Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ABSTRACT: Tumor suppressor function of Gata2 in Acute Promyelocytic Leukemia

PROVIDER: PRJNA699863 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	SRR13642000_1.fastq.gz	Fastqsanger.gz
	SRR13642000_2.fastq.gz	Fastqsanger.gz
	SRR13642001_1.fastq.gz	Fastqsanger.gz
	SRR13642001_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 97

Similar Datasets

DNA methylation changes are a late event in Acute Promyelocytic Leukemia and coincide with loss of transcription factor binding

Project description:This SuperSeries is composed of the following subset Series: GSE42044: DNA methylation changes are a late event in Acute Promyelocytic Leukemia and coincide with loss of transcription factor binding (sequencing) GSE42118: DNA methylation changes are a late event in Acute Promyelocytic Leukemia and coincide with loss of transcription factor binding (Illumina Methylation) Refer to individual Series

2012-11-08 | E-GEOD-42119 | biostudies-arrayexpress

NUP98RARG gene fusion

Project description:A novel NUP98/RARG gene fusion in acute myeloid leukemia resembling acute promyelocytic leukemia

2010-10-18 | E-MEXP-2928 | biostudies-arrayexpress

Anti-leukemia activity of bortezomib through GATA2-WT1 axis in acute myeloid leukemia

Project description:GATA2 is a transcription factor essential for hematopoietic differentiation and lymphatic system formation. High expression of GATA2 has been implicated in myelodysplastic syndrome and acute myeloid leukemia. Bortezomib has a good effect in MM. However, the mechanism of bortezomib possesses anti-self-renewal and leukemogenesis in AML is still unclear. Here, we reported that GATA2 and WT1 protein is degraded by bortezomib. The half-life of GATA2 mRNA was obviously shorter in Bortezomib-treated cells. Knockdown of GATA2 by small hairpin RNAs (shRNAs) has potential anti-leukemia activity in leukemic cells. Bortezomib inhibited cell proliferation and induced apoptotic death without activation of caspases pathway. Finally, bortezomib decreased xenograft tumor size in a xenograft leukemia mouse model, and prolonged the survival time in mouse C1498 AML model. Collectively, bortezomib might be a potential treatment for AML.

2021-11-14 | GSE188358 | GEO

STAT3β is a tumor suppressor in acute myeloid leukemia

Project description:STAT3β is a tumor suppressor in acute myeloid leukemia

| PRJNA484895 | ENA

Homo sapiens

Project description:SNP data of acute promyelocytic leukemia samples

| PRJNA112439 | ENA

LSK cells transfected with Hhex retrovirus

Project description:The Hematopoietically-expressed homeobox (Hhex) transcription factor is overexpressed in human myeloid leukemias. Conditional knockout models of murine acute myeloid leukemia (AML) indicate that Hhex maintains leukemia stem cell self-renewal by enabling Polycomb-mediated epigenetic repression of the Cdkn2a tumor suppressor locus, encoding p16Ink4a and p19Arf. However, whether Hhex overexpression also affects hematopoietic differentiation is unknown. To study this, we retrovirally overexpressed Hhex in hematopoietic progenitors. This enabled serial replating of myeloid progenitors, leading to the rapid establishment of IL-3-dependent promyelocytic cell lines. Use of a Hhex-ERT2 fusion protein demonstrated that continuous nuclear Hhex is required for transformation, and structure function analysis demonstrated a requirement of the DNA binding and N-terminal repressive domains of Hhex for promyelocytic transformation. This included the N-terminal Pml interaction domain, although deletion of Pml failed to prevent Hhex-induced promyelocyte transformation, implying other critical partners. Furthermore, deletion of p16Ink4a or p19Arf did not promote promyelocyte transformation, indicating that repression of distinct Hhex target genes is required for this process. Indeed, transcriptome analysis showed that Hhex overexpression resulted in repression of several myeloid developmental genes. To test potential for Hhex overexpression to contribute to leukemic transformation, Hhex-transformed promyelocyte lines were rendered growth factor-independent using a constitutively active IL-3 receptor common b subunit (bcV449E). The resultant cell lines resulted in a rapid promyelocytic leukemia in vivo. Thus Hhex overexpression can contribute to myeloid leukemia via multiple mechanisms including differentiation blockade and enabling epigenetic repression of the Cdkn2a locus.

2018-01-30 | GSE109793 | GEO

Expression profiling of NB4 cells after treatment with ATRA

Project description:In acute promyelocytic leukemia (APL), differentiation therapy with all-trans retinoic acid (ATRA)

2009-10-06 | GSE18397 | GEO

Genome-wide studies identify the role of PML/RARα phase separation in PML/RARα-driven transcriptional dysregulation.

2024-12-31 | GSE261293 | GEO

Genome-wide studies identify genes directly regulated by PML/RARα fusion protein

Project description:Acute promyelocytic leukemia (APL) is characterized by a specific t(15;17) chromosome translocation that generates the promyelocytic leukemia/retinoic acid receptor-α (PML/RARα) fusion gene. However, the global association between PML/RARα and transcriptional co-regulators, and the rules of their association in governing the key processes during the leukemogenesis remain obscure. Here, we performed the genome-wide binding profiling of PML/RARα, HDAC1 and P300, in NB4, an APL patient-derived cell line. We found that PML/RARα targets could be classified into two classes. Moreover, we also performed ChIP-seq of H3K27ac to determine super-enhancers in NB4. We identified a novel function of PML/RARα in super-enhancer regulation during the leukemogenesis of APL.

2020-08-26 | GSE126720 | GEO

Expression profiling of myeloid leukemia cell treated with vibsanin A, PMA and ATRA

Project description:All-trans retinoic acid (ATRA)-based differentiation therapy has achieved success with the treatment of acute promyelocytic leukemia (APL), a unique subtype of acute myeloid leukemia (AML). However, other subtypes of AML display resistance to ATRA-based treatment. Here, we demonstrate that a novel natural vibsane-type diterpenoid vibsanin A promotes the differentiation of myeloid leukemia cell lines and primary AML blasts. To reveal how vibsanin A function on promoting myeloid leukemia cell differentiation, we analyzed and compared the gene expression profiles in myeloid leukemia HL-60 cells treated with vibsanin A, PMA, and ATRA.

2016-02-28 | GSE78734 | 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