ArticlePloS one2011
hnRNP A1 and hnRNP F modulate the alternative splicing of exon 11 of the insulin receptor gene.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
46 citing papers in PubMed, 69 citations in OpenAlex.
- Review
- Nonsense-mediated mRNA decay and associated splicing patterns in neurodevelopmental disorders.Frontiers in molecular biosciences · 2026Review
- Comparative Transcriptomic Analysis Reveals Key Growth-Related Genes and Alternative Splicing Events in Siniperca scherzeri.Marine biotechnology (New York, N.Y.) · 2025Article
- Review
- Identification of Highly Repetitive Enhancers with Long-range Regulation Potential in Barley via STARR-seq.Genomics, proteomics & bioinformatics · 2024Article
- Insulin receptor alternative splicing in breast and prostate cancer.Cancer cell international · 2024Review
- Exploring the interplay between PARP1 and circRNA biogenesis and function.Wiley interdisciplinary reviews. RNA · 2023Review
- Insulin Receptor Isoforms and Insulin Growth Factor-like Receptors: Implications in Cell Signaling, Carcinogenesis, and Chemoresistance.International journal of molecular sciences · 2023Review
- The RNA-binding protein hnRNP F is required for the germinal center B cell response.Nature communications · 2023Article
- hnRNP A1 in RNA metabolism regulation and as a potential therapeutic target.Frontiers in pharmacology · 2022Review
- Current Studies on Molecular Mechanisms of Insulin Resistance.Journal of diabetes research · 2022Review
- PRMT5 Promotes Symmetric Dimethylation of RNA Processing Proteins and Modulates Activated T Cell Alternative Splicing and CaImmunoHorizons · 2021Article
- Mass Spectrometry-Based Proteomic Discovery of Prognostic Biomarkers in Adrenal Cortical Carcinoma.Cancers · 2021Article
- The RNA-binding protein Igf2bp3 is critical for embryonic and germline development in zebrafish.PLoS genetics · 2021Article
- Review
- Isoform- and Paralog-Switching in IR-Signaling: When Diabetes Opens the Gates to Cancer.Biomolecules · 2020Review
- Hyperinsulinaemia in cancer.Nature reviews. Cancer · 2020Review
- Multilateral Bioinformatics Analyses Reveal the Function-Oriented Target Specificities and Recognition of the RNA-Binding Protein SFPQ.iScience · 2020Article
- Alternative Splicing Enhances the Transcriptome Complexity ofFrontiers in plant science · 2020Article
- The Role of RNA Splicing Factors in Cancer: Regulation of Viral and Human Gene Expression in Human Papillomavirus-Related Cervical Cancer.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Exon 11 of the insulin receptor gene (INSR) is alternatively spliced in a developmentally and tissue-specific manner. Linker scanning mutations in a 5' GA-rich enhancer in intron 10 identified AGGGA sequences that are important for enhancer function. Using RNA-affinity purification and mass spectrometry, we identified hnRNP F and hnRNP A1 binding to these AGGGA sites and also to similar motifs at the 3' end of the intron. The hnRNPs have opposite functional effects with hnRNP F promoting and hnRNP A1 inhibiting exon 11 inclusion, and deletion of the GA-rich elements eliminates both effects. We also observed specific binding of hnRNP A1 to the 5' splice site of intron 11. The SR protein SRSF1 (SF2/ASF) co-purified on the GA-rich enhancer and, interestingly, also competes with hnRNP A1 for binding to the splice site. A point mutation -3U→C decreases hnRNP A1 binding, increases SRSF1 binding and renders the exon constitutive. Lastly, our data point to a functional interaction between hnRNP F and SRSF1 as a mutant that eliminates SRSF1 binding to exon 11, or a SRSF1 knockdown, which prevents the stimulatory effect of hnRNP F over expression.
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What OpenQuestion holds
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.