ArticleMolecular and cellular biology1998
Regulation of alternative polyadenylation by U1 snRNPs and SRp20.
Article in Molecular and cellular biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 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
101 citing papers in PubMed, 191 citations in OpenAlex.
- SRSF3 plays a key role in liver cancer sex disparity by facilitating hepatocyte expression of ERα and FOXA.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- The competition between splicing and 3' processing shapes the human transcriptome.Genes & development · 2026Article
- HSV ICP27 hijacks host splicing factor SRSF3 to regulate pre-mRNA splicing and export for viral gene expression and immune evasion.PLoS pathogens · 2026Article
- The role of alternative pre-mRNA splicing in cancer progression.Cancer cell international · 2023Review
- Role of the long non-coding RNAs in regulation of Gemcitabine response in tumor cells.Cancer cell international · 2023Review
- Oncogenic SRSF3 in health and diseases.International journal of biological sciences · 2023Review
- The rice blast fungus SR protein 1 regulates alternative splicing with unique mechanisms.PLoS pathogens · 2022Article
- Deciphering the impact of genetic variation on human polyadenylation using APARENT2.Genome biology · 2022Article
- The RNA-binding protein SRSF3 has an essential role in megakaryocyte maturation and platelet production.Blood · 2022Article
- Biological function and molecular mechanism of SRSF3 in cancer and beyond.Oncology letters · 2022Review
- SRSF3 Expression Serves as a Potential Biomarker for Prognostic and Immune Response in Pan-Cancer.Frontiers in oncology · 2022Article
- SRSF3 and SRSF7 modulate 3'UTR length through suppression or activation of proximal polyadenylation sites and regulation of CFIm levels.Genome biology · 2021Article
- The RNA-binding profile of the splicing factor SRSF6 in immortalized human pancreatic β-cells.Life science alliance · 2021Article
- Article
- Emerging Roles of SRSF3 as a Therapeutic Target for Cancer.Frontiers in oncology · 2020Review
- HNRNPA1-mediated 3' UTR length changes ofAging · 2019Article
- Oncogenic splicing factor SRSF3 regulates ILF3 alternative splicing to promote cancer cell proliferation and transformation.RNA (New York, N.Y.) · 2019Article
- Alternative polyadenylation dependent function of splicing factor SRSF3 contributes to cellular senescence.Aging · 2019Article
- Interference of DNAJB6/MRJ Isoform Switch by Morpholino Inhibits Replication of HIV-1 and RSV.Molecular therapy. Nucleic acids · 2019Article
- Distinct mechanisms govern the phosphorylation of different SR protein splicing factors.The Journal of biological chemistry · 2019Article
41 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Although considerable information is currently available about the factors involved in constitutive vertebrate polyadenylation, the factors and mechanisms involved in facilitating communication between polyadenylation and splicing are largely unknown. Even less is known about the regulation of polyadenylation in genes in which 3'-terminal exons are alternatively recognized. Here we demonstrate that an SR protein, SRp20, affects recognition of an alternative 3'-terminal exon via an effect on the efficiency of binding of a polyadenylation factor to an alternative polyadenylation site. The gene under study codes for the peptides calcitonin and calcitonin gene-related peptide. Its pre-mRNA is alternatively processed by the tissue-specific inclusion or exclusion of an embedded 3'-terminal exon, exon 4, via factors binding to an intronic enhancer element that contains both 3' and 5' splice site consensus sequence elements. In cell types that preferentially exclude exon 4, addition of wild-type SRp20 enhances exon 4 inclusion via recognition of the intronic enhancer. In contrast, in cell types that preferentially include exon 4, addition of a mutant form of SRp20 containing the RNA-binding domain but missing the SR domain inhibits exon 4 inclusion. Inhibition is likely at the level of polyadenylation, because the mutant SRp20 inhibits binding of CstF to the exon 4 poly(A) site. This is the first demonstration that an SR protein can influence alternative polyadenylation and suggests that this family of proteins may play a role in recognition of 3'-terminal exons and perhaps in the communication between polyadenylation and splicing.
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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.