Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA316816 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The chromatin immunoprecipitation coupled with high-throughput sequencing (ChIP-seq) was conducted in the human cancer cell lines H358 and AGS using FXR1, FXR2, STAT1/3 and H3K4me3 specific antibodies on the platform Illumina HiSeq 2000. ChIP-seq data quality was analyzed using FastQC. Target protein binding genomic regions (called ChIP-seq peaks) were identified by Model-based Analysis of ChIP-Seq (MACS) algorithm using the default p-value cutoff of 1e-5.
2017-09-01 | GSE79707 | GEO
Project description:Exploring the gene expression profile upon FXR1 knockdown in H358 cells using RNA-seq
| PRJNA395359 | ENA
Project description:We performed the RNA-seq in control samples and FXR1 knockdown samples, and compared the gene expression profiles to explore the effect of FXR1 knockdown on gene expression. The study was performed in H358 cells. Doxycycline inducible shRNA3 (sh3) was used to knockdown FXR1. Control shRNA (ctrl) samples were used to get rid of the effect of Doxycycline treatment. Both the Doxycycline treament for 3 days (D3) and 5 days (D5) samples were collected. Each sample has three repeats (rep 1, rep 2, and rep 3). The mRNA profiles were generated by deep sequencing using Illumina.Sequenced reads were trimmed for adaptor sequence, then mapped to hg19 whole genome using STAR v2.5.3 with parameters --bamRemoveDuplicatesType UniqueIdentical --outSAMmultNmax 1. Raw reads and Reads Per Kilobase per Megabase of library size (RPKM) were calculated using HOMER (PMID: 20513432). Differential gene expression was analyzed using R package DESeq2 using the raw reads.
2017-10-04 | GSE101754 | GEO
Project description:To identify SET1A genome-wide occupancy and further unveil its role in transcriptional regulation in mouse ES cells, we carried out chromatin immunoprecipitation followed by high sequencing (ChIP-seq).We established a stable ES cell line expressing 2X Flag tagged SET1A and performed ChIP with anti-Flag M2 beads, followed by deep sequencing. We found that the SET1A peaks show an outstanding enrichment in promoter region. Importantly, these SET1A binding loci revealed a clear co-localization with OCT4, and high H3K4me3 level, which is consistent with its interaction with OCT4 and intrinsic H3K4 methylase activity.
2016-01-20 | GSE66067 | GEO
Project description:AGS cell line and AGS-EBV cell line Genome sequencing
| PRJNA191915 | ENA
Project description:The RBP, FXR1, is overexpressed in many epithelial tumors containing a canonical RGG box domain. FXR1 controls post-transcriptional gene regulation through changes in mRNA turnover and translation of target genes. Here we show that arginine methyltransferase PRMT5- mediated specific arginine methylation of FXR1 increases its stability in cancer cells. FXR1-dependent gene signatures show decreased expression and instability of G4-rich sequences containing mRNAs such as CDKN1A, PLK2, TCN2, and TRAF4. Furthermore, structural features of FXR1 and G4-RNA interactions provide novel insights into the critical arginine amino acids of FXR1 essential for G4-RNA-binding and turnover activity. In addition, analysis of the eCLIP data provides various RNA targets and the G-rich sequence motifs of FXR1 in head and neck cancer cell line. Thus, our results indicate that PRMT5-mediated methylation of FXR1 binding with G4-RNAs favors mRNA stability and turnover, contributing to cancer cell growth and proliferation.
2024-04-08 | GSE252916 | GEO
Project description:FXR1 is an essential RNA-binding protein. This chromosome 3q26-28 gene is overexpressed in many epithelial tumors. FXR1 controls the turnover and translation of multiple mRNAs and is involved in cellular transformation. We identified critical residues in the protein that are post-translationally modified. These regulate the stability of FXR1 protein, its RNA-binding function, cell growth, and proliferation. Here we show that PRMT5-mediated arginine methylation of FXR1 increases the protein's binding to G-quadruplex RNAs in vivo and controls their expression in cancer cells. Independent point mutations of specific arginine residues in the nuclear export signal (R386, R388) and arginine-glycine rich (R453, R455, R459) domains of FXR1 abrogate the RNA-binding in vitro. Genetic and small molecule inhibition of PRMT5 minimizes methylation and levels of FXR1 and suppresses oral tumor growth and proliferation. RNA-seq analyses of FXR1 KD cells show an increase in the expression of PLK2, TCN2, and TRAF4 along with FXR1’s well-known target CDKN1A. Like CDKN1A, these targets possess strong G4 sequences. FXR1 and G4-RNA interactions provide new insights into the molecular mechanism of FXR1 and its interaction with target mRNAs. Furthermore, an increased expression of FXR1 and PRMT5 is colocalized in cancer tissues, leading to a poor patient prognosis. Thus, our data demonstrate that PRMT5-mediated arginine methylation of FXR1 arginine residues in the NES and RGG domains plays a critical role in binding and controlling G4-RNAs, which encode tumor suppressors and promote cancer cell growth and proliferation.
2023-09-30 | GSE212760 | GEO
Project description:AGS cell line and AGS-EBV cell line Transcriptome or Gene expression
| PRJNA192444 | ENA
Project description:Mapping STAT1 pS727 occupancy and effect of cortistatin A (CA) on STAT1 occupancy in JAK2-driven neoplasms
| PRJNA392122 | ENA
Project description:MicroRNAs predominantly decrease gene expression; however, specific mRNAs are translationally upregulated in quiescent (G0) mammalian cells and immature Xenopus laevis oocytes by an FXR1a-associated microRNP (microRNA-protein complex) that lacks the microRNP repressor, GW182. We conducted global proteomic analysis in THP1 cells depleted of FXR1 to globally identify activation targets of more than one microRNA, since FXR1 is required for microRNAmediated translation activation in THP1 G0 cells by FXR1-microRNPs.Since proteomic data changes could also be due to changes at the RNA level, total RNA levels in FXR1knockdown compared to control shRNA cells were examined in parallel by microarray analysis using Affymetrix Human GeneChip 2.0 ST. We used microarrays to get total RNA levels from FXR1 knockdown and control shRNA cells, to normalize the mass spectrometry data in order to provide normalized protein data or translation efficiency. FXR1 knockdown and shRNA control cells were induced with 1ug/ml of doxycycline continually to cause knockdown of FXR1; the cells were grown in serum for 3 days to induce the shRNAs, followed by 2 days of serum-starvation to induce G0. After harvesting, the cells were lysed in proteinase K buffer (Truesdell et al., 2012) and total RNA was isolated using Trizol (Invitrogen) and hybridized on Affymetrix Human GeneChip 2.0 ST microarray.
2016-02-03 | E-GEOD-77512 | biostudies-arrayexpress