ArticleNucleic acids research2002
A splicing silencer that regulates smooth muscle specific alternative splicing is active in multiple cell types.
Article in Nucleic acids research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 20 citations in OpenAlex.
- FBXO22 degrades nuclear PTEN to promote tumorigenesis.Nature communications · 2020Article
- Dissecting domains necessary for activation and repression of splicing by Muscleblind-like protein 1.BMC molecular biology · 2013Article
- MBNL1 and PTB cooperate to repress splicing of Tpm1 exon 3.Nucleic acids research · 2013Article
- Modulating alternative splicing by cotranscriptional cleavage of nascent intronic RNA.RNA (New York, N.Y.) · 2008Article
- Activation of alpha-tropomyosin exon 2 is regulated by the SR protein 9G8 and heterogeneous nuclear ribonucleoproteins H and F.Molecular and cellular biology · 2006Article
- A class of human exons with predicted distant branch points revealed by analysis of AG dinucleotide exclusion zones.Genome biology · 2006Article
- Exon selection in alpha-tropomyosin mRNA is regulated by the antagonistic action of RBM4 and PTB.Molecular and cellular biology · 2005Article
- The PTB interacting protein raver1 regulates alpha-tropomyosin alternative splicing.The EMBO journal · 2003Article
- Antagonistic regulation of alpha-actinin alternative splicing by CELF proteins and polypyrimidine tract binding protein.RNA (New York, N.Y.) · 2003Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Alternative splicing of alpha-tropomyosin (alpha-TM) involves mutually exclusive selection of exons 2 and 3. Selection of exon 2 in smooth muscle (SM) cells is due to inhibition of exon 3, which requires both binding sites for polypyrimidine tract-binding protein as well as UGC (or CUG) repeat elements on both sides of exon 3. Point mutations or substitutions of the UGC-containing upstream regulatory element (URE) with other UGC elements disrupted the alpha-TM splicing pattern in transfected cells. Multimerisation of the URE caused enhanced exon skipping in SM and various non-SM cells. In the presence of multiple UREs the degree of splicing regulation was decreased due to the high levels of exon skipping in non-SM cell lines. These results suggest that the URE is not an intrinsically SM- specific element, but that its functional strength is fine tuned to exploit differences in the activities of regulatory factors between SM and other cell types. Co-transfection of tropomyosin reporters with members of the CUG-binding protein family, which are candidate URE-binding proteins, indicated that these factors do not mediate repression of tropomyosin exon 3.
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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.