Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Identification of JMJD1C target genes in LN-229 glioblastoma cells.

ABSTRACT: Identification of JMJD1C target genes in LN-229 glioblastoma cells.

PROVIDER: PRJNA700586 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13651635_1.fastq.gz	Fastqsanger.gz
	SRR13651635_2.fastq.gz	Fastqsanger.gz
	SRR13651636_1.fastq.gz	Fastqsanger.gz
	SRR13651636_2.fastq.gz	Fastqsanger.gz
	SRR13651637_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Identification of JMJD1C target genes in LN-229 glioblastoma cells.

Project description:JMJD1C shows ubiquitous expression and is often downregulated in tumor entities compared to healthy tissues.JMJD1C inhibit growth of the glioblastoma cell line LN-229. Here, JMJD1C knockdown leads to malignant progression in the glioblastoma cell line LN-229.

2021-02-09 | GSE166351 | GEO

Effect of Vortioxetine treatment on gene expression of LN-229 glioblastoma cells over time

Project description:The atypical antidepressant Vortioxetine represents the most effective neuroactive drug with anti-glioblastoma efficacy across glioblastoma patient samples and model systems. To closer examine the temporal dynamics of Vortioxetine, we performed in-depth transcriptomic profiling of LN-229 cells following Vortioxetine treatment. We performed gene expression profiling analysis using data obtained from RNA-seq across 6 different time points during the 24 hours following Vortioxetine treatment.

2024-07-29 | GSE214968 | GEO

Expression data from WIF1 induced LN-229 (GBM cell line)

Project description:Glioblastoma is the most aggressive primary brain tumor in adults and due to the invasive nature it cannot be completely removed. We have recently shown that the WNT inhibitory factor 1 (WIF1), a secreted inhibitor of WNTs, is downregulated in glioblastoma and acts as strong tumor suppressor. In search of a mediator for this function differential gene expression profiles of WIF1-expressing cells were performed. MALAT1, a long non-coding RNA and key positive regulator of invasion, emerged as the top downregulated gene. Indeed, knock-down of MALAT1 reduced migration in glioblastoma cells, without effect on proliferation. LN-229 cells induced with Doxocyclin to express WIF1 were compared to the non-induced control (two biological replicates each)

2015-02-23 | E-GEOD-58525 | biostudies-arrayexpress

RNA sequencing analysis of LN-229-shControl and LN-229-shMOB2 cells

Project description:RNA sequencing analysis of LN-229-shControl and LN-229-shMOB2 cells

| PRJNA579353 | ENA

Effect of IDH1 mutation induced by doxycycline on gene expression during VSVΔ51 infection in LN-229-TRE-R132H glioblastoma cells

Project description:To investigate whether IDH1 mutation influence the effects of oncolytic virus VSVΔ51, we transduced doxycycline-inducible IDH1-R132H lentiviruses into LN-229 to establish the LN-229-TRE-R132H cell line. We then performed gene expression profiling analysis using data obtained from RNA-seq of LN-229-TRE-R132H cells infected with or without VSVΔ51 in the presence or absence of IDH1 mutation induced by doxycycline.

2023-09-19 | GSE208634 | GEO

Digital RNA with pertUrbation of Genes (DRUG-Seq) of LN-229 glioblastoma cells treated with 20 different drugs at two time points

Project description:DRUG-Seq is a miniatruized and multiplexed RNA-Seq protocol described in Ye et al., 2018 (https://www.nature.com/articles/s41467-018-06500-x) To determine transcriptional changes upon drug perturbation in LN-229 glioblastoma cells, we profiled 20 drug responses across two time-points (6 and 22 hours) by DRUG-Seq

2024-07-29 | GSE214965 | GEO

Comparative proteomic analysis of EV-derived from glioblastoma (LN 229 cell line) and healthy human astrocytes, neurons and endothelial brain cells

Project description:This study aims to identify EV-derived glioblastoma biomarkers through a comparative mass spectrometry-based bottom-up proteomic analysis of glioblastoma LN-229 cell line and healthy human neurons, astrocytes, and endothelial brain cells (HEBC). The work investigates cancer cells' communication with the healthy brain environment

2024-09-03 | PXD055487 |

Jmjd1c

Project description:Jmjd1c

| PRJNA304620 | ENA

Expression data from WIF1 induced LN-229 (GBM cell line)

2015-02-23 | GSE58525 | GEO

RNA expression analysis upon JMJD1C depletion

Project description:The AML1-ETO fusion protein, a transcription factor generated by the t(8;21) translocation in acute myeloid leukaemia (AML), dictates a leukemic program by increasing self-renewal and inhibiting differentiation. Here we demonstrate that the histone demethylase JMJD1C functions as a co-activator for AML1-ETO and is required for its transcriptional program. JMJD1C is directly recruited by AML1-ETO to its target genes and regulates their expression by maintaining low H3K9me2 levels. Analyses in JMJD1C knockout mice also establish a JMJD1C requirement for AML1-ETOâs ability to increase proliferation. We also show a critical role for JMJD1C in the survival of multiple human AML cell lines, suggesting that it is required for leukemic programs in different AML cell types through its association with key transcription factors. Examination of RNA expression when Kasumi-1 cells are treated with control shRNA or two different JMJD1C shRNAs; in duplicate. Please note that the 'shAML1_ETO_vs_shControl.all_gene_exp.tb.txtl' was generated comparing control and shRNA treated RNA abundance-using previously published data [GSE43834; GSM1071857 and GSM1071852].

2015-11-02 | E-GEOD-63485 | 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