ArticleFrontiers in cell and developmental biology2022
Increased Aurora B expression reduces substrate phosphorylation and induces chromosomal instability.
Article in Frontiers in cell and developmental biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Epigenetic Factor Dysregulation and Distinct Expression Signatures in Retinoblastoma: A Transcriptomic Analysis.Investigative ophthalmology & visual science · 2026Article
- An optimum rate of microtubule flux for error correction in metaphase spindle.Life science alliance · 2026Article
- Linking kinetochore attachment to checkpoint control: the role of Aurora B in BubR1 acetylation.Nucleic acids research · 2026Article
- Aurora kinase B as a therapeutic target in HPV-induced cervical cancer: mechanisms and future perspectives.Frontiers in oncology · 2026Review
- SPC24 boosts tumor progression and correlates with immune infiltrates in pancreatic adenocarcinoma.Frontiers in oncology · 2026Article
- Aurora B and INCENP co-overexpression severely disrupts mitosis and distinctly modifies the global transcriptional landscape.iScience · 2025Article
- Aurora kinases signaling in cancer: from molecular perception to targeted therapies.Molecular cancer · 2025Review
- Optimal strategies for correcting merotelic chromosome attachments in anaphase.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- RUNX3 exerts tumor-suppressive role through inhibiting EXOSC4 expression.Functional & integrative genomics · 2024Article
- Aurora-B: a novel biomarker in the invasion and metastasis of osteosarcoma.Biomarkers in medicine · 2024Review
- Double-checking chromosome segregation.The Journal of cell biology · 2023Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Increased Aurora B protein expression, which is common in cancers, is expected to increase Aurora B kinase activity, yielding elevated phosphorylation of Aurora B substrates. In contrast, here we show that elevated expression of Aurora B reduces phosphorylation of six different Aurora B substrates across three species and causes defects consistent with Aurora B inhibition. Complexes of Aurora B and its binding partner INCENP autophosphorylate in trans to achieve full Aurora B activation. Increased expression of Aurora B mislocalizes INCENP, reducing the local concentration of Aurora B:INCENP complexes at the inner centromere/kinetochore. Co-expression of INCENP rescues Aurora B kinase activity and mitotic defects caused by elevated Aurora B. However, INCENP expression is not elevated in concert with Aurora B in breast cancer, and increased expression of Aurora B causes resistance rather than hypersensitivity to Aurora B inhibitors. Thus, increased Aurora B expression reduces, rather than increases, Aurora B kinase activity.
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Registered trials
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