ArticleProceedings of the National Academy of Sciences of the United States of America2007
Intranuclear targeting and nuclear export of the adenovirus E1B-55K protein are regulated by SUMO1 conjugation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 97 citations in OpenAlex.
- The adenovirus oncoprotein E1B-55K reshapes epigenetic histone modifications in primary human cells.mBio · 2026Article
- Adenovirus E1B-55K regulates p53-dependent and -independent gene expression during infection.PLoS pathogens · 2025Article
- Adenovirus E1B-55K interferes with cellular IκB kinase complex subunit proteins.Frontiers in immunology · 2025Article
- Nanopore guided annotation of transcriptome architectures.mSystems · 2024Article
- The human adenovirus PI3K-Akt activator E4orf1 is targeted by the tumor suppressor p53.Journal of virology · 2024Article
- Nanopore Guided Annotation of Transcriptome Architectures.bioRxiv : the preprint server for biology · 2024Article
- Viral Subversion of the Chromosome Region Maintenance 1 Export Pathway and Its Consequences for the Cell Host.Viruses · 2023Review
- The human adenovirus E1B-55K oncoprotein coordinates cell transformation through regulation of DNA-bound host transcription factors.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The adenoviral E4orf3/4 is a regulatory polypeptide with cell transforming properties in vitro.Tumour virus research · 2023Article
- Article
- PML Alternative Splice Products Differentially Regulate HAdV Productive Infection.Microbiology spectrum · 2022Article
- Article
- SUMOylation in Viral Replication and Antiviral Defense.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Review
- Protein-Protein Interactions Facilitate E4orf6-Dependent Regulation of E1B-55K SUMOylation in HAdV-C5 Infection.Viruses · 2022Article
- Conserved E1B-55K SUMOylation in Different Human Adenovirus Species Is a Potent Regulator of Intracellular Localization.Journal of virology · 2022Article
- Human Adenovirus Type 5 Infection Leads to Nuclear Envelope Destabilization and Membrane Permeability Independently of Adenovirus Death Protein.International journal of molecular sciences · 2021Article
- Differential Regulation of Cellular FAM111B by Human Adenovirus C Type 5 E1 Oncogenes.Viruses · 2021Article
- A Tale of Usurpation and Subversion: SUMO-Dependent Integrity of Promyelocytic Leukemia Nuclear Bodies at the Crossroad of Infection and Immunity.Frontiers in cell and developmental biology · 2021Review
- Fluorescent protein tagging of adenoviral proteins pV and pIX reveals 'late virion accumulation compartment'.PLoS pathogens · 2020Article
- ATO (Arsenic Trioxide) Effects on Promyelocytic Leukemia Nuclear Bodies Reveals Antiviral Intervention Capacity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have investigated the requirements for CRM1-mediated nuclear export and SUMO1 conjugation of the adenovirus E1B-55K protein during productive infection. Our data show that CRM1 is the major export receptor for E1B-55K in infected cells. Functional inactivation of the E1B-55K CRM1-dependent nuclear export signal (NES) or leptomycin B treatment causes an almost complete redistribution of the viral protein from the cytoplasm to the nucleus and its accumulation at the periphery of the viral replication centers. Interestingly, however, this nuclear restriction imposed on the wild type and the NES mutant protein is fully compensated by concurrent inactivation of the adjacent SUMO1 conjugation site. Moreover, the same mutation fully reverses defects of the NES mutant in the nucleocytoplasmic transport of Mre11 and proteasomal degradation of p53. These results show that nuclear export of E1B-55K in infected cells occurs via CRM1-dependent and -independent pathways and suggest that SUMO1 conjugation and deconjugation provide a molecular switch that commits E1B-55K to a CRM1-independent export pathway.
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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.