Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Homo sapiens

ABSTRACT: mRNA sequencing in acute myeloid leukemia (AML) cells with and without knockdown of FTO

PROVIDER: PRJNA335858 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR3987612.fastq.gz	Fastqsanger.gz
	SRR3987613.fastq.gz	Fastqsanger.gz

Items per page:

1 - 2 of 2

Similar Datasets

N6-methyladenosine (m6A) sequencing of messenger RNAs in acute myeloid leukemia (AML) cells with and without knockdown of FTO

Project description:To identify potential mRNA targets of FTO whose m6A levels are influenced in acute myeloid leukemia (AML) cells, we conducted m6A-seq for mRNA isolated from MA9.3ITD cells with and without knockdown of FTO

2016-12-20 | GSE84944 | GEO

RNA seq with AML cells (NB4) upon FTO knockdown

Project description:To identify the potential targets genes of FTO in acute myeloid leukemia (AML), we peroformed RNA-seq of NB4 cells with or without FTO knockdown based on Illumina Hiseq system.

2019-04-29 | GSE103494 | GEO

Sequencing of messenger RNAs with N6-methyladenosine modifications in acute myeloid leukemia (AML) with and without forced expression of FTO

Project description:To identify potential mRNA targets of FTO whose m6A levels are affected by FTO in acute myeloid leukemia (AML) cells, we conducted m6A-seq for messenger RNAs isolated from AML cells with and without forced expression of FTO.

2016-12-20 | GSE76414 | GEO

Analysis of m6A levels in K562 treted with the FTO inhibitor FB23-3 by m6A-mRNA&lncRNA Epitranscriptomic Microarray

Project description:FTO, an N6-methyladenosine demethylase, has emerged as a promising target for the treatment of specific acute myeloid leukemia (AML) subtypes. Here, we investigate the antiproliferative effects of the FTO inhibitor FB23-2 in leukemia. We demonstrate that FB23-2 potently inhibits proliferation across both AML and CML cell lines, irrespective of their responsiveness to FTO depletion. Interestingly, FB23-2 induces cell cycle arrest without a concurrent increase in m6A levels, suggesting an alternative mechanism of action.

2024-12-26 | GSE254577 | GEO

Homo sapiens

Project description:N6-methyladenosine (m6A) sequencing of messenger RNAs in acute myeloid leukemia (AML) cells with and without knockdown of FTO

| PRJNA335722 | ENA

Homo sapiens

Project description:RNA-seq in acute myeloid leukemia (AML) cells with and without knockdown of METTL14

| PRJNA381786 | ENA

Homo sapiens

Project description:acute myeloid leukemia (AML)

| PRJNA87151 | ENA

Homo sapiens

Project description:acute myeloid leukemia (AML)

| PRJNA87153 | ENA

Homo sapiens

Project description:TARGET: Acute Myeloid Leukemia (AML)

| PRJNA89525 | ENA

Proteomics analysis for RBM17 in acute myeloid leukemia

Project description:Acute myeloid leukemia (AML) patients suffer from chemo-resistance, high relapse frequency, and low overall survival rate, outcomes driven by leukemic stem cells (LSCs). Understanding the molecular mechanisms that support these primitive leukemic cells is crucial for developing effective AML therapeutics. In the present study, we demonstrate that upregulation of the splicing factor RBM17 preferentially marks and sustains the primitive compartment of AML. We performed shotgun proteomics to characterize the proteome changes upon RBM17 knockdown in AMl cells. In addition, we used proteomics to analyze the proteome changes after knockdown of EIF4A2, a direct splicing substrate of RBM17 in AML cells.

2022-08-12 | PXD026780 | 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