ArticleEMBO reports2002
Functional inactivation of the SR family of splicing factors during a vaccinia virus infection.
Article in EMBO reports, 2002. 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, 38 citations in OpenAlex.
- Viral Modulation of Host Splicing.Annual review of virology · 2025Review
- Multi-omics characterization of the monkeypox virus infection.Nature communications · 2024Article
- Transcriptome Changes in Glioma Cells upon Infection with the Oncolytic Virus VV-GMCSF-Lact.Cells · 2023Article
- Virologs, viral mimicry, and virocell metabolism: the expanding scale of cellular functions encoded in the complex genomes of giant viruses.FEMS microbiology reviews · 2023Article
- Virus usurps alternative splicing to clear the decks for infection.Virology journal · 2023Review
- Serine-arginine protein kinases and their targets in viral infection and their inhibition.Cellular and molecular life sciences : CMLS · 2023Review
- Opposing roles of CLK SR kinases in controlling HIV-1 gene expression and latency.Retrovirology · 2022Article
- Vaccinia Virus as a Master of Host Shutoff Induction: Targeting Processes of the Central Dogma and Beyond.Pathogens (Basel, Switzerland) · 2020Review
- Viral modulation of cellular RNA alternative splicing: A new key player in virus-host interactions?Wiley interdisciplinary reviews. RNA · 2019Review
- A Cytoplasmic RNA Virus Alters the Function of the Cell Splicing Protein SRSF2.Journal of virology · 2017Article
- Regulation of human adenovirus alternative RNA splicing by the adenoviral L4-33K and L4-22K proteins.International journal of molecular sciences · 2015Review
- Protein kinase a-dependent phosphorylation of serine 119 in the proto-oncogenic serine/arginine-rich splicing factor 1 modulates its activity as a splicing enhancer protein.Genes & cancer · 2011Article
- Promotion of exon 6 inclusion in HuD pre-mRNA by Hu protein family members.Nucleic acids research · 2010Article
- Functional interplay between viral and cellular SR proteins in control of post-transcriptional gene regulation.The FEBS journal · 2009Review
- The E1circumflexE4 protein of human papillomavirus interacts with the serine-arginine-specific protein kinase SRPK1.Journal of virology · 2007Article
- Utilization of host SR protein kinases and RNA-splicing machinery during viral replication.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Acetylated Tat regulates human immunodeficiency virus type 1 splicing through its interaction with the splicing regulator p32.Journal of virology · 2006Article
- Chironomus tentans-repressor splicing factor represses SR protein function locally on pre-mRNA exons and is displaced at correct splice sites.Molecular biology of the cell · 2006Article
- Dilated cardiomyopathy caused by tissue-specific ablation of SC35 in the heart.The EMBO journal · 2004Article
- Convergence of RNA cis elements and cellular polyadenylation factors in the regulation of human cytomegalovirus UL37 exon 1 unspliced RNA production.Journal of virology · 2003Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
SR proteins are essential splicing factors required for constitutive splicing and function as key regulators of alternative RNA splicing. We have shown that SR proteins purified from late adenovirus-infected cells (SR-Ad) are functionally inactivated as splicing enhancer or splicing repressor proteins by a virus-induced partial de-phosphorylation. Here, we show that SR proteins purified from late vaccinia-virus-infected cells (SR-VV) are also hypo-phosphorylated and functionally inactivated as splicing regulatory proteins. We further show that incubating SR-Ad proteins under conditions that restore the phospho-epitopes to the SR proteins results in the restoration of their activity as splicing enhancer and splicing repressor proteins. Interestingly, re-phosphorylation of SR-VV proteins only partially restored the splicing enhancer or splicing repressor phenotype to the SR proteins. Collectively, our results suggest that viral control of SR protein activity may be a common strategy used by DNA viruses to take control of the host cell RNA splicing machinery.
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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.