Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

KDM4A depletion by siRNA in HEK293T cells

ABSTRACT: The goal of this study was to determine genes affected by depletion of KDM4A in HEK293T cells This data was used in Van Rechem et. al. Cancer Discovery 2014 to demonstrate that depletion of KDM4A did not alter expression of genese associated with translation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE63812 | GEO | 2015/03/31

SECONDARY ACCESSION(S): PRJNA269139

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

KDM4A depletion by siRNA in HEK293T cells

Project description:The goal of this study was to determine genes affected by depletion of KDM4A in HEK293T cells This data was used in Van Rechem et. al. Cancer Discovery 2014 to demonstrate that depletion of KDM4A did not alter expression of genese associated with translation. The experiment uses two different shRNA constructs; shKDM4A.2 in a pSuper backbone and shKDM4A.6 in a pLKO backbone. A corresponding empty vector control was conducted for each backbone. Each shRNA was compared to its own control.

2015-03-31 | E-GEOD-63812 | biostudies-arrayexpress

JMJD2A ChIP-chip from HEK293T cells

Project description:JMJD2A was chromatin immunoprecipitated from HEK293T cells overexpressing GFP-JMJD2A. From Van Rechem et al. 2011 JBC

2013-08-01 | GSE48765 | GEO

JMJD2A ChIP-chip from HEK293T cells

Project description:JMJD2A was chromatin immunoprecipitated from HEK293T cells overexpressing GFP-JMJD2A. From Van Rechem et al. 2011 JBC Determination of JMJD2A binding sites by MA2C analysis

2013-08-01 | E-GEOD-48765 | biostudies-arrayexpress

RNA-seq of KDM4A, B and C siRNA knockdown in NB cells

Project description:RNA-seq of KDM4A, B and C siRNA knockdown in NB cells

2024-03-04 | GSE207013 | GEO

Efficient Elimination of Acute Myeloid Leukaemia Cells through Inhibition of KDM4A

Project description:We previously identified an essential role for the H3K9me3 histone demethylase, KDM4A, in maintaining AML cell survival, with genetic depletion by shRNA of KDM4A inducing leukaemic cell death with little effect on normal haematopoiesis. We hypothesised KDM4A inhibition may represent a novel and effective strategy to treat AML. To address this, we provided proof-of-principle for the use of KDM4 inhibitors (KDM4Ai) and fully characterised their functional potential in AML cells and identified the epigenetic mechanisms underpinning the essential role of KDM4A activity in THP-1 cells using both ChIP-seq and RNA-seq, delineating and functionally validating the epigenomic network regulated by KDM4A, showing that selective loss of KDM4A is sufficient to induce apoptosis in a broad spectrum of human AML cells. This detrimental phenotype results from a global accumulation of H3K9me3 and H3K27me3 at KDM4A targeted genomic loci thereby causing down-regulation of a KDM4A-PAF1 controlled transcriptional program essential for leukemogenesis, distinct from that of KDM4C.

2022-12-31 | GSE173995 | GEO

Homo sapiens

Project description:KDM4A depletion by siRNA in HEK293T cells

| PRJNA269139 | ENA

Effect of depletion of alt-LAMA3 on gene expression of HEK293T cells

Project description:To investigate the depletion of altLAMA3, we established HEK293T cell lines in which alt-LAMA3 gene has been knocked out by CRISPR-Cas9. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells

2022-06-17 | GSE205869 | GEO

Riboflavin depletion regulates cell proliferation and cell cycle progression‑associated genes in HEK293T cells

Project description:Transcriptome analysis of RNA samples from riboflavin-depleted HEK293T cells. Riboflavin is an essential component of the human diet and its derivative cofactors have an established role in oxidative metabolism. Riboflavin deficiency has been linked with various human diseases. In this study, we have modelled riboflavin deficiency in HEK293T cell line, shown remarkable increase of cell proliferation. The aim of the present study is to develop a cell culture model of riboflavin depletion and analyze its molecular mechanism of acceleration cell proliferation. So, we used Affymetrix Human Transcriptome Array 2.0 to identify genes that were differentially expressed upon riboflavin-depleted HEK293T cells.

2017-05-16 | GSE98927 | GEO

KDM4A regulated genes in human squamous carcinoma cells

Project description:To establish a robust cellular model system for screening genes associated with cell invasion, we over-expressed the oncogenic translocated promoter region (Tpr)-MET proteins in SCC23 cells (SCC23/MET). Using a functional siRNA screen, we identified that the histone demethylase KDM4A played a critical role in the invasive growth and metastasis of SCC mediated by the Oncogenic MET. To investigate the molecular mechanism through which KDM4A inhibit the tumor cell invasion, we knock-down KDM4A in SCC23/MET cell and performed a gene microarray to examine which genes may be regulaged by kDM4A. We generated two stable cell lines. one was infected with virus containing scramble and another infected with virus infected with virus containing KDM4A shRNA. Total RNA were extracted from these two cell lines and subject to microarray.

2013-05-03 | E-GEOD-44238 | biostudies-arrayexpress

KDM4A regulated gene expression in human prostate cancer LNCaP cell

Project description:Histone lysine demethylase KDM4A is overexpressed in prostate cancer and plays a crucial role in tumor growth and survival. To understand the mechanisms underlying KDM4A-depedent cell growth and survival, microarray analysis was performed in LNCaP cells transduced with control or KDM4A specific-knockdown construct. The role of KDM4A in prostate carcinogenesis involves activation of E2F1 and androgen receptor transcriptional profiles. LNCaP cells were transduced by lentivirus carrying control pLKO.1 (empty vector) or shKDM4A construct (KDM4A-specific shRNA) for three days, followed by RNA extraction. Affymetrix GeneChip Human Genome U133 Plus 2.0 Arrays were used for microarray analysis.

2016-07-26 | E-GEOD-77928 | 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