ArticleRNA (New York, N.Y.)2004
A single polypyrimidine tract binding protein (PTB) binding site mediates splicing inhibition at mouse IgM exons M1 and M2.
Article in RNA (New York, N.Y.), 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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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Who cites it
27 citing papers in PubMed.
- Essential requirement for polypyrimidine tract binding proteins 1 and 3 in the maturation and maintenance of mature B cells in mice.European journal of immunology · 2021Article
- Intronic Determinants Coordinate Charme lncRNA Nuclear Activity through the Interaction with MATR3 and PTBP1.Cell reports · 2020Article
- Conservation of polypyrimidine tract binding proteins and their putative target RNAs in several storage root crops.BMC genomics · 2018Article
- Pathogenic variants that alter protein code often disrupt splicing.Nature genetics · 2017Article
- PSF contacts exon 7 of SMN2 pre-mRNA to promote exon 7 inclusion.Biochimica et biophysica acta · 2014Article
- Polypyrimidine tract binding protein inhibits IgM pre-mRNA splicing by diverting U2 snRNA base-pairing away from the branch point.RNA (New York, N.Y.) · 2014Article
- A 2-nt RNA enhancer on exon 11 promotes exon 11 inclusion of the Ron proto-oncogene.Oncology reports · 2014Article
- De novo prediction of PTBP1 binding and splicing targets reveals unexpected features of its RNA recognition and function.PLoS computational biology · 2014Article
- New insights into functional roles of the polypyrimidine tract-binding protein.International journal of molecular sciences · 2013Review
- Polypyrimidine tract binding protein (hnRNP I) is possibly a conserved modulator of miRNA-mediated gene regulation.PloS one · 2012Article
- The RNA polymerase II C-terminal domain promotes splicing activation through recruitment of a U2AF65-Prp19 complex.Genes & development · 2011Article
- Stoichiometry of a regulatory splicing complex revealed by single-molecule analyses.The EMBO journal · 2010Article
- Next-generation SELEX identifies sequence and structural determinants of splicing factor binding in human pre-mRNA sequence.RNA (New York, N.Y.) · 2009Article
- Multiple roles for polypyrimidine tract binding (PTB) proteins in trypanosome RNA metabolism.RNA (New York, N.Y.) · 2009Article
- Deletion of the N-terminus of SF2/ASF permits RS-domain-independent pre-mRNA splicing.PloS one · 2007Article
- Crossregulation and functional redundancy between the splicing regulator PTB and its paralogs nPTB and ROD1.Molecular cell · 2007Article
- hnRNP I/PTB can antagonize the splicing repressor activity of SRp30c.RNA (New York, N.Y.) · 2007Article
- Repression of alpha-actinin SM exon splicing by assisted binding of PTB to the polypyrimidine tract.RNA (New York, N.Y.) · 2007Article
- The polypyrimidine tract binding protein (PTB) represses splicing of exon 6B from the beta-tropomyosin pre-mRNA by directly interfering with the binding of the U2AF65 subunit.Molecular and cellular biology · 2006Article
- Functional coupling of RNAP II transcription to spliceosome assembly.Genes & development · 2006Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Splicing of mouse immunoglobulin (IgM) exons M1 and M2 is directed by two juxtaposed regulatory elements, an enhancer and an inhibitor, located within the M2 exon. A primary function of the enhancer is to counteract the inhibitor, allowing splicing to occur. Here we show that the inhibitor contains two binding sites for polypyrimidine tract binding protein (PTB). Mutational analysis indicates that only one of these sites is necessary and sufficient to direct splicing inhibition both in vitro and in vivo. We demonstrate that the difference in activity of the two sites is explained by proximity to the intron. We further show that the presence of the enhancer results in the disruption of the PTB-inhibitor interaction, enabling splicing to occur. In the absence of the enhancer, splicing can be artificially activated by immuno-inhibition of PTB. Collectively, our results indicate that a single PTB binding site can function as an inhibitor that regulates alternative splicing both in vitro and in vivo.
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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.