ArticleCell cycle (Georgetown, Tex.)2014
Role of Cdk1 in DNA damage-induced G1 checkpoint abrogation by the human papillomavirus E7 oncogene.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- An Overview of the Mechanisms of HPV-Induced Cervical Cancer: The Role of Kinase Targets in Pathogenesis and Drug Resistance.Cancers · 2026Review
- The Drivers, Mechanisms, and Consequences of Genome Instability in HPV-Driven Cancers.Cancers · 2022Review
- Linking Coregulated Gene Modules with Polycyclic Aromatic Hydrocarbon-Related Cancer Risk in the 3D Human Bronchial Epithelium.Chemical research in toxicology · 2021Article
- The dysregulation of microarray gene expression in cervical cancer is associated with overexpression of a unique messenger RNA signature.Iranian journal of microbiology · 2020Article
- Identification of hub genes and pathways in glioblastoma by bioinformatics analysis.Oncology letters · 2019Article
- The lysine acetyltransferase GCN5 contributes to human papillomavirus oncoprotein E7-induced cell proliferation via up-regulating E2F1.Journal of cellular and molecular medicine · 2018Article
- Regulator of chromatin condensation 1 abrogates the G1 cell cycle checkpoint via Cdk1 in human papillomavirus E7-expressing epithelium and cervical cancer cells.Cell death & disease · 2018Article
- 3-(2-Chloropropyl amide)-4-methoxy-N-phenylbenzamide inhibits expression of HPV oncogenes in human cervical cancer cell.Virology journal · 2017Article
- MYBL2 (B-Myb): a central regulator of cell proliferation, cell survival and differentiation involved in tumorigenesis.Cell death & disease · 2017Review
- Cdc6 contributes to abrogating the G1 checkpoint under hypoxic conditions in HPV E7 expressing cells.Scientific reports · 2017Article
- Whole exome-wide association study identifies a missense variant in SLC2A4RG associated with glioblastoma risk.American journal of cancer research · 2017Article
- 1-(2-Hydroxy-5-methylphenyl)-3-phenyl-1,3-propanedione Induces G1 Cell Cycle Arrest and Autophagy in HeLa Cervical Cancer Cells.International journal of molecular sciences · 2016Article
- Role of Cdc6 in re-replication in cells expressing human papillomavirus E7 oncogene.Carcinogenesis · 2016Article
- Role of WDHD1 in Human Papillomavirus-Mediated Oncogenesis Identified by Transcriptional Profiling of E7-Expressing Cells.Journal of virology · 2016Article
- Role of dual specificity tyrosine-phosphorylation-regulated kinase 1B (Dyrk1B) in S-phase entry of HPV E7 expressing cells from quiescence.Oncotarget · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
The high-risk human papillomavirus (HPV) E7 oncogene abrogates DNA damage-induced G1 checkpoint but the mechanism is not fully understood. The G1 kinase Cdk2 is activated in E7-expressing cells. However, whether Cdk2 is required for E7 to abrogate the G1 checkpoint is not known. Accumulating evidence implicates a role for the mitotic Cdk1 in G1/S phase transition in the absence of Cdk2. We therefore examined the expression and requirement of Cdk1 and Cdk2 in the G1 checkpoint abrogation in E7-expressing cells. Although both Cdk1 and Cdk2 were up-regulated in E7-expressing cells upon DNA damage, down-regulation of Cdk1 but not Cdk2 impairs the ability of E7 to abrogate the G1 checkpoint. Our study thus demonstrated an important role for Cdk1 in bypassing the G1 checkpoint in E7-expressing cells. To understand the mechanism by which E7 activates Cdk1, we examined the transcription factor B-Myb. Our studies demonstrated that downregulation of B-Myb reduced the steady-state level of Cdk1 and induced G1 arrest in E7-expressing cells upon DNA damage. In addition, it remains a mystery how E7 promotes cell cycle progression in the presence of Cdk inhibitor p21. As p21 binds Cdk1 with lower affinity than Cdk2, our results suggest a mechanism by which E7 bypasses the inhibitory effect of p21. Nonetheless, our studies demonstrated that p21 still possessed partial ability to arrest cells at G1 phase in E7-expressing cells. These studies shed light on mechanisms by which HPV E7 modulates cell cycle checkpoint.
Indexed as
Identifiers
What OpenQuestion holds
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.