ArticleThe Journal of biological chemistry2010
Alternative splicing and polyadenylation contribute to the generation of hERG1 C-terminal isoforms.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- Review
- Article
- The ERG1 KFrontiers in molecular neuroscience · 2022Review
- Regulation of Kv11.1 Isoform Expression by Polyadenylate Binding Protein Nuclear 1.International journal of molecular sciences · 2021Article
- Long QT Syndrome Type 2: Emerging Strategies for Correcting Class 2Biomolecules · 2020Review
- Regulation of Kv11.1 potassium channel C-terminal isoform expression by the RNA-binding proteins HuR and HuD.The Journal of biological chemistry · 2018Article
- Article
- Molecular pathogenesis of long QT syndrome type 2.Journal of arrhythmia · 2016Review
- Upregulation of functional Kv11.1 isoform expression by inhibition of intronic polyadenylation with antisense morpholino oligonucleotides.Journal of molecular and cellular cardiology · 2014Article
- Identification of Kv11.1 isoform switch as a novel pathogenic mechanism of long-QT syndrome.Circulation. Cardiovascular genetics · 2014Article
- Article
- Isoform-specific dominant-negative effects associated with hERG1 G628S mutation in long QT syndrome.PloS one · 2012Article
- Nonsense-mediated mRNA decay caused by a frameshift mutation in a large kindred of type 2 long QT syndrome.Heart rhythm · 2011Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The human ether-a-go-go-related gene 1 (hERG1) encodes the pore-forming subunit of the rapidly activating delayed rectifier potassium channel. Several hERG1 isoforms with different N- and C-terminal ends have been identified. The hERG1a, hERG1b, and hERG1-3.1 isoforms contain the full-length C terminus, whereas the hERG1(USO) isoforms, hERG1a(USO) and hERG1b(USO), lack most of the C-terminal domain and contain a unique C-terminal end. The mechanisms underlying the generation of hERG1(USO) isoforms are not understood. We show that hERG1 isoforms with different C-terminal ends are generated by alternative splicing and polyadenylation of hERG1 pre-mRNA. We identified an intrinsically weak, noncanonical poly(A) signal, AGUAAA, within intron 9 of hERG1 that modulates the expression of hERG1a and hERG1a(USO). Replacing AGUAAA with the strong, canonical poly(A) signal AAUAAA resulted in the predominant production of hERG1a(USO) and a marked decrease in hERG1 current. In contrast, eliminating the intron 9 poly(A) signal or increasing the strength of 5' splice site led to the predominant production of hERG1a and a significant increase in hERG1 current. We found significant variation in the relative abundance of hERG1 C-terminal isoforms in different human tissues. Taken together, these findings suggest that post-transcriptional regulation of hERG1 pre-mRNA may represent a novel mechanism to modulate the expression and function of hERG1 channels.
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