Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptome analysis to UHRF1 depletion in MUTU I cells

ABSTRACT: RNAseq was used to identify host and viral transcriptome changes in UHRF1 knock-out MUTU I cells. UHRF1 KO MUTU I cells were subjected to FACSort for ICAM1+/GP350- and ICAM1-/GP350+ subpopulations, which were further used for RNAseq analysis. The MUTU I cells expressing control sgRNA was used as the control.

ORGANISM(S): Homo sapiens

PROVIDER: GSE136609 | GEO | 2020/05/04

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcriptome analysis to UHRF1 depletion in RaeL cells

Project description:RNAseq was used to identify host and viral transcriptome changes in UHRF1 knock-out RaeL cells. UHRF1 KO RaeL cells were subjected to FACSort for ICAM1+ subpopulations, which were further used for RNAseq analysis. The RaeL cells expressing control sgRNA was used as the control.

2020-05-04 | GSE136596 | GEO

Transcriptome analysis to UHRF1 depletion in MUTU I cells

Project description:Transcriptome analysis to UHRF1 depletion in MUTU I cells

| PRJNA562857 | ENA

Overexpression of UHRF1 drives DNA hypomethylation and hepatocellular carcinoma

Project description:UHRF1 is an essential regulator of DNA methylation that is highly expressed in many cancers. Using transgenic zebrafish, cultured cells and human tumors, we demonstrate that UHRF1 is an oncogene. RNAseq was used to assess the variation in gene expression between control and experimental samples. Total small RNA from 2 batches of Tg(fabp10:has.UHRF1-GFP)High and age matched Tg(fabp10:nls-mCherry) control 5 dpf zebrafish livers was purified for preparation of high-throughput sequencing libraries.

2013-11-22 | E-GEOD-52605 | biostudies-arrayexpress

Overexpression of UHRF1 drives DNA hypomethylation and hepatocellular carcinoma

2013-11-22 | GSE52605 | GEO

UHRF1 is a mediator of KRAS driven oncogenesis in lung adenocarcinoma [CRISPR_screen]

Project description:We performed a focused CRISPR in KRAS mutant lung cancer cells (A549) using a minipool sgRNA library targeting 80 lung cancer specific tumor suppressor genes and 12 control genes. This screen identified tumor suppressor genes regulated by Uhrf1 in KRAS mutant lung cancer.

2023-05-25 | GSE233401 | GEO

Expression data from HeLa cell lines stably expressing shRNA targeting ctrl or UHRF1

Project description:We used microarrays to explore the expression profile from cells expressing wild type and UHRF1 S674A mutant. HeLa cells expressing UHRF1 WT and S674A mutant showed similar gene expression pattern without significant affecting the transcription of DNA repari genes. UHRF1 was depleted in HeLa cells by shRNA treatment. Total RNA was purified and used to determine the global gene transcription profiles by microarray assays. The UHRF1-related genes expression profiles were compared among control cells, UHRF1-depleted cells, UHRF1 WT reconstituting cells and UHRF1 S674A mutant reconstituting cells.

2016-01-05 | E-GEOD-73751 | biostudies-arrayexpress

Transcriptome analysis of CHAF1B depletion in Akata EBV+ Burkitt Lymphoma cells

Project description:RNAseq was used to identify host and EBV viral transcriptome changes in CHAF1B knock-out Akata EBV+ cells. CHAF1B KO Akata EBV+ cells were subjected to RNAseq analysis. The Akata EBV+ cells expressing control sgRNA was used as the control.

2020-10-15 | GSE148910 | GEO

Transcriptome analysis of MUTU I and MUTU III cells

Project description:RNAseq was used to identify host and viral transcriptome changes in MUTU I and MUTU III cells.

2020-05-04 | GSE136597 | GEO

RNA sequencing of WT and Uhrf1 KO iNKT cells

Project description:Deletion of Uhrf1 resulted in stage 1-specific defects during iNKT cell development. To investigate the molecular mechanism, we sorted WT and Uhrf1-KO stage 1 iNKT cells and performed RNA-seq. By comparing gene expression profile, we found metabolic defects in Uhrf1-KO stage 1 iNKT cells. The expression of CD71 (Tfrc), two subunits of CD98 (Slc3a2 and Slc7a5) and Glut3 (Slc2a3) was reduced in stage 1 iNKT cells. Besides, the downstream pathways of AKT-mTOR axis were significantly reduced. Collectively, our results suggest that Uhrf1 is required for iNKT cell development by regulating the Akt-mTOR signaling pathway. We first sorted WT and Uhrf1-KO stage 1 iNKT cells, extracted the mRNA and performed RNA-seq. We then analyzed the differentially expressed genes and performed KEGG pathway analysis. We used RT-PCR to verify the expression of the key nutrient related genes (Tfrc, Slc3a2, Slc7a5 and Slc2a3) and used flow cytometry to test the protein level of metabolic related molecules. Besides, we also analyzed the expression of genes of mTOR downstream pathways to demonstrate that Uhrf1 mediated AKt-mTOR axis regulates iNKT cell development.

2016-03-10 | E-GEOD-77941 | biostudies-arrayexpress

Gene expression profiles of uhrf1 mutant zebrafish

Project description:UHRF1 (Ubiquitin-like, containing PHD and RING finger domains, 1) recruits DNMT1 to hemimethylated DNA during replication, is essential for maintaining DNA methylation patterns during cell division and is suggested to direct additional repressive epigenetic marks. Uhrf1 mutation in zebrafish results in multiple embryonic defects including failed hepatic outgrowth, but the epigenetic basis of these phenotypes is not known. We find that DNA methylation is the only epigenetic mark that is depleted in uhrf1 mutants and make the surprising finding that despite the reduced organ size in uhrf1 mutants, genes regulating DNA replication and S-phase progression were highly upregulated. Further, there is a striking increase in BrdU incorporation in uhrf1 mutant cells, and they retained BrdU labeling over several days, indicating they are arrested in S-phase. Moreover, some of the label retaining nuclei co-localized with TUNEL positive nuclei, suggesting that arrested cells are responsible for apoptosis. Importantly, dnmt1 mutation phenocopies the S-phase arrest and hepatic outgrowth defects in uhrf1 mutants and Dnmt1 knock-down enhances the uhrf1 hepatic phenotype. Together, these data indicate that DNA hypomethylation is sufficient to generate the uhrf1 mutant phenotype by promoting an S-phase arrest. We thus propose that cell cycle arrest is a mechanism to restrict propagation of epigenetically deranged cells during embryogenesis. Genome-wide expression profiling was performed on 2 uhrf1 mutant and 2 wildtype zebrafish larvae (120 hours post fertilization) by using Zebrafish Genome Array (Affymetrix) according to manufacturer's instruction.

2015-02-09 | E-GEOD-55339 | 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