ArticleRNA (New York, N.Y.)2009
A nonsense exon in the Tpm1 gene is silenced by hnRNP H and F.
Article in RNA (New York, N.Y.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Competitive regulation of alternative splicing and alternative polyadenylation by hnRNP H and CstF64 determines acetylcholinesterase isoforms.Nucleic acids research · 2017Article
- HnRNPH1/H2, U1 snRNP, and U11 snRNP cooperate to regulate the stability of the U11-48K pre-mRNA.RNA (New York, N.Y.) · 2013Article
- Identification of evolutionarily conserved exons as regulated targets for the splicing activator tra2β in development.PLoS genetics · 2011Article
- Molecular design of a splicing switch responsive to the RNA binding protein Tra2β.Nucleic acids research · 2011Article
- Position-dependent alternative splicing activity revealed by global profiling of alternative splicing events regulated by PTB.Nature structural & molecular biology · 2010Article
- Structural basis of G-tract recognition and encaging by hnRNP F quasi-RRMs.Nature structural & molecular biology · 2010Article
- A glycine-rich domain of hnRNP H/F promotes nucleocytoplasmic shuttling and nuclear import through an interaction with transportin 1.Molecular and cellular biology · 2010Article
- The intronic splicing code: multiple factors involved in ATM pseudoexon definition.The EMBO journal · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
As well as generating protein isoform diversity, in some cases alternative splicing generates RNAs that harbor premature termination codons and that are subject to nonsense-mediated decay (NMD). We previously identified an apparent pseudo-exon in the rat alpha-tropomyosin (Tpm1) gene as a probable genuine alternatively spliced exon that causes NMD when spliced into Tpm1 RNA. Here, we report the analysis of cis-acting splicing regulatory elements within this "nonsense exon." Guided by the data set of predicted splicing enhancer and silencer elements compiled by Zhang and Chasin, we made a series of mutations through the nonsense exon and found that like authentic exons it is densely packed with enhancer and silencer elements. Strikingly, 11 of 13 tested mutations behaved as predicted computationally. In particular, we found that a G-rich silencer at the 5' end, which is crucial for skipping of the nonsense exon, functions by binding hnRNP-H and F.
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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.