Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

33 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The effect of miR-294 and miR-181 on the transcriptome during OSK reprogramming of MEFs

ABSTRACT: Study designed to determine the immediate effects of supplementing OSK reprogramming with miR-294 or miR-181. MEFs were infected on day 0, and transfected with miR-294, miR-181 or control mimic on day 1. On day 3 RNA was extracted. OSK infected MEFs samples were compared to non-infected MEFs and to fully reprogrammed iPSCs. Performed in biological triplicate, with each sample containing different OSK viral stocks, different preparations of MEFs and independent transfections. Biological triplicate iPSCs represent three independent and clonally expanded iPSC lines. Total RNA collected with Trizol. All processing conducted at the UCLA Neuroscience Genomics Core. MouseRef-8 v2.0 Expression BeadChips.

ORGANISM(S): Mus musculus

SUBMITTER: Robert Blelloch

PROVIDER: E-GEOD-49556 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Similar Datasets

The effect of miR-294 and miR-181 on the transcriptome during OSK reprogramming of MEFs

Project description:Study designed to determine the immediate effects of supplementing OSK reprogramming with miR-294 or miR-181. MEFs were infected on day 0, and transfected with miR-294, miR-181 or control mimic on day 1. On day 3 RNA was extracted. OSK infected MEFs samples were compared to non-infected MEFs and to fully reprogrammed iPSCs.

2013-09-15 | GSE49556 | GEO

Expression analysis of OSK and Sall4+OSK reprogramming cells sorted for expression of miR-290 and/or miR-302.

2014-03-31 | GSE54341 | GEO

Expression analysis of OSK and Sall4+OSK reprogramming cells sorted for expression of miR-290 and/or miR-302.

Project description:MEFs were infected with Oct4, Sox2, Klf4 (+/- Sall4), sorted for miR-290/302 reporter expression at day 9 (OSK) or 12 (Sall4+OSK), and then profiled. Resulting iPSCs were also profiled. Mouse ES cells were differentiated and sorted for miR-290/302 reporter expression during Fgf/Activin differentiation (day 4 or day 7). Performed in biological triplicate. Biological triplicate samples represent three independent lines. Total RNA collected with Trizol. All processing conducted at the UCLA Neuroscience Genomics Core. MouseRef-8 v2.0 Expression BeadChips.

2014-03-31 | E-GEOD-54341 | biostudies-arrayexpress

Mus musculus

Project description:The effect of miR-294 and miR-181 on the transcriptome during OSK reprogramming of MEFs

| PRJNA214243 | ENA

miR-181 regulates colonic inflammation

Project description:The intestinal epithelium is a key physical interface that integrates dietary and microbial signals to regulate nutrient uptake and mucosal homeostasis. Intestinal epithelial cells (IECs) have a high turnover rate driven by the death of terminally differentiated cells with concurrent stem cell proliferation, a process critical for maintaining intestinal homeostasis and protecting against mucosal inflammation. The transcriptional programs that regulate IEC quiescence, proliferation, and differentiation have been well-characterized. However, how gene expression networks critical for IEC functions are regulated at the post-transcriptional level during homeostasis or inflammatory disease remains poorly understood. Herein, we show that a conserved family of microRNAs, miR-181, is significantly downregulated in IECs from patients with inflammatory bowel disease and mice with chemical-induced colitis. Strikingly, we showed that miR-181 expression within IECs, but not the hematopoietic system, is required for protection against the development of severe colonic inflammation in response to epithelial injury in mice. Mechanistically, we showed that miR-181 expression increases the proliferative capacity of IECs, likely through the regulation of Wnt signaling, independently of gut microbiota composition. As epithelial reconstitution is crucial for restoring intestinal homeostasis after injury, the miR-181 family represents a potential novel therapeutic target in IECs for protection against severe intestinal inflammation.

2022-07-25 | GSE208410 | GEO

miR-181 regulates colonic inflammation

Project description:miR-181 regulates colonic inflammation

| PRJNA859816 | ENA

Analysis of HeLa cells after transfection with miR-1, miR-124 and miR-181.

Project description:Analysis of HeLa cells at 24 hours after transfection with wild type miR-1, miR-124, miR-181 versus control transfected HeLa cells. Results were compared to protein down-regulation at 48 hours measured by SILAC-MS. Analysis of HeLa cells at 24 hours after transfection with wild type miR-1, miR-124, miR-181 versus control transfected HeLa cells. Results were compared to protein down-regulation at 48 hours measured by SILAC-MS.

2010-05-25 | E-GEOD-11968 | biostudies-arrayexpress

Analysis of HeLa cells after transfection with miR-1, miR-124 and miR-181.

2008-07-31 | GSE11968 | GEO

Transcription profiling by array of Jurkat cells following miR-181 over-expression

Project description:miR-181 is often dysregulated in several types of cancer. This dataset can represent a further insight into gene expression changes and GO Terms associated with miR-181 over-expression. miR-181 was over-expressed in Jurkat cells by transduction with a lentiviral transgenic construct encoding for miR-181 under a PGK promoter. A cognate vector encoding for a control hairpin was used to generate control cell line. mRNA Microarray gene expression profiling of Jurkat cells tranduced with either a miR-181 sponge or control construct. 3 biological replicas have been performed. Note that the control samples are the same as those used in the related experiment E-MTAB-4588

2016-03-24 | E-MTAB-4602 | biostudies-arrayexpress

Global Transcriptional Analysis of Nuclear Reprogramming in the Transition from MEFs to iPSCs

Project description:Here, we focused on the intermediate stages of SCR by comparing the somatic cell line induced by OCT4, SOX2, and KLF4 (OSK) for 7 days with mouse embryonic fibroblasts (MEFs), iPSCs, and embryonic stem cells (ESCs). Transcriptional profiles of these four cell lines were analyzed by microarray, and we found that the transition process from day 7 to the formation of iPSCs is crucial for SCR and that the reverse expression patterns can provide more candidate markers to distinguish ESCs and somatic cells iPSC. Data confirmed that the viral infection results in defense innate immunity, DNA damage, and apoptosis in MEFs, which slows down cell proliferation and immortalization to inhibit SCR. Although SCR is initiated by OSK, the p53 signaling pathway can affect the transcriptional regulatory networks through cell cycle and genomic instability as a powerful core node. MEFs were derived from embryonic day 13.5 C57BL6 mice embryos. Cell line day7 is MEF induced by OCT4, SOX2, and KLF4 (OSK) for 7 days with mouse embryonic fibroblasts (MEFs), iPSCs, and embryonic stem cells (ESCs).

2012-10-01 | E-GEOD-37397 | 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