Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The Epigenetic Regulator Landscape of HOX/MEIS Expression in AML [scRNA-seq]

ABSTRACT: The Epigenetic Regulator Landscape of HOX/MEIS Expression in AML [scRNA-seq]

PROVIDER: PRJNA900364 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR22259371_1.fastq.gz	Fastqsanger.gz
	SRR22259371_2.fastq.gz	Fastqsanger.gz
	SRR22259372_1.fastq.gz	Fastqsanger.gz
	SRR22259372_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

The Epigenetic Regulator Landscape of HOX/MEIS Expression in AML [scRNA-seq]

Project description:Aberrant and constitutive activation of the clustered homeobox (HOX) genes and the three-amino-acid loop extension (TALE) domain-containing HOX co-factor MEIS1 (henceforth termed HOX/MEIS) is a recurrent feature in several types of myeloid and lymphoid leukemias. HOX/MEIS misexpression is linked to aberrant self-renewal and therapy resistance in leukemia, but the therapeutic targeting of this important pathway has remained elusive. Using AF10-rearranged leukemia as a prototypical example of HOX/MEIS dysregulation, we sought to comprehensively characterize chromatin regulators that sustain aberrant expression of these genes. We deployed a GFP-MEIS1 knock-in reporter cell line to conduct small-molecule inhibitor screens and a high-density domain-focused CRISPR-Cas9 screen targeting epigenetic regulators. We identified members of at least six distinct chromatin-modifying complexes as HOX/MEIS regulators, including previously characterized HOX/MEIS regulators such as DOT1L, AF10, ENL, and HBO1 as well as less well-characterized and completely novel HOX/MEIS regulators including AFF2, JADE3, casein kinase 2 and the chromatin reader SGF29. These HOX/MEIS regulators were important for the growth of AML cell lines representing diverse leukemia subtypes characterized by HOX/MEIS dysregulation including leukemias with AF10 rearrangements, MLL rearrangements, and NPM1 mutation. Determination of gene expression changes after perturbing each of these MEIS1 regulators in parallel using CROP-seq demonstrated that the deletion of DOT1L, ENL, AFF2, or SGF29 led to the downregulation of several genes associated with stem cell self-renewal and upregulation of differentiation-associated genes.

2023-11-10 | GSE217779 | GEO

Epigenetic regulator landscape of HOX/MEIS expression in AML

Project description:Epigenetic regulator landscape of HOX/MEIS expression in AML

| PRJNA900618 | ENA

Axial skeleton anterior-posterior patterning is regulated through feedback regulation between Meis and retinoic acid

Project description:Vertebrate axial skeletal patterning is controlled by coordinated collinear expression of Hox genes and axial level-dependent activity of Hox protein combinations. Transcription factors of the Meis family act as cofactors of Hox proteins and profusely bind to Hox complex DNA, however their roles in mammalian axial patterning have not been established. Similarly, retinoic acid (RA) is known to regulate axial skeletal element identity through the transcriptional activity of its receptors, however whether this role is related to Meis/Hox regulation or functions in axial patterning remains unknown. Here we study the role of Meis factors in axial skeleton formation and its relationship to the RA pathway by characterizing Meis1, Meis2 and Raldh2 mutant mice. We report that Meis and Raldh2 regulate each other in a positive feedback regulatory loop that controls axial skeletal identity. Meis elimination produces homeotic transformations similar to those found in Raldh2 and anterior-Hox mutants and disrupts the expression of Hox target genes without changing the transcriptional profiles of Hox complexes. We propose that Meis regulates vertebrate axial skeleton patterning by exclusively affecting Hox protein function, and that alterations in RA levels can produce homeotic transformations without altering Hox transcription through regulating Meis expression.

2020-12-22 | GSE146301 | GEO

Gene regulation in t(6 9) AML resembles that of FLT3-ITD/NPM1 AML with an altered HOX/MEIS axis

Project description:Gene regulation in t(6 9) AML resembles that of FLT3-ITD/NPM1 AML with an altered HOX/MEIS axis

| PRJNA1003067 | ENA

Gene regulation in t(6 9) AML resembles that of FLT3-ITD/NPM1 AML with an altered HOX/MEIS axis [DNase-hypersensitivity]

Project description:Gene regulation in t(6 9) AML resembles that of FLT3-ITD/NPM1 AML with an altered HOX/MEIS axis [DNase-hypersensitivity]

| PRJNA1003073 | ENA

Gene regulation in t(6 9) AML resembles that of FLT3-ITD/NPM1 AML with an altered HOX/MEIS axis [RNA-seq]

Project description:Gene regulation in t(6 9) AML resembles that of FLT3-ITD/NPM1 AML with an altered HOX/MEIS axis [RNA-seq]

| PRJNA1003070 | ENA

Epigenetic regulator landscape of HOX/MEIS expression in AML

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-11-10 | GSE217829 | GEO

Gene regulation in t(6;9) AML resembles that of FLT3-ITD/NPM1 AML with an altered HOX/MEIS axis [RNA-seq]

Project description:Acute Myeloid Leukemia (AML) represents a heterogeneous group of hematological malignancies. The t(6;9)(p23;q34) translocation, giving rise to the DEK::NUP214 fusion protein, is a rare mutation which produces a highly aggressive AML associated with extremely poor prognosis. Here, we utilise genome-wide chromatin accessibility to elucidate how a normal gene regulatory networks is disrupted by DEK::NUP214. We find that DEK::NUP214 AML forms a specific GRN related to that of mutant NPM1 AML, but also displays an elevated leukemic stem cell signature, suggesting both similar and unique therapeutic vulnerabilities.

2024-01-04 | GSE240267 | GEO

Gene regulation in t(6;9) AML resembles that of FLT3-ITD/NPM1 AML with an altered HOX/MEIS axis [DNase-hypersensitivity]

2024-01-04 | GSE240268 | GEO

Gene expression profiling of Hox-driven AML overexpressing JMJD1C

Project description:JMJD1C, a Jumonji C (JmjC) domain-containing histone demethylase, has been reported as a direct cofactor of oncogenic transcription factor HOXA9. To identify JMJD1C downstream effectors, we performed a genome-wide gene expression profiling experiment. Our microarray analysis identified a new role for JMJD1C in regulating a cancer metabolic program in HOX-driven AML. GFP+ HOXA9/MEIS1-mediated pre-leukemic stem cells were transduced with retroviruses carrying JMJD1C or empty vector for the microarray experiment. Each group has 4 samples.

2018-12-30 | E-MTAB-5760 | biostudies-arrayexpress

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