Effects of deletion of a portion of the Alu element from MIR205HG transcript
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE103655 | GEO | 2019/01/23
REPOSITORIES: GEO
Similar Datasets
Project description:Aside serving as host gene for the microRNA miR-205, MIR205HG transcribes for a nuclear chromatin-associated long noncoding RNA (lncRNA) able to restrain the differentiation of prostate basal cells, a finding that led to its reannotation as LEADR (Long Epithelial Alu-interacting Differentiation-related RNA). In our previous work (PMID: 30659180), we showed that genes that are modulated upon manipulation of MIR205HG/LEADR are characterized by the presence of an Alu sequence in their promoters. Notably, an Alu element also spans the first and second exon of MIR205HG/LEADR, thus suggesting its possible involvement in target selection and binding. Here, we performed Chromatin Isolation by RNA precipitation followed by DNA-sequencing (ChIRP-seq) to map MIR205HG/LEADR chromatin occupancy at a genome-wide level in prostate basal cells.
2022-06-07 | GSE201567 | GEO
Project description:We aimed at analyzing the transcriptome changes associated with MIR205HG knock-down in RWPE-1 cells
2019-01-23 | GSE103656 | GEO
Project description:We aimed at analyzing the transcriptome changes associated with MIR205HG knock-down in RWPE-1 cells or overexpression in DU145 cells
2019-01-23 | GSE103654 | GEO
Project description:Effects of deletion of a portion of the Alu element from MIR205HG transcript
| PRJNA407464 | ENA
Project description:Alu element-containing RNAs maintain nucleolar structure and function
| PRJEB9105 | ENA
Project description:An extrachromosomal replication system was established to examine the perturbation of Alu-carrying genes in response to elevated Alu RNAs in the opposite direction. The null hypothesis is that the Alu-carrying RNA duplex cannot trigger subsequent post-transcriptional regulation, manifesting a random perturbation of expression levels. Comparing HEK293 cells transfected and not-transfected with pDR2-Alu vectors.
2013-05-13 | E-GEOD-39822 | biostudies-arrayexpress
Project description:Alu element is a major contributor to lineage-specific new exons in the primate and human genomes. Recent studies indicate that some Alu exons have high transcript inclusion levels or tissue-specific splicing profiles, and may play important regulatory roles in modulating mRNA degradation or translational efficiency. However, the contribution of Alu exons to the human proteome remains unclear and controversial. The prevailing view is that exons derived from young repetitive elements (such as Alu) are restricted to regulatory functions but do not have adequate evolutionary time to be incorporated into stable, functional proteins. In this work, we adopt a proteotranscriptomics approach to systematically assess the contribution of Alu exons to the human proteome. Using RNA sequencing, ribosome profiling, and mass spectrometry data of diverse human tissues and cell lines, we provide evidence for the translational activities of Alu exons and the presence of Alu exon derived peptides in human proteins. These Alu exon peptides represent species-specific protein differences between primates and other mammals, and in certain instances even between humans and closely related nonhuman primates. In the RNA editing enzyme ADARB1, which contains an Alu exon peptide in its catalytic domain, RNA editing analyses of RNA-sequencing data demonstrate that both the Alu exon skipping and inclusion isoforms encode active RNA editing enzymes, while the Alu exon peptide may fine tune the editing activities of the ADARB1 protein products . Together, our data indicate that Alu elements have contributed to the acquisition of novel protein sequences during primate and human evolution. Comparing the A-I RNA editing levels during HEK293 (control), ADARB1 long isoform (with Alu exon) transfected, and short isoform (without Alu exon) transfected cells, each group has 3 replicates.
2015-12-10 | E-GEOD-65999 | biostudies-arrayexpress
Project description:An extrachromosomal replication system was established to examine the perturbation of Alu-carrying genes in response to elevated Alu RNAs in the opposite direction. The null hypothesis is that the Alu-carrying RNA duplex cannot trigger subsequent post-transcriptional regulation, manifesting a random perturbation of expression levels.
2013-05-13 | GSE39822 | GEO
Project description:Alu is a primate-specific repeat element in the human genome and has been increasingly appreciated as a regulatory element in many biological processes. But the role of Alu has not been studied comprehensively in brain tumor because an evolutionary perspective has been the subject of little research in brain tumor. We aim to investigate the relevance of Alu to the gliomagenesis.
2021-01-27 | GSE165595 | GEO
Project description:Enhancers determine spatiotemporal gene expression programs by engaging with long-range promoters. However, it remains unknown how enhancers find their cognate promoters. We recently developed a RIC-seq technology to identify enhancer-promoter connectivity using pairwise interacting enhancer RNAs and promoter-derived noncoding RNAs in HeLa cells. Here, we apply this technology to generate high-confidence enhancer-promoter RNA interaction (EPRI) maps in six additional cell lines. Using these maps, we discover that 37.9% of the enhancer-promoter RNA interaction sites are overlapped with Alu sequences. These pairwise interacting Alu and non-Alu RNA sequences tend to be complementary and potentially form duplexes. Knockout of Alu elements compromises enhancer-promoter looping, whereas Alu insertion or CRISPR-dCasRx-mediated Alu tethering to unregulated promoter RNAs can create new loops to homologous enhancers. Importantly, mapping 535,404 noncoding risk variants back to the EPRI maps enabled us to construct variant-to-function maps for interpreting their molecular functions, including 15,318 deletions or insertions in 11,677 Alu elements that affect 6,497 protein-coding genes. We further demonstrate that polymorphic Alu insertion at PTK2 enhancer can promote tumorigenesis. Our study uncovers a principle for determining enhancer-promoter pairing specificity and provides a framework to link noncoding risk variants to their molecular functions.
2023-05-11 | GSE190214 | GEO