Adenovirus and cell cycle control
- PMID: 11991831
- DOI: 10.2741/ben
Adenovirus and cell cycle control
Abstract
Adenovirus infection of quiescent cells induces transition from G0 or G1 into the S phase of the cell cycle and allows cellular proliferation. This is beneficial for the virus since cells in S phase provide optimal conditions for viral replication. Adenovirus E1A, E1B and E4 gene products contribute to cell cycle deregulation. E1A proteins inactivate the pRb checkpoint, allowing the E2F transcription factor to activate genes involved in nucleotide metabolism and DNA replication, which are required in S phase. E1A also interacts with transcriptional modulators, including histone acetyltransferases, histone deacetylases, and other chromatin remodeling factors. These interactions affect transcription of several cellular and viral genes, some of which are involved in cell cycle regulation. Cell cycle deregulation by E1A results in stabilization and accumulation of p53. To prevent cell cycle arrest and apoptosis that would be triggered by p53, the adenovirus E1B and E4orf6 gene products employ various mechanisms to inactivate the tumor suppressor. Additional E4 gene products also interact with and modulate cell cycle regulators. Cell cycle checkpoints targeted by adenovirus proteins are often compromised in human tumors as well. Thus, understanding the interactions between adenovirus and the cell cycle has facilitated the generation of adenovirus mutants, which can replicate only in cells with inactivated checkpoints. Such "oncolytic" viruses are being tested for their ability to specifically replicate in and lyse cancer cells.
Similar articles
-
The role of p53 in coordinated regulation of cyclin D1 and p21 gene expression by the adenovirus E1A and E1B oncogenes.Oncogene. 1995 Jun 15;10(12):2421-5. Oncogene. 1995. PMID: 7784093
-
Recent lessons in gene expression, cell cycle control, and cell biology from adenovirus.Oncogene. 2005 Nov 21;24(52):7673-85. doi: 10.1038/sj.onc.1209040. Oncogene. 2005. PMID: 16299528 Review.
-
Genetically modified adenoviruses against gliomas: from bench to bedside.Neurology. 2004 Aug 10;63(3):418-26. doi: 10.1212/01.wnl.0000133302.15022.7f. Neurology. 2004. PMID: 15304571 Review.
-
E1B55K-deleted adenovirus (ONYX-015) overrides G1/S and G2/M checkpoints and causes mitotic catastrophe and endoreduplication in p53-proficient normal cells.Cell Cycle. 2006 Oct;5(19):2244-52. doi: 10.4161/cc.5.19.3263. Epub 2006 Oct 1. Cell Cycle. 2006. PMID: 16969092
-
DNA replication of first-generation adenovirus vectors in tumor cells.Hum Gene Ther. 2000 Sep 1;11(13):1933-48. doi: 10.1089/10430340050129549. Hum Gene Ther. 2000. PMID: 10986565
Cited by
-
Adenovirus with DNA Packaging Gene Mutations Increased Virus Release.Viruses. 2016 Dec 20;8(12):333. doi: 10.3390/v8120333. Viruses. 2016. PMID: 27999391 Free PMC article.
-
Adenovirus E4orf4 hijacks rho GTPase-dependent actin dynamics to kill cells: a role for endosome-associated actin assembly.Mol Biol Cell. 2006 Jul;17(7):3329-44. doi: 10.1091/mbc.e05-12-1146. Epub 2006 May 10. Mol Biol Cell. 2006. PMID: 16687574 Free PMC article.
-
Role of E1B55K in E4orf6/E1B55K E3 ligase complexes formed by different human adenovirus serotypes.J Virol. 2013 Jun;87(11):6232-45. doi: 10.1128/JVI.00384-13. Epub 2013 Mar 27. J Virol. 2013. PMID: 23536656 Free PMC article.
-
Development of an Oncolytic Adenovirus with Enhanced Spread Ability through Repeated UV Irradiation and Cancer Selection.Viruses. 2016 Jun 14;8(6):167. doi: 10.3390/v8060167. Viruses. 2016. PMID: 27314377 Free PMC article.
-
Production of rAAV by plasmid transfection induces antiviral and inflammatory responses in suspension HEK293 cells.Mol Ther Methods Clin Dev. 2023 Jan 16;28:272-283. doi: 10.1016/j.omtm.2023.01.002. eCollection 2023 Mar 9. Mol Ther Methods Clin Dev. 2023. PMID: 36819978 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Other Literature Sources
Research Materials
Miscellaneous