Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA297859 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2566080.fastq.gz | Fastqsanger.gz | |||
| SRR2566090.fastq.gz | Fastqsanger.gz | |||
| SRR2566100.fastq.gz | Fastqsanger.gz | |||
| SRR2566110.fastq.gz | Fastqsanger.gz | |||
| SRR2566120.fastq.gz | Fastqsanger.gz |
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Project description:Understanding the roles of splicing factors and splicing events during human tumorigenesis would open new avenues for targeted therapeutics. Here we identify an oncofetal splicing factor MBNL3, which indicates poor prognosis, and promotes hepatocellular carcinoma (HCC) tumorigenesis. Genetic MBNL3 inhibition almost completely abolishes HCC tumorigenesis. Transcriptomic analysis revealed that MBNL3 induces PXN antisense transcript 1 exon 4 inclusion. The transcript lacking exon 4 binds to coding sequences of PXN mRNA, causes dissociation of translation elongation factors from PXN mRNA, thereby inhibiting PXN mRNA translation. Whereas the transcript containing exon 4 preferentially binds to 3' untranslated region of PXN mRNA, protects PXN mRNA from microRNA-24-AGO2 complex-induced degradation, thereby increasing PXN expression. Through inducing exon 4 inclusion, MBNL3 upregulates PXN expression, which mediates the pro-tumorigenic roles of MBNL3. Collectively, these data demonstrate detailed mechanistic links between oncofetal splicing factor, splicing event, and tumorigenesis, and establish splicing factors and splicing events would be potential therapeutic targets.
2017-03-08 | GSE95778 | GEO
Project description:Understanding the roles of splicing factors and splicing events during tumorigenesis would open new avenues for targeted therapies. Here we identify an oncofetal splicing factor, heterogeneous nuclear ribonucleoprotein M (HNRNPM), which promotes tumorigenesis and predicts poor prognosis of hepatocellular carcinoma (HCC) patients. HNRNPM knockdown almost completely abolishes HCC tumorigenesis. Transcriptomic analysis combined with RNA-immunoprecipatation sequencing revealed that HNRNPM induces lncRNA-TRIM7-AS exon 2 inclusion. The transcript containing exon 2 binds to coding sequences of TRIM7 mRNA, causes dissociation of translation elongation factors from TRIM7 mRNA, and thereby inhibits TRIM7 mRNA translation. In contrast, the transcript including exon 3 preferentially binds to the 3’ untranslated region of TRIM7 mRNA, protects TRIM7 mRNA from microRNA-145-5p induced degradation, and thereby increases TRIM7 expression. Through inducing exon 2 inclusion, HNRNPM downregulates TRIM7 protein expression, which mediates the pro-tumorigenic roles of HNRNPM. Collectively, these data demonstrate detailed mechanistic links between an oncofetal splicing factor, a splicing event and tumorigenesis, and establish splicing factors and splicing events as potential therapeutic targets.
2022-06-01 | GSE169223 | GEO
Project description:In the present study, we performed HITS-CLIP analysis for FUS using mouse brain to extensively characterize tits RNA-binding sites and functional roles in RNA metabolisms. We identified preferential binding of FUS to stem-and-loop structures but without any discernible consensus motifs. FUS was preferentially bound to introns and 3' untranslated regions, but the exon/intron boundaries were mostly devoid of FUS-tags. Analysis of position-dependence of FUS-binding sites in regulating inclusion and skipping of exons disclosed that FUS is bound broadly around the alternatively spliced exons. Among them, however, noticeable CLIP-tags were observed in the downstream introns. We also noticed that FUS occasionally binds to the antisense strands in the promoter regions. Global analysis of CLIP-tags and expression profiles revealed that binding of FUS to the promoter antisense regions downgregulates transcription of the sense strand. HITS-CLIP (High Throughput Sequencing after Crosslinking and Immunoprecipitation) experiments targeting FUS in mouse cerebrums derived from 12-week-old C57BL/6 mice
2012-07-26 | E-GEOD-37190 | biostudies-arrayexpress
Project description:In the present study, we performed HITS-CLIP analysis for FUS using mouse brain to extensively characterize tits RNA-binding sites and functional roles in RNA metabolisms. We identified preferential binding of FUS to stem-and-loop structures but without any discernible consensus motifs. FUS was preferentially bound to introns and 3' untranslated regions, but the exon/intron boundaries were mostly devoid of FUS-tags. Analysis of position-dependence of FUS-binding sites in regulating inclusion and skipping of exons disclosed that FUS is bound broadly around the alternatively spliced exons. Among them, however, noticeable CLIP-tags were observed in the downstream introns. We also noticed that FUS occasionally binds to the antisense strands in the promoter regions. Global analysis of CLIP-tags and expression profiles revealed that binding of FUS to the promoter antisense regions downgregulates transcription of the sense strand.
2012-07-26 | GSE37190 | GEO
Project description:Maturation of the 3¢ end of almost all eukaryotic messenger RNAs (mRNAs) requires cleavage and polyadenylation. Most mammalian mRNAs are polyadenylated at different sites within the last exon, generating alternative polyadenylation (APA) isoforms that have the same coding region but distinct 3¢ untranslated regions (UTRs). The 3¢UTR contains motifs that regulate mRNA metabolism; thus, changing the 3¢UTR length via APA can significantly impact gene expression. Endochondral ossification is a central process in bone healing, and the impact of APA on gene expression during this process is unknown. Here, we report widespread utilization of APA that impacts multiple pathways with established roles in bone healing. Importantly, progression of endochondral ossification is typified by global 3¢UTR shortening that is coupled with an increased abundance of shortened transcripts as compared to all other transcripts, underscoring the role of APA in promoting gene expression during endochondral bone formation. Our mechanistic studies of genes that undergo APA in the fracture callus uncover an intricate regulatory network in which APA boosts the expression of collagen, type I, alpha 1 (Col1a1) and Col1a2 genes, which encode the 2 subunits of the abundantly expressed protein collagen 1. APA does so via shortening the 3¢UTRs of Col1a1 and Col1a2 mRNAs, which removes the binding sites of miR-29a-3p that otherwise potently triggered the degradation of both transcripts. Taken together, our study takes the lead in characterizing crucial roles of APA in tailoring the 3¢UTR landscape and regulating gene expression during fracture healing.
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Project description:The epithelial splicing regulatory proteins, ESRP1 and ESRP2 are essential for mammalian development through regulation of a global program of alternative splicing of genes involved in maintenance of epithelial cell function. To further inform our understanding of the molecular functions of ESRP1 we performed enhanced crosslinking immunoprecipitation coupled with high throughput sequencing (eCLIP) in epithelial cells of mouse epidermis. The genome-wide binding sites of ESRP1 were integrated with RNA-Seq analysis of alterations in splicing and total gene expression that result from epidermal ablation of Esrp1 and Esrp2. These studies demonstrated that ESRP1 functions in splicing regulation occur primarily through direct binding in a position-dependent manner to either promote exon inclusion or skipping. In addition, we also identified widespread binding of ESRP1 in 3’ and 5’ untranslated regions (UTRs) of genes involved in epithelial cell function, suggesting that its post-transcriptional functions extend beyond splicing regulation.
2022-09-12 | GSE212306 | GEO
Project description:The epithelial splicing regulatory proteins, ESRP1 and ESRP2 are essential for mammalian development through regulation of a global program of alternative splicing of genes involved in maintenance of epithelial cell function. To further inform our understanding of the molecular functions of ESRP1 we performed enhanced crosslinking immunoprecipitation coupled with high throughput sequencing (eCLIP) in epithelial cells of mouse epidermis. The genome-wide binding sites of ESRP1 were integrated with RNA-Seq analysis of alterations in splicing and total gene expression that result from epidermal ablation of Esrp1 and Esrp2. These studies demonstrated that ESRP1 functions in splicing regulation occur primarily through direct binding in a position-dependent manner to either promote exon inclusion or skipping. In addition, we also identified widespread binding of ESRP1 in 3’ and 5’ untranslated regions (UTRs) of genes involved in epithelial cell function, suggesting that its post-transcriptional functions extend beyond splicing regulation.
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Project description:Alternative splicing (AS) generates transcript variants by the definition of different exonic and intronic regions and causes a massive expansion of transcriptome diversity. Changes in AS patterns have been found to be linked to manifold biological processes, yet fundamental aspects such as the regulation of AS and the functional implications of altered AS programs largely remain to be addressed. In this work, widespread AS regulation by Arabidopsis Polypyrimidine tract-binding protein homologues (AtPTBs) was revealed. In total 452 AS events derived from 308 distinct genes were found to be responsive to the levels of the splicing factors AtPTB1 and AtPTB2, which predominantly triggered splicing of regulated introns, inclusion of cassette exons, and usage of upstream 5' splice sites. In contrast, alternative 3' splice site events were strongly underrepresented among the AtPTB1/2 targets and no major AS regulatory function of the distantly related AtPTB3 was found. Dependent on their position within the mRNA, AtPTB-regulated events can both modify the untranslated regions and give rise to alternative protein products. Gene ontology analysis revealed a connection of AtPTB-mediated AS control with diverse biological processes, and the functional implications of selected AS events were further elucidated in the context of seed germination and flowering time control. Specifically, AtPTB misexpression changes AS of the PHYTOCHROME INTERACTING FACTOR 6 (PIF6) pre-mRNA, coinciding with altered rates of abscisic acid-dependent seed germination. Furthermore, AS patterns as well as the expression of key flowering regulators were massively changed in an AtPTB1/2 level-dependent manner. In conclusion, our work has revealed widespread AS regulatory functions of the AtPTB splicing factors with important functional implications in various fundamental processes of Arabidopsis development. Analysis of alternative splicing patterns in plants with increased and decreased levels of the 3 Arabidopsis Polypyrimidine-tract binding protein homologues in comparison to wild type samples, determined in duplicates
2012-10-22 | E-GEOD-41433 | biostudies-arrayexpress