ArticleCells2019
Activation of Cryptic 3' Splice-Sites by SRSF2 Contributes to Cassette Exon Skipping.
Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Three exonic variants in theFrontiers in genetics · 2024Article
- SRSF2 plays an unexpected role as reader of mMolecular cell · 2023Article
- Identification and in-silico characterization of splice-site variants from a large cardiogenetic national registry.European journal of human genetics : EJHG · 2023Article
- HBV Enhances Sorafenib Resistance in Hepatocellular Carcinoma by Reducing Ferroptosis via SRSF2-Mediated Abnormal PCLAF Splicing.International journal of molecular sciences · 2023Article
- The Impact of Pro-Inflammatory Cytokines on Alternative Splicing Patterns in Human Islets.Diabetes · 2021Article
- SRSF9 Regulates Cassette Exon Splicing of Caspase-2 by Interacting with Its Downstream Exon.Cells · 2021Article
- Splicing factor SRSF2-centric gene regulation.International journal of biological sciences · 2021Review
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Authors and funding
8 authors.
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Abstract
Here we show that the serine/arginine rich splicing factor 2 (SRSF2) promotes cryptic 3' splice-site (3'AG') usage during cassette exon exclusion in survival of motor neuron (SMN2) minigenes. Deletion of the 3'AG' (3'AG'1), its associated branch point (BP') and polypyrimidine tract (PPT') sequences directs SRSF2 to promote a second 3'AG' (3'AG'2) with less conserved associated region for intron splicing. Furthermore, deletion of both 3'AG'1 and 3'AG'2 and their associated sequences triggered usage of a third 3'AG'3 that has very weak associated sequences. Interestingly, when intron splicing was directed to the 3'AG' cryptic splice-sites, intron splicing from the canonical 3'AG splice-site was reduced along with a decrease in cassette exon inclusion. Moreover, multiple SRSF2 binding sites within the intron are responsible for 3'AG' activation. We conclude that SRSF2 facilitates exon exclusion by activating a cryptic 3'AG' and inhibiting downstream intron splicing.
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