Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA seq with AML cells (NB4) upon FTO knockdown

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE103494 | GEO | 2019/04/29

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA seq with AML (NB4) cells upon FTO inhibition

Project description:To determine the potential targets of FTO and identify treatment significance of FTO inhibition in AML, we conducted transcriptome wide RNA seq with NB4 cells upon DMSO and FTO inhibitors (FB23 and FB23-2) treatment.

2019-04-29 | GSE103495 | GEO

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

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

NB4 cell line treatment with WEB-2170

Project description:This study reports the ability of WEB-2170, an antagonist of platelet-activating-factor receptor, to induce apoptosis in human acute myelogenous leukemia (AML) cells. Action mechanisms of WEB-2170 were first investigated in promyelocytic NB4 cells by DNA microarray profiling followed by morphologic, cytofluorimetric and biological analyses which were then extended to other AML cell lines including KG1, NB4-MR4, THP1 and U937, and, eventually, to blasts from patients with different AML subtypes (M0-M5).

2011-03-22 | E-GEOD-12645 | biostudies-arrayexpress

Sequencing of mRNA with N6-methyladenosine (m6A) modification in AML cells upon DMSO or FTO inhibitor treatment

Project description:To identify the potential mRNA targets of FTO inhibitor, we conducted m6A-seq with mRNA samples enriched from AML cells upon DMSO and FB23-2 (FTO inhibitor) treatment

2019-04-29 | GSE103496 | GEO

Proteome dynamics of HL-60, NB4, and K562 cells under the ATRA treatment

Project description:Searching for new strategies of acute myeloid leukemia (AML) treatment is of particular interest. Cell lines, e. g. HL-60 and NB4, represent model systems to study molecular features of leukemic cells. The all-trans-retinoic acid (ATRA) has proven itself to be an effective treatment for one of AML subtypes, i.e., acute promyelocytic leukemia (APL). At the same time, ATRA causes granulocytic differentiation of non-APL leukemic cells in vitro. Combination of new therapeutics with ATRA could improve efficiency of treatment. Studying the proteome perturbation in leukemic cells under the ATRA treatment allows to determine potential regulatory molecules that could be affected pharmacologically. Thus, the TMT-based proteomic profiles of HL-60, NB4, and K562 cell lines under the ATRA treatment were obtained at 0, 3, 12, 24, and 72 h after the ATRA treatment.

2024-06-23 | PXD050317 | Pride

Next generation sequencing analysis of transcriptomes at different timepoints after chlorprothixene treatment in NB4 and Kasumi-1 cells

Project description:To understand the mechanisms of chlorprothixene in acute myeloblastic leukemia (AML) therapy, gene expression changes of NB4 and Kasumi-1cells after chlorprothixene treatment were analyzed by RNA-seq

2019-12-23 | GSE124316 | GEO

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

Project description:To identify the expression of mRNAs after knockdown of FTO, we performed RNA-Seq in MA9.3ITD cells with or without knockdown of FTO.

2016-12-20 | GSE85008 | GEO

Identify genome-wide binding sites of GFI1 in NB4 cells

Project description:Abarrent transcriptional regulation is one of hallmarks of leukemia. GFI1 is a transcriptional regulator with context-dependent roles in hematopoiesis and leukemogenesis. Reduced or loss of GFI1 expression has been reported in myeloid malignancies, while high GFI1 expression has been observed in AML1-ETO-positive acute myeloid leukemia (AML) and acute lymphoid leukemia, but without clear roles defined for GFI1 in APL pathogenesis. We here performed ChIP-seq analysis using antibodies against GFI1 and identified genome-wide binding site of GFI1 in NB4 cells.

2020-08-26 | GSE154269 | GEO

Effect of FTO overexpression and knockdown on transcriptome of HEK293 cells

Project description:To gain insight into FTO function, we knocked down and overexpressed FTO in HEK293 cells.Genetrail analyses of expression profiles pointed to the RNA splicing and processing machinery. Intriguingly, using immunocytochemistry and confocal laser scanning microscopy, we observed strong enrichment of FTO in nuclear speckles and - to a lesser extent - in nucleoli, but not in other known nuclear bodies. We also studied RNA samples of Fto knockout and wild type mice with regard to content of methylated and unmethylated nucleosidesand observed that ratios of modified and unmodified uracil and adenine were different depending on the presence of FTO. Taken together, our data suggest that FTO is involved in RNA processing and modification. We used microarrays to investigate global gene expression changes depending on the level of FTO We compared FTO overexpressing and FTO depleted cells to cells with endogeneus level of FTO to determine global gene expression changes.

2012-11-13 | E-GEOD-33870 | 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