Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

HoxBlinc lncRNA reprograms CTCF-independent TADs to drive leukemic transcription and HSC dysregulation in NUP98 fusion transformed leukemia

ABSTRACT: HoxBlinc lncRNA reprograms CTCF-independent TADs to drive leukemic transcription and HSC dysregulation in NUP98 fusion transformed leukemia

PROVIDER: PRJNA1120835 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	SRR29306201_1.fastq.gz	Fastqsanger.gz
	SRR29306201_2.fastq.gz	Fastqsanger.gz
	SRR29306202_1.fastq.gz	Fastqsanger.gz
	SRR29306202_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 117

Similar Datasets

Hoxblinc lncRNA reprograms CTCF-independent TADs to drive leukemic transcription and HSC dysregulation in NUP98 fusion transformed leukemia [scRNA-Seq]

Project description:We found NUP98 fusions activate Hoxb-associated lncRNA, HoxBlinc that occupies homeotic/oncogenic topologically associated domain (TAD) boundaries in malignant hematopoiesis. Aberration of HoxBlinc led to recruitment of MLL1 complex and reorganization of homeotic/oncogenicTADs that enhanced chromatin accessibilities and aberrantly activated homeotic/hematopoietic oncogenes defined by Hoxblinc chromatin occupancies in NUP98-PHF23 related murine leukemia cells. Eliminated HoxBlinc in NUP98 fusion-driven leukemic cells resulted in loss of Hoxblinc binding, TAD integrity, recruitment of MLL complex, and MLL driven H3K4me3 and chromatin accessibility within the HoxBlinc defined domain in a CTCF independent manner, leading to inhibiting homeotic/leukemic oncogenes and mitigating NUP98 fusion-driven leukemia in xenografted mouse models. Moreover, overexpression of HoxBlinc in mouse bone marrow hematopoietic compartment developed multiple leukemia resembling NUP98-PHF23 knock-in mice via enhancing HoxBlinc binding and TAD formation to transcriptionally expanding HS/PC and myeloid/lymphoid subpopulations leading to leukemogenesis. Our studies reveal a CTCF independent role of HoxBlinc in leukemic TAD organization and oncogenic gene regulatory networks in NUP98-fusion related leukemia.

2025-01-31 | GSE269219 | GEO

Hoxblinc lncRNA reprograms CTCF-independent TADs to drive leukemic transcription and HSC dysregulation in NUP98 fusion transformed leukemia [Hi-C]

2025-01-31 | GSE269218 | GEO

Hoxblinc lncRNA reprograms CTCF-independent TADs to drive leukemic transcription and HSC dysregulation in NUP98 fusion transformed leukemia [ChIP-Seq]

2025-01-31 | GSE269217 | GEO

Hoxblinc lncRNA reprograms CTCF-independent TADs to drive leukemic transcription and HSC dysregulation in NUP98 fusion transformed leukemia [ChIRP-seq]

2025-01-31 | GSE269224 | GEO

Hoxblinc lncRNA reprograms CTCF-independent TADs to drive leukemic transcription and HSC dysregulation in NUP98 fusion transformed leukemia [CUT&Run]

2025-01-31 | GSE269221 | GEO

Hoxblinc lncRNA reprograms CTCF-independent TADs to drive leukemic transcription and HSC dysregulation in NUP98 fusion transformed leukemia [ATAC-Seq]

2025-01-31 | GSE269216 | GEO

Hoxblinc lncRNA reprograms CTCF-independent TADs to drive leukemic transcription and HSC dysregulation in NUP98 fusion transformed leukemia [RNA-Seq]

Project description:We found NUP98 fusions activate Hoxb-associated lncRNA, HoxBlinc that occupies and regulates homeotic/oncogenic topologically associated domain (TAD) in malignant hematopoiesis. Aberration of HoxBlinc led to recruitment of MLL1 complex , altered chromatin landscape (both H3K4me3 and chromatin accessibility), and HOX/homeotic gene activatiion in NUP98-PHF23 fusion driven leukemia and HoxBlinc -Tg models. Conversely, eliminated HoxBlinc in NUP98 fusion-driven leukemic cells resulted in loss of Hoxblinc binding, TAD integrity, recruitment of MLL complex, and MLL driven H3K4me3 and chromatin accessibility within the HoxBlinc defined domain in a CTCF independent manner, leading to inhibiting homeotic/leukemic oncogenes and mitigating NUP98 fusion-driven leukemia in xenografted mouse models. Thus, our studies revealed a CTCF independent role of HoxBlinc in leukemic TAD organization and oncogenic gene regulatory networks in NUP98-fusion related leukemia.

2025-01-31 | GSE269226 | GEO

Hoxblinc lncRNA reprograms CTCF-independent TADs to drive leukemic transcription and HSC dysregulation in NUP98 fusion transformed leukemia [CTCF-HiChIP-seq]

2025-01-31 | GSE283303 | GEO

Hoxblinc lncRNA reprograms CTCF-independent TADs to drive leukemic transcription and HSC dysregulation in NUP98 fusion transformed leukemia [ATAC-Seq]

Project description:Hoxblinc lncRNA reprograms CTCF-independent TADs to drive leukemic transcription and HSC dysregulation in NUP98 fusion transformed leukemia [ATAC-Seq]

| PRJNA1120741 | ENA

Hoxblinc lncRNA reprograms CTCF-independent TADs to drive leukemic transcription and HSC dysregulation in NUP98 fusion transformed leukemia [scRNA-Seq]

Project description:Hoxblinc lncRNA reprograms CTCF-independent TADs to drive leukemic transcription and HSC dysregulation in NUP98 fusion transformed leukemia [scRNA-Seq]

| PRJNA1120753 | ENA

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