To investigate whether U1C plays a role in splicing regulation in human system, we performed siRNA-mediated knockdown of U1C in HeLa cells and analyzed alternative splicing patterns by high-throughput RNA sequencing (RNAseq) Overall design: RNAseq performed with poly(A)+ selected total RNA from U1C-knockdown and control-treated HeLa cells
A novel intra-U1 snRNP cross-regulation mechanism: alternative splicing switch links U1C and U1-70K expression.
Cell line, Treatment, Subject
View SamplesRecently a genome of Russian individual (somatic DNA from blood) was sequenced (Skryabin et al. 2009). That study was continued to find a linkage between genetic differences in parental alleles and bias in biallelic expression of genes.
Individual genome sequencing identified a novel enhancer element in exon 7 of the CSFR1 gene by shift of expressed allele ratios.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Crosslinking-immunoprecipitation (iCLIP) analysis reveals global regulatory roles of hnRNP L.
Cell line, Treatment
View SamplesTransient siRNA-mediated knockdown of hnRNP L, followed by cycloheximide treatment to eliminate NMD.
Crosslinking-immunoprecipitation (iCLIP) analysis reveals global regulatory roles of hnRNP L.
Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genome-wide profiles of CtBP link metabolism with genome stability and epithelial reprogramming in breast cancer.
Specimen part, Cell line, Treatment
View SamplesCtBP is a global co-repressor by serving as transcriptional factor in multiple pathways. CtBP functioned as transcriptional factor by recruiting other cofactors such as G9a, HDAC1 and PcG proteins. CtBP is found to be over enriched in several type of tumor samples. To dipict the role of CtBP in globally regulating gene expression, we applied gene microarray technology to find out what subgroups of genes are mainly affected.
Genome-wide profiles of CtBP link metabolism with genome stability and epithelial reprogramming in breast cancer.
Cell line, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Conserved and species-specific molecular denominators in mammalian skeletal muscle aging.
Sex, Specimen part
View SamplesAging is a complex phenomenon involving functional decline in multiple physiological systems. We focused on skeletal muscle to identify pathways that modulate function and healthspan by global expression profiles and specific mechanisms fundamental to aging processes. Our experimental design integrated comparative analysis of mice, rats, rhesus monkeys and humans and targeted three key time points during their lifespans. Pathways related to oxidative stress, inflammation and nutrient signaling, which function collectively to affect the quality and status of mitochondria, emerged across all species with age. Notably, mitochondrial transcript levels were better preserved in aging human muscle, suggesting an evolution-driven fitness more robust than in other species. The identification of these conserved pathways uncovers common molecular mechanisms intrinsic to health and lifespan, while unveiling of species-specific pathways emphasizes the importance of human studies for devising optimal therapeutic modalities to slow the aging process.
Conserved and species-specific molecular denominators in mammalian skeletal muscle aging.
Sex, Specimen part
View SamplesAging is a complex phenomenon involving functional decline in multiple physiological systems. We focused on skeletal muscle to identify pathways that modulate function and healthspan by global expression profiles and specific mechanisms fundamental to aging processes. Our experimental design integrated comparative analysis of mice, rats, rhesus monkeys and humans and targeted three key time points during their lifespans. Pathways related to oxidative stress, inflammation and nutrient signaling, which function collectively to affect the quality and status of mitochondria, emerged across all species with age. Notably, mitochondrial transcript levels were better preserved in aging human muscle, suggesting an evolution-driven fitness more robust than in other species. The identification of these conserved pathways uncovers common molecular mechanisms intrinsic to health and lifespan, while unveiling of species-specific pathways emphasizes the importance of human studies for devising optimal therapeutic modalities to slow the aging process.
Conserved and species-specific molecular denominators in mammalian skeletal muscle aging.
Sex, Specimen part
View SamplesAging is a complex phenomenon involving functional decline in multiple physiological systems. We focused on skeletal muscle to identify pathways that modulate function and healthspan by global expression profiles and specific mechanisms fundamental to aging processes. Our experimental design integrated comparative analysis of mice, rats, rhesus monkeys and humans and targeted three key time points during their lifespans. Pathways related to oxidative stress, inflammation and nutrient signaling, which function collectively to affect the quality and status of mitochondria, emerged across all species with age. Notably, mitochondrial transcript levels were better preserved in aging human muscle, suggesting an evolution-driven fitness more robust than in other species. The identification of these conserved pathways uncovers common molecular mechanisms intrinsic to health and lifespan, while unveiling of species-specific pathways emphasizes the importance of human studies for devising optimal therapeutic modalities to slow the aging process.
Conserved and species-specific molecular denominators in mammalian skeletal muscle aging.
Sex, Specimen part
View Samples