ArticleMolecular and cellular biology2003
Roles for SR proteins and hnRNP A1 in the regulation of c-src exon N1.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 88 citations in OpenAlex.
- Review
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- The Roles of hnRNP Family in the Brain and Brain-Related Disorders.Molecular neurobiology · 2024Review
- hnRNP A1 in RNA metabolism regulation and as a potential therapeutic target.Frontiers in pharmacology · 2022Review
- Nucleotides in both donor and acceptor splice sites are responsible for choice in NAGNAG tandem splice sites.Cellular and molecular life sciences : CMLS · 2021Article
- Splicing Enhancers at Intron-Exon Borders Participate in Acceptor Splice Sites Recognition.International journal of molecular sciences · 2020Article
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- TCF3 mutually exclusive alternative splicing is controlled by long-range cooperative actions between hnRNPH1 and PTBP1.RNA (New York, N.Y.) · 2019Article
- SRSF2 mutations drive oncogenesis by activating a global program of aberrant alternative splicing in hematopoietic cells.Leukemia · 2018Article
- SRSF6 is upregulated in asthmatic horses and involved in the MYH11 SMB expression.Physiological reports · 2018Article
- SPSB1-mediated HnRNP A1 ubiquitylation regulates alternative splicing and cell migration in EGF signaling.Cell research · 2017Article
- Article
- Diverse regulation of 3' splice site usage.Cellular and molecular life sciences : CMLS · 2015Review
- RNA-Binding Proteins: Splicing Factors and Disease.Biomolecules · 2015Review
- Mitochondrial retrograde signaling at the crossroads of tumor bioenergetics, genetics and epigenetics.Mitochondrion · 2013Review
- hnRNP A1: the Swiss army knife of gene expression.International journal of molecular sciences · 2013Review
- 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.Nucleic acids research · 2012Article
- c-Myc regulates RNA splicing of the A-Raf kinase and its activation of the ERK pathway.Cancer research · 2011Article
- Interaction between the RNA binding domains of Ser-Arg splicing factor 1 and U1-70K snRNP protein determines early spliceosome assembly.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Elevated copper remodels hepatic RNA processing machinery in the mouse model of Wilson's disease.Journal of molecular biology · 2011Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The splicing of the c-src exon N1 is controlled by an intricate combination of positive and negative RNA elements. Most previous work on these sequences focused on intronic elements found upstream and downstream of exon N1. However, it was demonstrated that the 5' half of the N1 exon itself acts as a splicing enhancer in vivo. Here we examine the function of this regulatory element in vitro. We show that a mutation in this sequence decreases splicing of the N1 exon in vitro. Proteins binding to this element were identified as hnRNP A1, hnRNP H, hnRNP F, and SF2/ASF by site-specific cross-linking and immunoprecipitation. The binding of these proteins to the RNA was eliminated by a mutation in the exonic element. The activities of hnRNP A1 and SF2/ASF on N1 splicing were examined by adding purified protein to in vitro splicing reactions. SF2/ASF and another SR protein, SC35, are both able to stimulate splicing of c-src pre-mRNA. However, splicing activation by SF2/ASF is dependent on the N1 exon enhancer element whereas activation by SC35 is not. In contrast to SF2/ASF and in agreement with other systems, hnRNP A1 repressed c-src splicing in vitro. The negative activity of hnRNP A1 on splicing was compared with that of PTB, a protein previously demonstrated to repress splicing in this system. Both proteins repress exon N1 splicing, and both counteract the enhancing activity of the SR proteins. Removal of the PTB binding sites upstream of N1 prevents PTB-mediated repression but does not affect A1-mediated repression. Thus, hnRNP A1 and PTB use different mechanisms to repress c-src splicing. Our results link the activity of these well-known exonic splicing regulators, SF2/ASF and hnRNP A1, to the splicing of an exon primarily controlled by intronic factors.
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