ArticleCell cycle (Georgetown, Tex.)2013
Glycogen synthase kinase 3 β activity is required for hBora/Aurora A-mediated mitotic entry.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- BORA regulates cell proliferation and migration in bladder cancer.Cancer cell international · 2020Article
- Article
- Off-target based drug repurposing opportunities for tivantinib in acute myeloid leukemia.Scientific reports · 2019Article
- Characterization of Apoptosis in a Breast Cancer Cell Line after IL-10 SilencingAsian Pacific journal of cancer prevention : APJCP · 2018Article
- Self-oligomerization regulates stability of survival motor neuron protein isoforms by sequestering an SCFMolecular biology of the cell · 2018Article
- Inhibition of Polo-like kinase 1 during the DNA damage response is mediated through loss of Aurora A recruitment by Bora.Oncogene · 2017Article
- Mitotic entry: The interplay between Cdk1, Plk1 and Bora.Cell cycle (Georgetown, Tex.) · 2016Article
- Deciphering the Interplay among Multisite Phosphorylation, Interaction Dynamics, and Conformational Transitions in a Tripartite Protein System.ACS central science · 2016Article
- Cdk1 plays matchmaker for the Polo-like kinase and its activator SPAT-1/Bora.Cell cycle (Georgetown, Tex.) · 2015Article
- Landscape of Pin1 in the cell cycle.Experimental biology and medicine (Maywood, N.J.) · 2015Review
- Bora downregulation results in radioresistance by promoting repair of double strand breaks.PloS one · 2015Article
- GSK3 inhibitors stabilize Wee1 and reduce cerebellar granule cell progenitor proliferation.Cell cycle (Georgetown, Tex.) · 2015Article
- Phosphorylation-mediated stabilization of Bora in mitosis coordinates Plx1/Plk1 and Cdk1 oscillations.Cell cycle (Georgetown, Tex.) · 2014Article
- BRCA1 downregulates the kinase activity of Polo-like kinase 1 in response to replication stress.Cell cycle (Georgetown, Tex.) · 2013Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The synthesis and degradation of hBora is important for the regulation of mitotic entry and exist. In G 2 phase, hBora can complex with Aurora A to activate Plk1 and control mitotic entry. However, whether the post-translational modification of hBora is relevant to the mitotic entry still unclear. Here, we used the LC-MS/MS phosphopeptide mapping assay to identify 13 in vivo hBora phosphorylation sites and characterized that GSK3β can interact with hBora and phosphorylate hBora at Ser274 and Ser278. Pharmacological inhibitors of GSK3β reduced the retarded migrating band of hBora in cells and diminished the phosphorylation of hBora by in vitro kinase assay. Moreover, as well as in GSK3β activity-inhibited cells, specific knockdown of GSK3β by shRNA and S274A/S278 hBora mutant-expressing cells also exhibited the reduced Plk1 activation and a delay in mitotic entry. It suggests that GSK3β activity is required for hBora-mediated mitotic entry through Ser274 and Ser278 phosphorylation.
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