Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression of in vitro cultivated preB cells before and after 8, 16 and 24 hours induction of miR-221

ABSTRACT: PreB cells were analyzed for differences in gene expression before and after the overexpression of miR-221. In order to dissect possible targets for the miR-221, gene expression profiles of preB cells un-induced or induced for the miR-221 expression after 8, 16 and 24 hours were compared. All induction time-points, e.g. after 8, 16 and 24 hours were compared to un-induced preB cells and to each other group.

ORGANISM(S): Mus musculus

PROVIDER: GSE47643 | GEO | 2013/06/05

SECONDARY ACCESSION(S): PRJNA207006

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Gene expression of in vitro cultivated preB cells before and after 8, 16 and 24 hours induction of miR-221

Project description:PreB cells were analyzed for differences in gene expression before and after the overexpression of miR-221. In order to dissect possible targets for the miR-221, gene expression profiles of preB cells un-induced or induced for the miR-221 expression after 8, 16 and 24 hours were compared. All induction time-points, e.g. after 8, 16 and 24 hours were compared to un-induced preB cells and to each other group. Gene expression profiles of un-induced preB cells, preB cells induced for miR-221 expression after 8, 16, and 24 hours were analyzed using Affymetrix MG 430 2.0 whole genome arrays. Each time-point was performed in triplicates for un-induced preB cells and preB cells induced for miR-221 expression after 8, 16, and 24 hours (12 arrays in total). To obtain genes significantly downregulated upon induction of miR-221, the expression profiles of un-induced preB cells were compared to preB cells activated for 8, 16, or 24 h and were also compared to each other. After total RNA extraction, reverse transcription, cDNA extraction, the biotinylated cRNA was transcribed, fragmented, and 15 M-BM-5g cRNA hybridized in triplicates for each of the four groups to the 12 GeneChip arrays: Group1, un-induced preB cells, Group2, preB cells induced for miR-221 expression after 8h, Group3, preB cells induced for miR-221 expression after 16h, Group4, preB cells induced for miR-221 expression after 24h.

2013-06-05 | E-GEOD-47643 | biostudies-arrayexpress

Klebsiella pneumoniae strain:221-24 | isolate:221-24

Project description:Klebsiella pneumoniae strain:221-24 | isolate:221-24 Genome sequencing

| PRJNA1182958 | ENA

Mus musculus

Project description:Gene expression of in vitro cultivated preB cells before and after 8, 16 and 24 hours induction of miR-221

| PRJNA207006 | ENA

MicroRNA expression profiling of NGF-treated PC12 cells revealed a critical role for miR-221 in neuronal differentiation

Project description:MicroRNAs (miRNAs) are small non-coding RNAs that control protein expression through translational inhibition or mRNA degradation. MiRNAs have been implicated in diverse biological processes such as development, proliferation, apoptosis and differentiation. Upon treatment with nerve growth factor (NGF), rat pheochromocytoma PC12 cells elicit neurite outgrowth and differentiae into neuron-like cells. NGF plays a critical role not only in neuronal differentiation but also in protection against apoptosis. In an attempt to identify NGF-regulated miRNAs in PC12 cells, we performed miRNAM-cM-^@M-^@microarray analysis using total RNAs harvested from cells treated with NGF. In response to NGF treatment, expression of 8 and 12 miRNAs were up- and down-regulated, respectively. Quantitative RT-PCR analysis confirmed increased expression of miR-221, miR-181a* and miR-326, and decreased expression of miR-143, miR-210 and miR-532-3p after NGF treatment, among which miR-221 was drastically up-regulated. Overexpression of miR-221 induced neurite outgrowth of PC12 cells in the absence of NGF treatment, and also enhanced neurite outgrowth caused by low-dose NGF. More importantly, knockdown of miR-221 by antagomir attenuated NGF-mediated neurite outgrowth. Finally, miR-221 decreased expression of Foxo3a and Apaf-1, both of which are involved in apoptosis in PC12 cells. Our results indicate that miR-221 plays a critical role for neuronal differentiation as well as protection against apoptosis in PC12 cells. NGF induced miRNAs expression in rat pheochromocytoma PC12 cells was measured in cells treated with 100 ng/ml NGF for 0, 12, 24 and 48 hr.

2012-05-15 | E-GEOD-32122 | biostudies-arrayexpress

Liver cancer progression through increased miR-221 mediated tumorigenesis

Project description:Hepatocellular carcinoma (HCC) is the third leading malignancy worldwide. MiR-221 have oncogenic functions and play a seminal role in carcinogenesis regulation including in high risk- human HCC. However, the molecular mechanism and biological functions of miR-221 has not been investigated thoroughly in HCC. In the present work, the role of miR-221 in HCC was evaluated using microarray and miR-221target genes expressions were analyzed in miR-221 inhibitor transfected HCC cell lines HepG2, Huh-7, WRL-68. Finally, we found that 89 upregulated and 52 downregulated genes by miR-221 in HCC cell lines.l

2020-08-01 | GSE135375 | GEO

Gene expression profiling of MCF10A (miR-221/222 vs control)

Project description:Analysis of gene expression of MCF10A to identify the targets of miR-221 and miR-222 Keywords: MCF10, miR-221, miR-222

2011-06-14 | GSE29327 | GEO

miR-221 is required for endothelial tip cell behaviors during vascular development

Project description:Through deep sequencing and functional screening in zebrafish, we find that miR-221 is essential for angiogenesis. miR-221 knockdown phenocopied defects associated with loss of the tip cell-expressed Flt4 receptor. Furthermore, miR-221 was required for tip cell proliferation and migration, as well as tip cell potential in mosaic blood vessels. miR-221 knockdown also prevented “hyper-angiogenesis” defects associated with Notch deficiency and miR-221 expression was inhibited by Notch signaling. Finally, miR-221 promoted tip cell behavior through repression of two targets: cyclin-dependent kinase inhibitor 1b (cdkn1b) and phosphoinositide-3-kinase regulatory subunit 1 (pik3r1). These results identify miR-221 as an important regulatory node through which tip cell migration and proliferation are controlled during angiogenesis.

2012-02-28 | GSE35078 | GEO

miR-221 is required for endothelial tip cell behaviors during vascular development

2012-02-28 | E-GEOD-35078 | biostudies-arrayexpress

Gene expression profiling of MCF10A (miR-221/222 vs control)

Project description:Analysis of gene expression of MCF10A to identify the targets of miR-221 and miR-222 Keywords: MCF10, miR-221, miR-222 RNA profiles of human MCF10A cell line

2011-06-14 | E-GEOD-29327 | biostudies-arrayexpress

C/EBPb cooperates with BLNK mutation in preB leukemogenesis (BLNK2)

Project description:BLNK (BASH/SLP-65) encodes an adaptor protein within the B-cell receptor signaling. Loss-of-function mutations of BLNK are observed in human preB-ALL, and a subset of Blnk knock-out mice develop preB-ALL. To understand the molecular mechanism of preB-ALL development associated with the Blnk mutation, retroviral tagging was applied on Blnk KO mice using Moloney murine leukemia virus (MoMLV). The Blnk mutation significantly accelerated the disease onset of MoMLV-induced leukemia and increased the incidence of preB-ALL. Cebpb was identified as the most frequent common retroviral integration site, suggesting that Cebpb upregulation cooperates with Blnk mutation. Transgenic expression of the LAP (liver-enriched activator protein) isoform of C/EBP-beta significantly accelerated preB-ALL development of Blnk ko mice. We used microarrays to detail the global program of gene expression in mouse preB-ALL

2021-10-27 | GSE110738 | GEO

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