ArticleThe Journal of investigative dermatology2013
Aurora kinase-A deficiency during skin development impairs cell division and stratification.
Article in The Journal of investigative dermatology, 2013. 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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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.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Aurka-Bhlhe41 axis prevents premature aging-like microglial dysfunction and promotes remyelination.Nature communications · 2026Article
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- Predictors for hepatocellular carcinoma recurrence after microwave ablation.Clinical and experimental hepatology · 2020Article
- Tenacigenin B Has Anti-Tumor Effect in Lymphoma by In Vitro and In Vivo Study.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Activation of S6 signaling is associated with cell survival and multinucleation in hyperplastic skin after epidermal loss of AURORA-A Kinase.Cell death and differentiation · 2019Article
- Aurora kinases: novel therapy targets in cancers.Oncotarget · 2017Review
- Epiboly generates the epidermal basal monolayer and spreads the nascent mammalian skin to enclose the embryonic body.Journal of cell science · 2016Article
- Article
- Transient PLK4 overexpression accelerates tumorigenesis in p53-deficient epidermis.Nature cell biology · 2016Article
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Aurora kinase-A (Aurora-A) promotes timely entry into mitosis, centrosome maturation, and formation of bipolar spindles. To address the role of Aurora-A in skin development and homeostasis, we interbred a floxed Aurora-A (Aurora-A(fl)) mouse with the Cre-deleter strain, K14.Cre. Aurora-A(fl/fl);Krt14.Cre (Aurora-A(-/-)) mice died shortly after birth. These mice had translucent skin, and histological evaluation showed that the dorsal skin was very thin and fragile with frank erosions. Although the expression of the basal layer marker keratin 14 and the differentiation marker keratin 1 was evident in Aurora-A(-/-) epidermis, there was a marked reduction in the number of suprabasal layers and basal keratinocytes. Dye exclusion assays also showed defects in barrier function. Unlike wild-type cells, Aurora-A(-/-) basal progenitors were delayed in forming two layers at embryonic day (E)13.5 when embryonic skin begins to stratify. Increased numbers of mitotic cells, apoptotic bodies, and polyploid keratinocytes were evident in Aurora-A(-/-) epidermis, indicating that a deficiency in Aurora-A promotes aberrant mitosis, mitotic slippage, and cell death. Finally, Aurora-A(-/-) keratinocytes displayed centrosomal abnormalities that included centrosomes located at nonapical sites in basal cells. Thus, the deletion of Aurora-A in the developing epidermis alters centrosome function of basal keratinocytes and markedly impairs their ability to divide and stratify.
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Registered trials
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