ArticleJournal of virology2013
Dissection of the C-terminal region of E1A redefines the roles of CtBP and other cellular targets in oncogenic transformation.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- CtBP promoted P4HB mediates SLC7A11 maturation to confer ferroptosis resistance in triple-negative breast cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- Reciprocal stabilization of CtBP and TRIM28 represses autophagy to promote metastasis.Nature structural & molecular biology · 2025Article
- DYRK1A in blood and immune function: implications in leukemia, inflammatory disorders, infection and Down syndrome.Frontiers in cell and developmental biology · 2025Review
- Article
- Adenovirus E1A binding to DCAF10 targets proteasomal degradation of RUVBL1/2 AAA+ ATPases required for quaternary assembly of multiprotein machines, innate immunity, and responses to metabolic stress.Journal of virology · 2023Article
- High-throughput discovery and characterization of viral transcriptional effectors in human cells.Cell systems · 2023Article
- DYRK1A promotes viral entry of highly pathogenic human coronaviruses in a kinase-independent manner.PLoS biology · 2023Article
- Metabolic modulation of CtBP dimeric status impacts the repression of DNA damage repair genes and the platinum sensitivity of ovarian cancer.International journal of biological sciences · 2023Article
- Insights from the protein interaction Universe of the multifunctional "Goldilocks" kinase DYRK1A.Frontiers in cell and developmental biology · 2023Review
- Interplay Between CMGC Kinases Targeting SR Proteins and Viral Replication: Splicing and Beyond.Frontiers in microbiology · 2021Review
- NAD-linked mechanisms of gene de-repression and a novel role for CtBP in persistent adenovirus infection of lymphocytes.Virology journal · 2019Article
- C-Terminus of E1A Binding Protein 1 Stimulates Malignant Phenotype in Human Hepatocellular Carcinoma.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Review
- DYRK1A regulates the recruitment of 53BP1 to the sites of DNA damage in part through interaction with RNF169.Cell cycle (Georgetown, Tex.) · 2019Article
- Molecular Evolution of Human Adenovirus (HAdV) Species C.Scientific reports · 2019Article
- The Transcriptional Repressor BS69 is a Conserved Target of the E1A Proteins from Several Human Adenovirus Species.Viruses · 2018Article
- Review
- Article
- Article
- The Adenovirus E1A C Terminus Suppresses a Delayed Antiviral Response and Modulates RAS Signaling.Cell host & microbe · 2017Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Human adenovirus E1A makes extensive connections with the cellular protein interaction network. By doing so, E1A can manipulate many cellular programs, including cell cycle progression. Through these reprogramming events, E1A functions as a growth-promoting oncogene and has been used extensively to investigate mechanisms contributing to oncogenesis. Nevertheless, it remains unclear how the C-terminal region of E1A contributes to oncogenic transformation. Although this region is required for transformation in cooperation with E1B, it paradoxically suppresses transformation in cooperation with activated Ras. Previous analysis has suggested that the interaction of E1A with CtBP plays a pivotal role in both activities. However, some C-terminal mutants of E1A retain CtBP binding and yet exhibit defects in transformation, suggesting that other targets of this region are also necessary. To explore the roles of these additional factors, we performed an extensive mutational analysis of the C terminus of E1A. We identified key residues that are specifically required for binding all known targets of the C terminus of E1A. We further tested each mutant for the ability to both localize to the nucleus and transform primary rat cells in cooperation with E1B-55K or Ras. Interaction of E1A with importin α3/Qip1, dual-specificity tyrosine-regulated kinase 1A (DYRK1A), HAN11, and CtBP influenced transformation with E1B-55K. Interestingly, the interaction of E1A with DYRK1A and HAN11 appeared to play a role in suppression of transformation by activated Ras whereas interaction with CtBP was not necessary. This unexpected result suggests a need for revision of current models and provides new insight into transformation by the C terminus of E1A.
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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.