ArticleMolecular and cellular biology2006
An apparent pseudo-exon acts both as an alternative exon that leads to nonsense-mediated decay and as a zero-length exon.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- A single-cell strategy for the identification of intronic variants related to mis-splicing in pancreatic cancer.NAR genomics and bioinformatics · 2024Article
- Features of CFTR mRNA and implications for therapeutics development.Frontiers in genetics · 2023Review
- Genetic variants in S-adenosyl-methionine synthesis pathway and nonsyndromic cleft lip with or without cleft palate in Chile.Pediatric research · 2021Article
- Cutting a Long Intron Short: Recursive Splicing and Its Implications.Frontiers in physiology · 2016Article
- Recursive splicing in long vertebrate genes.Nature · 2015Article
- Molecular biology: Splicing does the two-step.Nature · 2015Article
- Splicing of many human genes involves sites embedded within introns.Nucleic acids research · 2015Article
- Dual role of G-runs and hnRNP F in the regulation of a mutation-activated pseudoexon in the fibrinogen gamma-chain transcript.PloS one · 2013Article
- Identification of evolutionarily conserved exons as regulated targets for the splicing activator tra2β in development.PLoS genetics · 2011Article
- hnRNP F directs formation of an exon 4 minus variant of tumor-associated NADH oxidase (ENOX2).Molecular and cellular biochemistry · 2011Article
- Molecular design of a splicing switch responsive to the RNA binding protein Tra2β.Nucleic acids research · 2011Article
- Common genetic variation in Neuregulin 3 (NRG3) influences risk for schizophrenia and impacts NRG3 expression in human brain.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Unconstrained mining of transcript data reveals increased alternative splicing complexity in the human transcriptome.Nucleic acids research · 2010Article
- The intronic splicing code: multiple factors involved in ATM pseudoexon definition.The EMBO journal · 2010Article
- The peculiarities of large intron splicing in animals.PloS one · 2009Article
- An Alu-derived intronic splicing enhancer facilitates intronic processing and modulates aberrant splicing in ATM.Nucleic acids research · 2009Article
- A nonsense exon in the Tpm1 gene is silenced by hnRNP H and F.RNA (New York, N.Y.) · 2009Article
- Propionic and methylmalonic acidemia: antisense therapeutics for intronic variations causing aberrantly spliced messenger RNA.American journal of human genetics · 2007Article
- Unfolding the mystery of alternative splicing through a unique method of in vivo selection.Frontiers in bioscience : a journal and virtual library · 2007Article
- RNA structure is a key regulatory element in pathological ATM and CFTR pseudoexon inclusion events.Nucleic acids research · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Pseudo-exons are intronic sequences that are flanked by apparent consensus splice sites but that are not observed in spliced mRNAs. Pseudo-exons are often difficult to activate by mutation and have typically been viewed as a conceptual challenge to our understanding of how the spliceosome discriminates between authentic and cryptic splice sites. We have analyzed an apparent pseudo-exon located downstream of mutually exclusive exons 2 and 3 of the rat alpha-tropomyosin (TM) gene. The TM pseudo-exon is conserved among mammals and has a conserved profile of predicted splicing enhancers and silencers that is more typical of a genuine exon than a pseudo-exon. Splicing of the pseudo-exon is fully activated for splicing to exon 3 by a number of simple mutations. Splicing of the pseudo-exon to exon 3 is predicted to lead to nonsense-mediated decay (NMD). In contrast, when "prespliced" to exon 2 it follows a "zero length exon" splicing pathway in which a newly generated 5' splice site at the junction with exon 2 is spliced to exon 4. We propose that a subset of apparent pseudo-exons, as exemplified here, are actually authentic alternative exons whose inclusion leads to NMD.
Indexed as
Identifiers
What OpenQuestion holds
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.