ArticleJournal of virology2003
Interactions between human cytomegalovirus IE1-72 and cellular p107: functional domains and mechanisms of up-regulation of cyclin E/cdk2 kinase activity.
Article in Journal of virology, 2003. 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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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
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- Revisiting promyelocytic leukemia protein targeting by human cytomegalovirus immediate-early protein 1.PLoS pathogens · 2020Article
- The DNA damage response induced by infection with human cytomegalovirus and other viruses.Viruses · 2014Review
- Identification of cellular proteins that interact with human cytomegalovirus immediate-early protein 1 by protein array assay.Viruses · 2013Article
- Polycomb repressive complex 2 targets murine cytomegalovirus chromatin for modification and associates with viral replication centers.PloS one · 2012Article
- Transcriptional activation of endoplasmic reticulum chaperone GRP78 by HCMV IE1-72 protein.Cell research · 2011Article
- B55alpha PP2A holoenzymes modulate the phosphorylation status of the retinoblastoma-related protein p107 and its activation.The Journal of biological chemistry · 2010Article
- The human cytomegalovirus major immediate-early proteins as antagonists of intrinsic and innate antiviral host responses.Viruses · 2009Article
- Human cytomegalovirus IE1-72 protein interacts with p53 and inhibits p53-dependent transactivation by a mechanism different from that of IE2-86 protein.Journal of virology · 2009Article
- Regulation of the retinoblastoma proteins by the human herpesviruses.Cell division · 2009Article
- Human cytomegalovirus IE1 protein enhances herpes simplex virus type 1-induced syncytial formation in U373MG cells.Journal of Korean medical science · 2008Article
- Binding STAT2 by the acidic domain of human cytomegalovirus IE1 promotes viral growth and is negatively regulated by SUMO.Journal of virology · 2008Article
- Cell cycle-independent expression of immediate-early gene 3 results in G1 and G2 arrest in murine cytomegalovirus-infected cells.Journal of virology · 2008Article
- Human cytomegalovirus UL97 kinase activity is required for the hyperphosphorylation of retinoblastoma protein and inhibits the formation of nuclear aggresomes.Journal of virology · 2008Article
- Evidence that the human cytomegalovirus IE2-86 protein binds mdm2 and facilitates mdm2 degradation.Journal of virology · 2006Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Previous work has demonstrated that the human cytomegalovirus IE1-72 protein is able to bind to the N terminus of p107, and IE1-72 alone is sufficient for alleviation of p107-mediated cell growth suppression. However, the mechanism of this alleviation is unclear. Here, we show that IE1-72 can alleviate p107 inhibition of cyclin E/cdk2 kinase activity. We cotransfected various IE1-72 and p107 constructs into C33A cells and demonstrated that IE1-72 could activate the kinase activity of cyclin E/cdk2. Conversely, IE2-86 did not activate this activity, suggesting that the interaction between p107 and IE1-72 and the subsequent kinase activation are specific. By the use of a series of deletion and point mutants of IE1-72 and p107, we observed that a mutation of the loop region of helix-loop-helix-turn-helix in exon 3 of IE1-72 as well as a mutation of the leucine zipper-2 region in exon 4 of IE1-72 abolished binding to p107. In addition, these two IE1-72 mutants did not alleviate p107 inhibition of cyclin E/cdk2 kinase activity and also failed to alleviate p107 inhibition of the E2F-responsive promoter. Meanwhile, deletion of the N-terminal aa 1 to 175 of p107 abolished both p107 binding with IE1-72 and p107 inhibition of cyclin E/cdk2 kinase activity. This result confirms that the N-terminus aa 1 to 175 region of p107 is a common region where both IE1-72 protein and cyclin E/cdk2 bind. We propose a mechanism in which binding of IE1-72 to p107 displaces cyclin E/cdk2 from p107. Once released from p107, cyclin E/cdk2 is able to function as an active kinase.
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