLM-13 AML cells following KAT6A CRISPR targeting

Project description:Transcriptional profiling of MOLM-13 AML cells following KAT6A CRISPR targeting

| PRJNA659646 | ENA

Epigenetic profiling of cells following KAT6A CRISPR targeting

Project description:ChIP-seq analysis of MOLM-13 human leukemia cells transduced with lentivirus containing CRISPR-Cas9 EV or sgKAT6A for 5 days.

2021-10-20 | GSE157041 | GEO

Transcriptional profiling of MOLM-13 AML cells following KAT6A CRISPR targeting

Project description:RNA-seq analysis of MOLM-13 human leukemia cells transduced with lentivirus containing CRISPR-Cas9 EV or sgKAT6A for 5 days

2021-10-20 | GSE156948 | GEO

Targeting KAT6A/KAT6B dependencies in breast cancer with a novel selective, orally bioavailable KAT6 inhibitor, CTx-648/PF-9363 [RNA-Seq]

Project description:KAT6A, and its paralog KAT6B, are histone lysine acetyltransferases (HAT) that acetylate histone H3K23 and regulate diverse biological processes including transcription, cell-cycle progression, and stem cell development. KAT6A exerts an oncogenic role in several tumor types including breast cancer where it is amplified in 10-15% of patients. However, pharmacologic targeting of KAT6A to achieve therapeutic benefit has been a challenge. Here we describe identification of a highly potent, selective and orally bioavailable KAT6A/KAT6B inhibitor CTx-648 (PF-9363), derived from a novel benzisoxazole series, which demonstrates anti-tumor activity in correlation with H3K23Ac inhibition in KAT6A over-expressing breast cancer. Transcriptional and epigenetic profiling studies show reduced RNA Pol II binding and downregulation of genes involved in estrogen signaling, cell cycle and stem cell pathways associated with CTx-648 anti-tumor activity in ER-positive (ER+) breast cancer. CTx-648 treatment leads to potent tumor growth inhibition in ER+ breast cancer in vivo models, including models refractory to endocrine therapy, highlighting the potential for targeting KAT6A in ER+ breast cancer.

2023-06-05 | GSE233783 | GEO

Targeting KAT6A/KAT6B dependencies in breast cancer with a novel selective, orally bioavailable KAT6 inhibitor, CTx-648/PF-9363 [BrU-Seq]

2023-06-05 | GSE233787 | GEO

Targeting KAT6A/KAT6B dependencies in breast cancer with a novel selective, orally bioavailable KAT6 inhibitor, CTx-648/PF-9363 [ATAC-Seq]

2023-06-05 | GSE233784 | GEO

Targeting KAT6A/KAT6B dependencies in breast cancer with a novel selective, orally bioavailable KAT6 inhibitor, CTx-648/PF-9363 [ChIP-Seq - CUT&RUN]

2023-06-05 | GSE233788 | GEO

The histone acetyltransferase KAT6A is recruited to unmethylated CpG islands via a DNA-binding winged helix domainThe histone acetyltransferase KAT6A is recruited to unmethylated CpG islands via a DNA-binding winged helix domain

Project description:The lysine acetyltransferase KAT6A (MOZ, MYST3) belongs to the MYST family of chromatin regulators, facilitating histone acetylation. Dysregulation of KAT6A has been implicated in developmental syndromes and the onset of acute myeloid leukemia (AML). Previous work suggests that KAT6A is recruited to its genomic targets by a combinatorial function of histone binding PHD fingers, transcription factors and chromatin binding interaction partners. Here, we demonstrated that a winged helix domain at the N-terminus of KAT6A specifically interacts with unmethylated CpG motifs. This DNA binding function leads to the association of KAT6A to unmethylated CpG islands (CGIs) genome wide. Mutation of the essential amino acids completely abrogates the enrichment of KAT6A at CGIs. Overexpression of a KAT6A WH1 mutant has a dominant negative effect on H3K9 histone acetylation, which is comparable to the effects upon overexpression of a KAT6A HAT domain mutant. Taken together, our work revealed a previously unrecognized chromatin recruitment mechanism of KAT6A, offering a new perspective on the role of KAT6A in gene regulation and human diseases

2023-01-14 | PXD034833 | Pride

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