ArticleNucleic acids research2019
Star-PAP controlled alternative polyadenylation coupled poly(A) tail length regulates protein expression in hypertrophic heart.
Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Alternative cleavage and polyadenylation: key regulatory mechanisms in health and disease.RNA biology · 2025Review
- The poly(A) polymerase Star-PAP is regulated by stably associated phosphoinositide messengers.The Journal of biological chemistry · 2025Article
- Genome-scale CRISPRi screen identifies pcnB repression conferring improved physiology for overproduction of free fatty acids in Escherichia coli.Nature communications · 2025Article
- The emerging role of circular RNAs in cisplatin resistance in ovarian cancer: From molecular mechanism to future potential.Non-coding RNA research · 2024Review
- Impact of NQO1 dysregulation in CNS disorders.Journal of translational medicine · 2024Review
- Landscape of molecular crosstalk between SARS-CoV-2 infection and cardiovascular diseases: emphasis on mitochondrial dysfunction and immune-inflammation.Journal of translational medicine · 2023Article
- Downregulation of apoptotic repressorProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Alternative polyadenylation regulation in cardiac development and cardiovascular disease.Cardiovascular research · 2023Review
- Tyrosine phosphorylation controlled poly(A) polymerase I activity regulates general stress response in bacteria.Life science alliance · 2023Article
- Dynamic alternative polyadenylation during iPSC differentiation into cardiomyocytes.Computational and structural biotechnology journal · 2022Article
- Emerging roles of alternative cleavage and polyadenylation (APA) in human disease.Journal of cellular physiology · 2022Review
- Cleavage Stimulation Factor Subunit 2: Function Across Cancers and Potential Target for Chemotherapeutic Drugs.Frontiers in pharmacology · 2022Article
- circPTN Promotes the Progression of Non-Small Cell Lung Cancer through Upregulation of E2F2 by Sponging miR-432-5p.International journal of genomics · 2022Article
- Dynamic Variations of 3'UTR Length Reprogram the mRNA Regulatory Landscape.Biomedicines · 2021Review
- Transgenesis of mammalian PABP reveals mRNA polyadenylation as a general stress response mechanism in bacteria.iScience · 2021Article
- Star-PAP RNA Binding Landscape Reveals Novel Role of Star-PAP in mRNA Metabolism That Requires RBM10-RNA Association.International journal of molecular sciences · 2021Article
- Emerging Roles of RNA 3'-end Cleavage and Polyadenylation in Pathogenesis, Diagnosis and Therapy of Human Disorders.Biomolecules · 2020Review
- CircRNA-PTN Sponges miR-326 to Promote Proliferation in Hepatocellular Carcinoma.OncoTargets and therapy · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Alternative polyadenylation (APA)-mediated 3'-untranslated region (UTR) shortening is known to increase protein expression due to the loss of miRNA regulatory sites. Yet, mRNAs with longer 3'-UTR also show enhanced protein expression. Here, we identify a mechanism by which longer transcripts generated by the distal-most APA site leads to increased protein expression compared to the shorter transcripts and the longer transcripts are positioned to regulate heart failure (HF). A Star-PAP target gene, NQO1 has three poly(A) sites (PA-sites) at the terminal exon on the pre-mRNA. Star-PAP selects the distal-most site that results in the expression of the longest isoform. We show that the NQO1 distal-specific mRNA isoform accounts for the majority of cellular NQO1 protein. Star-PAP control of the distal-specific isoform is stimulated by oxidative stress and the toxin dioxin. The longest NQO1 transcript has increased poly(A) tail (PA-tail) length that accounts for the difference in translation potentials of the three NQO1 isoforms. This mechanism is involved in the regulation of cardiac hypertrophy (CH), an antecedent condition to HF where NQO1 downregulation stems from the loss of the distal-specific transcript. The loss of NQO1 during hypertrophy was rescued by ectopic expression of the distal- but not the proximal- or middle-specific NQO1 mRNA isoforms in the presence of Star-PAP expression, and reverses molecular events of hypertrophy in cardiomyocytes.
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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.