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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Asha Nair

PROVIDER: E-GEOD-73751 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

2016-01-05 | GSE73751 | GEO

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

Gene expression profiles of uhrf1 mutant zebrafish

2015-02-09 | GSE55339 | GEO

PHD finger recognition of unmodified histone H3R2 links UHRF1 to regulation of euchromatic gene expression

Project description:Histone methylation occurs on both lysine and arginine residues and its dynamic regulation plays a critical role in chromatin biology. Here we identify the UHRF1 PHD domain (PHDUHRF1), an important regulator of DNA CpG methylation, as an unanticipated histone H3 unmodified arginine 2 (H3R2)-recognition modality. This conclusion is based on binding studies and co-crystal structures of the PHDUHRF1 bound to histone H3 peptides, where the guanidinium group of unmodified R2 forms an extensive intermolecular hydrogen bond network, with methylation of H3R2, but not H3K4 or H3K9, disrupting complex formation. We have identified direct target genes of UHRF1 from microarray and ChIP studies. Importantly, we show that UHRF1’s ability to repress its direct target gene expression is dependent on PHDUHRF1 binding to unmodified H3R2, thereby demonstrating the functional importance of this recognition event and supporting the potential for crosstalk between histone arginine methylation and UHRF1 function. UHRF1 protein was depleted in HCT116 cells by shRNA treatment. Total RNA was purified and used to determine the global gene transcription profiles by microarray assays. The UHRF1-regulated genes were identified by comparing the gene expression profiles of control and UHRF1-depleted HCT116 cells.

2011-07-07 | E-GEOD-30478 | biostudies-arrayexpress

Epigenome analyses of HCT116 cells stably expressing UHRF1 mutant [Illumina EPIC]

Project description:Epigenome analyses of HCT116 cells stably expressing UHRF1 mutant [Illumina EPIC]

| PRJNA637514 | ENA

Epigenome analyses of HCT116 cells stably expressing UHRF1 mutant [Illumina EPIC]

Project description:UHRF1 is a key regulator of DNA methylation maintenance. In this study, we investigated whether acetylation of UHRF1 affects its hemimethylated DNA binding affinity and alters genome-wide DNA methylation pattern. We show that cells with mutation in K490 of UHRF1 have distinct methylation profile versus wildtype UHRF1 expressing cells.

2020-06-06 | GSE151862 | GEO

Tumor-promoting functions of UHRF1 in retinoblastoma

Project description:UHRF1 (ubiquitin-like with PHD and ring finger domains 1) is an epigenetic regulator that is involved in the regulation of DNA and histone methylation and many other cellular events. The UHRF1 is frequently found to be overexpressed in various human cancers including retinoblastoma, and its overexpression has been associated with tumor-promoting effects such as inhibition of apoptosis and high metastatic potential. However, the detailed mechanisms underlying these tumor-promoting functions of UHRF1 in retinoblastoma still remain unclear. In this study, we uncovered that UHRF1 depletion in retinoblastoma cells sensitizes the cells to histone deacetylase (HDAC) inhibitors, augmenting apoptotic cell death. To understand the molecular mechanisms underlying the enhanced sensitivity to HDAC inhibitors in the UHRF1-depleted retinoblastoma cells, we performed the gene expression profiling in UHRF1-knockdown Y79 cells in comparison with control-knockdown cells by RNA-sequencing to identify differentially expressed genes. Our RNA-seq results revealed that UHRF1 depletion downregulates redox-responsive genes such as GSTA4 and TXN2, leading to increased intracellular oxidative stress and higher susceptibility to HDAC inhibitor treatment.

2020-02-10 | GSE135424 | GEO

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: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.

2020-05-04 | GSE136609 | 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

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