ArticleNucleic acids research2012
Mutually exclusive splicing regulates the Nav 1.6 sodium channel function through a combinatorial mechanism that involves three distinct splicing regulatory elements and their ligands.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 16 papers.
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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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Who cites it
16 citing papers in PubMed, 34 citations in OpenAlex.
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- Poison exon annotations improve the yield of clinically relevant variants in genomic diagnostic testing.Genetics in medicine : official journal of the American College of Medical Genetics · 2023Article
- Developmental dynamics of voltage-gated sodium channel isoform expression in the human and mouse brain.Genome medicine · 2021Article
- Sodium channelopathies in neurodevelopmental disorders.Nature reviews. Neuroscience · 2021Review
- Aberrant regulation of a poison exon caused by a non-coding variant in a mouse model of Scn1a-associated epileptic encephalopathy.PLoS genetics · 2021Article
- Aberrant Inclusion of a Poison Exon Causes Dravet Syndrome and Related SCN1A-Associated Genetic Epilepsies.American journal of human genetics · 2018Article
- Microprocessor-dependent processing of splice site overlapping microRNA exons does not result in changes in alternative splicing.RNA (New York, N.Y.) · 2018Article
- The landscape of human mutually exclusive splicing.Molecular systems biology · 2017Article
- The determinants of alternative RNA splicing in human cells.Molecular genetics and genomics : MGG · 2017Review
- Dissection of voltage-gated sodium channels in developing cochlear sensory epithelia.Protein & cell · 2015Article
- The Nav channel bench series: Plasmid preparation.MethodsX · 2014Article
- Linking spermatid ribonucleic acid (RNA) binding protein and retrogene diversity to reproductive success.Molecular & cellular proteomics : MCP · 2013Article
- Sodium channel SCN8A (Nav1.6): properties and de novo mutations in epileptic encephalopathy and intellectual disability.Frontiers in genetics · 2013Review
- Alternative pre-mRNA splicing in neurons: growing up and extending its reach.Trends in genetics : TIG · 2013Review
- Four Promoters of IRF5 Respond Distinctly to Stimuli and are Affected by Autoimmune-Risk Polymorphisms.Frontiers in immunology · 2013Article
Corrections and comments
- Expression of concern · 2023-11-21Concerns/Issues about Image · Duplication of/in Image · Investigation by Company/Institution · Investigation by Journal/Publisher · Original Data and/or Images not Provided and/or not Available · Unreliable Results and/or Conclusions · Upgrade/Update of Prior Notice(s) ·
- Expression of concern · 2023-04-11Concerns/Issues about Image · Investigation by Company/Institution · Updated to Retraction ·
- Expression of concern
- Retracted
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutually exclusive splicing is a form of alternative pre-mRNA processing that consists in the use of only one of a set of two or more exons. We have investigated the mechanisms involved in this process for exon 18 of the Na(v) 1.6 sodium channel transcript and its significance regarding gene-expression regulation. The 18N exon (neonatal form) has a stop codon in phase and although the mRNA can be detected by amplification methods, the truncated protein has not been observed. The switch from 18N to 18A (adult form) occurs only in a restricted set of neural tissues producing the functional channel while other tissues display the mRNA with the 18N exon also in adulthood. We demonstrate that the mRNA species carrying the stop codon is subjected to Nonsense-Mediated Decay, providing a control mechanism of channel expression. We also map a string of cis-elements within the mutually exclusive exons and in the flanking introns responsible for their strict tissue and temporal specificity. These elements bind a series of positive (RbFox-1, SRSF1, SRSF2) and negative (hnRNPA1, PTB, hnRNPA2/B1, hnRNPD-like JKTBP) splicing regulatory proteins. These splicing factors, with the exception of RbFox-1, are ubiquitous but their levels vary during development and differentiation, ensuing unique sets of tissue and temporal levels of splicing factors. The combinatorial nature of these elements is highlighted by the dominance of the elements that bind the ubiquitous factors over the tissue specific RbFox-1.
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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.