ArticleMolecules and cells2014
Pressure-overload cardiac hypertrophy is associated with distinct alternative splicing due to altered expression of splicing factors.
Article in Molecules and cells, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- PRMT1 alleviates isoprenaline-induced myocardial hypertrophy by methylating SRSF1.Acta biochimica et biophysica Sinica · 2024Article
- PTBP1 as a potential regulator of disease.Molecular and cellular biochemistry · 2024Review
- Aberrant spliceosome activity via elevated intron retention and upregulation and phosphorylation of SF3B1 in chronic lymphocytic leukemia.Molecular therapy. Nucleic acids · 2024Article
- Dynamic Variations of 3'UTR Length Reprogram the mRNA Regulatory Landscape.Biomedicines · 2021Review
- Review
- Alternative splicing in cardiomyopathy.Biophysical reviews · 2018Review
- Article
- Identification of the Mtus1 Splice Variant as a Novel Inhibitory Factor Against Cardiac Hypertrophy.Journal of the American Heart Association · 2016Article
- Abnormalities in Alternative Splicing of Apoptotic Genes and Cardiovascular Diseases.International journal of molecular sciences · 2015Review
- Gain of a New Exon by a Lineage-Specific Alu Element-Integration Event in the BCS1L Gene during Primate Evolution.Molecules and cells · 2015Article
- Article
- Transcriptome complexity in cardiac development and diseases--an expanding universe between genome and phenome.Circulation journal : official journal of the Japanese Circulation Society · 2014Review
- Challenges in Therapeutically Targeting the RNA-Recognition Motif.Wiley interdisciplinary reviews. RNAReview
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic pressure-overload cardiac hypertrophy is associated with an increased risk of morbidity/mortality, largely due to maladaptive remodeling and dilatation that progresses to dilated cardiomyopathy. Alternative splicing is an important biological mechanism that generates proteomic complexity and diversity. The recent development of next-generation RNA sequencing has improved our understanding of the qualitative signatures associated with alternative splicing in various biological conditions. However, the role of alternative splicing in cardiac hypertrophy is yet unknown. The present study employed RNA-Seq and a bioinformatic approach to detect the RNA splicing regulatory elements involved in alternative splicing during pressure-overload cardiac hypertrophy. We found GC-rich exonic motifs that regulate intron retention in 5' UTRs and AT-rich exonic motifs that are involved in exclusion of the AT-rich elements that cause mRNA instability in 3' UTRs. We also identified motifs in the intronic regions involved in exon exclusion and inclusion, which predicted splicing factors that bind to these motifs. We found, through Western blotting, that the expression levels of three splicing factors, ESRP1, PTB and SF2/ASF, were significantly altered during cardiac hypertrophy. Collectively, the present results suggest that chronic pressure-overload hypertrophy is closely associated with distinct alternative splicing due to altered expression of splicing factors.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.