Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA profiling of two endothelial cells (MPEC and AKT-HUVEC) and one human fibroblast line (BJ)

ABSTRACT: RNA profiling of two endothelial cells (MPEC and AKT-HUVEC) and one human fibroblast line (BJ)

PROVIDER: PRJNA269242 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

RNA profiling of two endothelial cells (MPEC and AKT-HUVEC) and one human fibroblast line (BJ)

Project description:Analysis of overall gene expression in endothelial cells, MPEC and AKT-HUVEC, comparing to a human fibroblast line, BJ. We are looking for the highly abundant genes in endothelial cells comparing to fibroblasts. Total RNA isolated from MPEC, AKT-HUVEC and BJ Fig 3b in publication.

2014-12-04 | E-GEOD-63843 | biostudies-arrayexpress

RNA profiling of two endothelial cells (MPEC and AKT-HUVEC) and one human fibroblast line (BJ)

2014-12-04 | GSE63843 | GEO

GRO-seq analysis of BJ cells

Project description:We used GRO-seq to examine RNA transcription rates in human fibroblast BJ cells.

2017-06-13 | GSE96717 | GEO

Expression data from transfected BJ fibroblast cell line

Project description:Skeletal muscle differentiation is a highly coordinated multistep process in which proliferating mononucleated myoblasts ?rst withdraw from the cell cycle, then differentiate into postmitotic mononucleated myocytes, and subsequently fuse into multinucleated myotubes which ?nally bundle to form mature muscle ?bers. All these processes are controlled by the sequential activation of myogenic regulatory factors, and especially MYOD1 is activated in the early phase to promote the transcription of muscle-specific genes coding for muscle proteins such as alpha-actin, myosin heavy chain and muscle creatine kinase. We used microarrays to detail the global gene expression changes associated with MYOD1 L122R mutation and identified MYOD1 L122R blocked myogenic differentiation and had a MYC-like transcriptional potential. wild type MYOD1, MYOD1 L122R, MYC, and GFP were introduced into BJ human fibroblast cells by retroviral infection. For retrovirus production, the pcx4 and pBabe vectors system were used. Retroviruses were obtained by using 293T cells as packaging cells, and were infected into BJ cell lines and selected with 500 ?g/ml Zeocin (Invitrogen, Carlsbad, CA, USA). After selection, RNAs were extracted and processed at MSKCC according to procedures recommended by Affymetrix (Santa Clara, CA, USA).

2014-05-01 | E-GEOD-56078 | biostudies-arrayexpress

Copy number variation between BJ cells and BJ-derived iPS cells

Project description:Copy number variation analysis between BJ cells and BJ cells derived iPS cells which were established by using non-transmissible measles virus vector

2016-06-22 | GSE79604 | GEO

Transcriptome-profiling (RNA-seq) and Ribosome-profiling (Ribo-seq) of BJ cells treated with Nutlin-3a, an MDM2 inhibitor, which induces p53.

Project description:We applied in parallel RNA-Seq and Ribosome-profiling analyses to immortalized human primary BJ fibroblast cells in which p53 was induced by Nutlin-3a

2013-06-01 | GSE45785 | GEO

Effect of CCAR2 depletion on the gene expression profile of BJ-hTERT cells

Project description:CCAR2 is a nuclear protein recently emerged as a pivotal player of the DNA damage response since it has been found involved in both apoptosis induction and DNA repair. Differently, its role in tumorigenesis and cancer progression is still elusive. In our studies we found that CCAR2 depletion impairs the proliferation of human cancer cell lines, but leaves unaffected the growth of normal immortalized cells. To better investigate this point we performed a genome wide gene expression analyses in U2OS and BJ-hTERT depleted of CCAR2 and we found that loss of this protein causes the deregulation of genes implicated in the AKT pathway specifically in U2OS cells, but not in BJ-hTERT. In accordance with these results we found a reduction in AKT activation in all the tested cancer cell lines depleted of CCAR2, but not in the normal ones. The defective activation of AKT is caused by the upregulation of TRB3 gene in cancer cells depleted of CCAR2 and finally results in the reduction of GSK3β phosphorylation, prevention of G1/S transition and inhibition of cancer cell growth.

2017-03-08 | GSE87362 | GEO

Bj Paraquat

Project description:This SuperSeries is composed of the following subset Series: GSE26236: Bj Paraquat fulminant shock vs. non-treatment GSE26252: Bj Paraquat prolonged exposure vs. non-treatment Refer to individual Series

2011-05-15 | E-GEOD-26531 | biostudies-arrayexpress

H3K9me3 ChIP-Seq in BJ-HELT cells

Project description:We generated H3K9me3 profile of reads and peaks of BJ fibroblasts expressing hTERT and SV40 early region (BJ-HELT cell line).

2018-08-04 | GSE102278 | GEO

LEOPARD Syndrome iPS, BJ iPS and Fibroblasts

Project description:Expression data from LEOPARD Syndrome-iPS clones, BJ-iPS cells and parental Fibroblasts 9 samples in total are analyzed. Among 22011 genes in expression data, there are 3657 genes with at least 2 fold expression change between the average of the three fibroblast lines versus all of the iPS lines/HES samples. A heatmap can be generated for the expression levels for the 3657 genes and 9 samples.

2010-06-24 | E-GEOD-20473 | 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