ArticleMolecular biology of the cell2008
Id1 overexpression induces tetraploidization and multiple abnormal mitotic phenotypes by modulating aurora A.
Article in Molecular biology of the cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Deletion of a core APC/C component reveals APC/C function in regulating neuronal USP1 levels and morphology.Frontiers in molecular neuroscience · 2024Article
- ATAD5 suppresses centrosome over-duplication by regulating UAF1 and ID1.Cell cycle (Georgetown, Tex.) · 2020Article
- A novel role for the deubiquitinase USP1 in the control of centrosome duplication.Cell cycle (Georgetown, Tex.) · 2016Article
- Niche-Based Screening in Multiple Myeloma Identifies a Kinesin-5 Inhibitor with Improved Selectivity over Hematopoietic Progenitors.Cell reports · 2015Article
- Aurora-A inactivation causes mitotic spindle pole fragmentation by unbalancing microtubule-generated forces.Molecular cancer · 2011Article
- Illicit survival of cancer cells during polyploidization and depolyploidization.Cell death and differentiation · 2011Review
- Id1 interacts and stabilizes the Epstein-Barr virus latent membrane protein 1 (LMP1) in nasopharyngeal epithelial cells.PloS one · 2011Article
- Inhibitor of differentiation 1 (ID1) promotes cell survival and proliferation of prostate epithelial cells.Cellular & molecular biology letters · 2010Article
- Elevated endogenous expression of the dominant negative basic helix-loop-helix protein ID1 correlates with significant centrosome abnormalities in human tumor cells.BMC cell biology · 2010Article
- Temporal profiling of rat transcriptomes in retinol-replenished vitamin A-deficient testis.Systems biology in reproductive medicine · 2009Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The basic helix-loop-helix transcription factor, Id1, was shown to induce tetraploidy in telomerase-immortalized nasopharyngeal epithelial cells in this study. Using both transient and stable Id1-expressing cell models, multiple mitotic aberrations were detected, including centrosome amplification, binucleation, spindle defects, and microtubule perturbation. Many of these abnormal phenotypes have previously been reported in cells overexpressing Aurora A. Further experiments showed that Id1 could stabilize Aurora A, whereas knocking down Aurora A expression in Id1-expressing cells could rescue some of the mitotic defects. The mechanisms by which Aurora A could be modulated by Id1 were explored. DNA amplification of the Aurora A locus was not involved. Id1 could only weakly activate the transcriptional activity of the Aurora A promoter. We found that Id1 overexpression could affect Aurora A degradation, leading to its stabilization. Aurora A is normally degraded from mitosis exit by the APC/C(Cdh1)-mediated proteasomal proteolysis pathway. Our results revealed that Id1 and Cdh1 are binding partners. The association of Id1 and Cdh1 was found to be dependent on the canonical destruction box motif of Id1, the increased binding of which may compete with the interaction between Cdh1 and Aurora A, leading to stabilization of Aurora A in Id1-overexpressing cells.
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