Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression profiling upon Knockdown of KDM5A and 5C in Gliobastoma stem-like cells

ABSTRACT: Investigating the changes of gene expression upon knockdown of KDM5A/5C and the mechanisms underlying the observed apoptotic phenotype.

ORGANISM(S): Homo sapiens

PROVIDER: GSE117962 | GEO | 2021/06/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression profiling upon Knockdown of KDM5A and 5C in Gliobastoma stem-like cells

Project description:Gene expression profiling upon Knockdown of KDM5A and 5C in Gliobastoma stem-like cells

| PRJNA483796 | ENA

Expression profiling of human medulloblastoma cell line ONS76 upon siRNA-mediated knockdown of KDM5A/LSD1

Project description:KDM5A/LSD1 is an important epigenetic regulator in medulloblastoma, the most frequent brain tumor of childhood. Here, the response of ONS76 medulloblastoma cells upon siRNA-mediated knockdown of KDM5A is analysed. The expression profile of ONS76 cells upon KDM5A knockdown was compared to mock control. Both conditions were run in triplicate.

2013-08-01 | E-GEOD-43552 | biostudies-arrayexpress

Expression profiling of human medulloblastoma cell line ONS76 upon siRNA-mediated knockdown of KDM5A/LSD1

2013-08-01 | GSE43552 | GEO

SK-NEP-1 treated with SKI-5C

Project description:Wilm’s tumor(WT) is the most common malignant renal tumor in children, representing approximately 6-14% of all childhood cancers and about 95% of all pediatric renal malignancies. SKI-5C is a newly developed Sphk1 inhibitor. This small molecular inhibitor was firstly reported at 2009 by Wang et al. This study investigated the antitumor activity of SKI-5C in SK-NEP-1 cells. SKI-5C inhibited cell proliferation of SK-NEP-1 cells in a dose-dependent manner. Annexin V, Tunel and Hochest 33342 staining analysis showed that SKI-5C-treated cells showed more apoptotic features compared with the control.

2016-12-31 | GSE72980 | GEO

Gene expression profiles of KDM5A-/- MEFs with wild-type KDM5A or KDM5A-H483A mutant

Project description:Gene expression profiles of Immortalized KDM5A-/- MEFs with re-introduction of wild-type KDM5A or KDM5A-H483A mutant.

2017-02-08 | GSE84309 | GEO

Genome-wide maps of KDM5A/JARID1A/RBP2 in mouse ES cells.

Project description:We report the identification of genomic regions bound by KDM5A in mouse embryonic stem (ES) cells and define the functional categories that these regions represent. KDM5A modifies methylated lysine residues on histone tails. We developed anti-KDM5A antibodies and set to detect genomic regions enriched with these antibodies using cells with normal Kdm5a or cells from Kdm5a knockout mice as a control. We found high enrichment with the KDM5A antibodies in normal cells when compared with the genomic background. We found striking identity in the regions enriched with these antibodies in normal cells when compared with the total genomic DNA or with KDM5A ChIP assays from Kdm5a KO cells, showing that the antibodies are specific. Examination of target genes in ES cells

2012-10-04 | E-GEOD-28343 | biostudies-arrayexpress

Profiling non-small cell lung carcinoma cell line PC9 treated with erlotinib, KDM5A inhibitor, or viruses expressing KDM5 shRNAs or cDNA

Project description:The non-small cell lung carcinoma (NSCLC) PC9 cell line is an established preclinical model for tyrosine kinase inhibitors. Recent evidence suggests that KDM5A protein is required for emerging drug-resistant cell population. To better understand the dependence of cell survival on KDM5A, we treated EGFR-mutant PC9 cells with erlotinib, KDM5A inhibitor or KDM5A and KDM5B shRNAs and performed Drop-seq. We were able to clearly distinguish cells with KDM5A knockdown from cells with KDM5A overexpression. We were able to identify specific biomarkers associated with varying dose of KDM5A, for each cell population. The results of this study will address clinical usefulness of KDM5A-targeted strategies in overcoming drug resistance, particularly in NSCLC.

2022-07-25 | GSE134840 | GEO

ChIP-seq analyses for KDM5A, H3K4me3, RNAPII and TAF3 in human multiple myeloma cell line MM.1S

Project description:Recent studies have highlighted the oncogenic roles of KDM5A; however, its molecular mechanism has not been fully delineated. Here we identifies KDM5A as a transcriptional activator of MYC target genes in multiple myeloma (MM). Genetic ablation of KDM5A or pharmacologic inhibition of KDM5 by novel inhibitor JQKD82 impairs MM cell growth. Gene expression profile reveals that JQKD82 decreases expression of MYC targets. Expression of MYC targets is similarly downregulated by KDM5A depletion, but little affected by KDM5B knockdown. Mechanistically, KDM5A co-localizes with MYC across the genome, and KDM5A and MYC coordinately promote MYC target gene transcription. The treatment with JQKD82 reduces phosphorylation level of RNA polymerase II (RNAPII), resulting in RNAPII pausing, accompanied by hyper-H3K4me3 status at the MYC loci. Finally, we shows that JQKD82 exerts anti-MM activity and prolongs overall survival in vivo mouse xenograft models. Our results delineate KDM5A function that reinforces MYC transcriptional program, and identify KDM5A as a potential therapeutic target in MM.

2021-03-22 | GSE148046 | GEO

Function of 5C medium in somatic cell reprogramming

Project description:We induced reprogramming by mES and 5C medium, and collected mRNA profiles of the GFP+ and GFP- reprogramming cells sorted by FACS. We found that 5C iPSCs showed differences with mES iPSCs, with different influences on GFP+ and GFP- cells on MET. And we picked the 5C iPSCs single colony, cultured with naive and primed medium. We showed that 5C iPSCs could be converted to naive and primed state respectively.

2019-04-14 | GSE103765 | GEO

Genome-wide KDM5A occupancy after MK2206/DMSO treatment of T47D cells

Project description:We perfomed ChIP-seq using KDM5A antibodies in T47D cells after 24 hour treatment with the AKT inhibitor MK2206 or DMSO. We show that the cistrome of the H3K4 demethylase KDM5A is affected by AKT inhibition. Comparison of genome-wide KDM5A binding after AKT inhibition vs vehicle

2016-06-14 | E-GEOD-80593 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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