Sense exon profiling across human, mouse, and rat
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PROVIDER: PRJNA177584 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcription profiling of sense and antisense transcripts of 10 tissues each from human, mouse, and rat. This SuperSeries is composed of the following subset Series: GSE41462: Antisense exon profiling across human, mouse, and rat GSE41464: Sense exon profiling across human, mouse, and rat We profiled the sense and antisense transcription level of 10 tissues each from human, mouse, and rat. Only Affymetrix core probesets were used. Two technical replicates per sample. Reference for protocol: Ge, X., Rubinstein, W.S., Jung, Y.C., and Wu, Q. (2008). Genome-wide analysis of antisense transcription with Affymetrix exon array. BMC Genomics 9, 27.
2012-10-10 | E-GEOD-41409 | biostudies-arrayexpress
Project description:Transcription profiling of sense transcripts of 10 tissues each from human, mouse, and rat.
2012-10-10 | GSE41464 | GEO
Project description:Transcription profiling of sense and antisense transcripts of 10 tissues each from human, mouse, and rat. This SuperSeries is composed of the SubSeries listed below.
2012-10-10 | GSE41409 | GEO
Project description:Transcription profiling of sense transcripts of 10 tissues each from human, mouse, and rat. We profiled the sense transcription level of 10 tissues each from human, mouse, and rat. Only Affymetrix core probesets were used. Two technical replicates per sample.
2012-10-10 | E-GEOD-41464 | biostudies-arrayexpress
Project description:Antisense exon profiling across human, mouse, and rat
| PRJNA177583 | ENA
Project description:Transcription profiling of antisense transcripts of 10 tissues each from human, mouse, and rat. We profiled the antisense transcription level of 10 tissues each from human, mouse, and rat. Only Affymetrix core probesets were used. Two technical replicates per sample. Reference for protocol: Ge, X., Rubinstein, W.S., Jung, Y.C., and Wu, Q. (2008). Genome-wide analysis of antisense transcription with Affymetrix exon array. BMC Genomics 9, 27.
2012-10-10 | E-GEOD-41462 | biostudies-arrayexpress
Project description:Transcription profiling of antisense transcripts of 10 tissues each from human, mouse, and rat.
2012-10-10 | GSE41462 | GEO
Project description:Increasing numbers of sense–antisense transcripts (SATs), which are transcribed from the same chromosomal location but in opposite directions, have been identified in various eukaryotic species, but the biological meanings of most SATs remain unclear. To improve understanding of natural sense–antisense transcription, we performed comparative expression profiling of SATs conserved among humans and mice. Using custom oligo-arrays loaded with probes that represented SATs with both protein-coding and non-protein–coding transcripts, we showed that 33% of the 291 conserved SATs displayed identical expression patterns in the two species. Among these SATs, expressional balance inversion of sense–antisense genes was mostly observed in testis at a tissue-specific manner. Northern analyses of the individual conserved SAT loci revealed that: (1) a smeary hybridization pattern was present in mice, but not in humans, and (2) small RNAs (about 60 to 80 nt) were detected from the exon-overlapping regions of SAT loci. In addition, further analyses showed marked alteration of sense–antisense expression balance throughout spermatogenesis in testis. These results suggest that conserved SAT loci are rich in potential regulatory roles that will help us understand this new class of transcripts underlying the mammalian genome. Keywords: Expression profile of mouse and human sense-antisense transcript
2008-02-20 | GSE9581 | GEO
Project description:Expression of Mouse and Human Sense-Antisense Transcript
| PRJNA103413 | ENA
Project description:Mutations in the dystrophin (DMD) gene can cause muscle-wasting disorders ranging from the milder Becker muscular dystrophy (BMD) to the more severe Duchenne muscular dystrophy (DMD). Exon 45 deletion is the most frequently reported single-exon deletion in DMD patients worldwide. In this study, we generated a novel rat model with an exon 45 deletion using the CRISPR/Cas9 technology. The DmdΔ45 rat recapitulate key clinical and molecular features of DMD, including progressive skeletal muscle degeneration, impaired muscle and cardiac function, cognitive deficits, elevated circulating muscle damage biomarkers and an overall reduced lifespan. Transcriptomics analyses confirmed the deletion of exon 45 and revealed gene expression patterns consistent with dystrophin deficiency. In the skeletal muscle, RNA-seq profiles demonstrated a transition from early stress responses and regenerative activity at 6 months to chronic inflammation, fibrosis, and metabolic dysfunction by 12 months. Similarly, the cardiac transcriptomic shifted from an early inflammatory and stress-responsive state to one characterized by fibrotic remodelling and metabolic impairment. Despite these pathological features, the DmdΔ45 rats exhibited a milder phenotype than other DMD rat models. This attenuation may be attributed to spontaneous exon 44 skipping, which partially restores the reading frame and results in an age-dependent increase in revertant dystrophin-positive fibres. Further analysis indicated downregulation of spliceosome-related genes, suggesting a potential mechanism driving exon skipping in this model. In summary, the DmdΔ45 rat represents a valuable model for investigating both the molecular determinants of phenotypic variability and the endogenous mechanisms of exon skipping. These findings offer important insights for the development of personalized exon-skipping therapies, particularly for DMD patients with exon 45 deletions.
2025-09-18 | GSE308065 | GEO