ArticleThe Biochemical journal2003
Differential effects of hyperphosphorylation on splicing factor SRp55.
Article in The Biochemical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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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Who cites it
20 citing papers in PubMed, 43 citations in OpenAlex.
- C9ORF72 poly-PR disrupts expression of ALS/FTD-implicated STMN2 through SRSF7.Acta neuropathologica communications · 2025Article
- Review
- Opposing roles of CLK SR kinases in controlling HIV-1 gene expression and latency.Retrovirology · 2022Article
- Targeting Splicing Factor SRSF6 for Cancer Therapy.Frontiers in cell and developmental biology · 2021Review
- Cdc-Like Kinases (CLKs): Biology, Chemical Probes, and Therapeutic Potential.International journal of molecular sciences · 2020Review
- Exploiting differential RNA splicing patterns: a potential new group of therapeutic targets in cancer.Expert opinion on therapeutic targets · 2018Review
- Overexpression of Antiangiogenic Vascular Endothelial Growth Factor Isoform and Splicing Regulatory Factors in Oral, Laryngeal and Pharyngeal Squamous Cell CarcinomasAsian Pacific journal of cancer prevention : APJCP · 2017Article
- Therapeutic targeting of splicing in cancer.Nature medicine · 2016Review
- Article
- Inhibitors of CLK protein kinases suppress cell growth and induce apoptosis by modulating pre-mRNA splicing.PloS one · 2015Article
- VEGF gene alternative splicing: pro- and anti-angiogenic isoforms in cancer.Journal of cancer research and clinical oncology · 2012Review
- Acetylation and phosphorylation of SRSF2 control cell fate decision in response to cisplatin.The EMBO journal · 2011Article
- DDX3 regulates cell growth through translational control of cyclin E1.Molecular and cellular biology · 2010Article
- Akt2 regulation of Cdc2-like kinases (Clk/Sty), serine/arginine-rich (SR) protein phosphorylation, and insulin-induced alternative splicing of PKCbetaII messenger ribonucleic acid.Endocrinology · 2009Article
- Control of alternative splicing by signal-dependent degradation of splicing-regulatory proteins.The Journal of biological chemistry · 2009Article
- Regulation of SR protein phosphorylation and alternative splicing by modulating kinetic interactions of SRPK1 with molecular chaperones.Genes & development · 2009Article
- Expression of pro- and anti-angiogenic isoforms of VEGF is differentially regulated by splicing and growth factors.Journal of cell science · 2008Article
- Protein kinase C-dependent control of Bcl-x alternative splicing.Molecular and cellular biology · 2007Article
- Exon selection in alpha-tropomyosin mRNA is regulated by the antagonistic action of RBM4 and PTB.Molecular and cellular biology · 2005Article
- RNA polymerase II carboxy-terminal domain phosphorylation is required for cotranscriptional pre-mRNA splicing and 3'-end formation.Molecular and cellular biology · 2004Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Members of the serine/arginine-rich (SR) protein family play an important role in both constitutive and regulated splicing of precursor mRNAs. Phosphorylation of the arginine/serine dipeptide-rich domain (RS domain) can modulate the activity and the subcellular localization of SR proteins. However, whether the SR protein family members are individually regulated and how this is achieved remain unclear. In this report we show that 5,6-dichloro-1 beta-D-ribofuranosyl-benzimidazole (DRB), an inhibitor of RNA polymerase II-dependent transcription, specifically induced hyperphosphorylation of SRp55 but not that of any other SR proteins tested. Hyperphosphorylation of SRp55 occurs at the RS domain and appears to require the RNA-binding activity. Upon DRB treatment, hyperphosphorylated SRp55 relocates to enlarged nuclear speckles. Intriguingly, SRp55 is specifically targeted for degradation by the proteasome upon overexpression of the SR protein kinase Clk/Sty. Although a destabilization signal is mapped within the C-terminal 43-amino acid segment of SRp55, its adjacent lysine/serine-rich RS domain is nevertheless critical for the Clk/Sty-mediated degradation. We report for the first time that SRp55 can be hyperphosphorylated under different circumstances whereby its fate is differentially influenced.
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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.