ArticleMolecular and cellular biochemistry2019
The nuclear GSK-3β regulated post-transcriptional processing of mRNA through phosphorylation of SC35.
Article in Molecular and cellular biochemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 6 citations in OpenAlex.
- Poison cassette exon splicing of SRSF6 regulates nuclear speckle dispersal and the response to hypoxia.Nucleic acids research · 2023Article
- Proteomic characterization of post-mortem human brain tissue following ultracentrifugation-based subcellular fractionation.Brain communications · 2022Article
- Splicing factor SRSF2-centric gene regulation.International journal of biological sciences · 2021Review
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Authors and funding
9 authors at 2 institutions in 1 country.
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Abstract
Glycogen synthase kinase-3β (GSK-3β) is a multifunctional serine/threonine kinase and regulates a variety of biological processes. Recent studies show GSK-3β can regulate pre-mRNA processing and transcription through phosphorylation of multiple splicing factors, but the detailed mechanism is still undetermined. In this study, we further proved that GSK-3β could specifically co-localize with SC35 in nuclear speckles depending on its kinase activity. Immunofluorescence and FISH studies showed the activity of nuclear GSK-3β regulated the assembly of nuclear speckles and consequently modulated the post-transcriptional processing of mRNA. In addition, GSK-3β phosphorylated SC35 and promoted its hyperphosphorylation, in which the unique C-terminal sequences were particularly important to efficiently sequential multiple phosphorylation of SC35. Hyperphosphorylated SC35 converged into cluster and lost its ability to perform splicing in nuclear speckles. More importantly, the nuclear GSK-3β activity could be a part of Wnt/β-catenin signaling activation by TCF4 and might take part in embryonic or tumorigenesis of cells.
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