Aurora A is a member of the Aurora/Ipl1-related kinase family, a family of serine/threonine kinases crucial for cell cycle control. The first Aurora kinase was discovered in Drosophila
(1). Mutations of this kinase cause monopolar spindles surrounded by kinase, and the appearance of this was reminiscent of the Aurora borealis at the poles of the earth (1). Mammals express three closely related Aurora kinases, specifically Aurora A, Aurora B, and Aurora C. To download a sequence alignment of the 3 human Aurora proteins go here
. Aurora A is overexpressed in various types of cancer and considered to play critical roles in tumorigenesis (2,3). Overexpression of Aurora A overrides the cell cycle checkpoint, interferes with mitotic exit (4), and induces transformation in mammalian cells (2,3). In contrast, silencing of Aurora A interrupts centrosome seperation, spindle assembly and arrests G2-M transition in C. elegans
and human cells (5,6). Moreover, Aurora A plays an essential role for neuronal migration by modulation of microtubule organization and is required for normal axon formation (7,8). Aurora A is activated by phosphorylation at Thr-288 and activated Aurora A phosphorylates numerous target proteins including p53, TPX2 and BRCA1. Expression of Aurora A is cell-cycle regulated, low in G1/S, accumulates during G2/M, and decreases rapidly afterwards. Aurora A localizes next to the centrosome late in the G1/S phase. As the cell cycle progresses, Aurora A associates with the mitotic poles and the adjacent spindle microtubules. It remains associated with the spindles through telophase and relocalizes to the mid-zone of the spindle right before mitotic exit (9). Monoclonal antibody MCA-1A11 was raised against full length recombinant human Aurora A expressed in and purified from E. coli
. The antibody was tested for binding to recombinant human Aurora A, B, C and shown to react with only Aurora A and without cross-reaction with Aurora B and C (see Blot image). The HGNC
name for this protein is AURKA
1. Glover DM, Leibowitz MH, McLean DA, Parry H. Mutations in aurora prevent centrosome separation leading to the formation of monopolar spindles. Cell 81:95-105 (1995).
2. Bischoff JR, Anderson L, Zhu Y, et al. A homologue of Drosophila aurora kinase is oncogenic and amplified in human colorectal cancers. EMBO J. 17:3052-65 (1998).
3. Zhou H, Kuang J, Zhong L, et al. Tumour amplified kinase STK15/BTAKinduces centrosome amplification, aneuploidy and transformation. Nat. Genet. 20:189-93 (1998).
4. Marumoto T, Hirota T, Morisaki T, Kunitoku N, Zhang D, Ichikawa Y, Sasayama T, Kuninaka S, Mimori T, Tamaki N, Kimura M, Okano, Roles of aurora-A kinase in mitotic entry and G2 checkpoint in mammalian cells. Genes Cells 7: 1173-1182 (2002).
5. Hannak E, Kirkham M, Hyman AA, Oegema K. Aurora-A kinase is required
for centrosome maturation in Caenorhabditis elegans. J. Cell Biol. 155:1109-16 (2001).
6. Du J, Hannon GJ. Suppression of p160ROCK bypasses cell cycle arrest after
Aurora-A/STK15 depletion. Proc Natl Acad Sci U S A 101:8975-80 (2004).
7. Mori D, Yamada M, Mimori-Kiyosue Y, Shirai Y, Suzuki A, Ohno S, Saya H, Wynshaw-Boris A, Hirotsune S. An essential role of the aPKC-Aurora A-NDEL1 pathway in neurite elongation by modulation of microtubule dynamics. Nat Cell Biol. 11(9):1057-68 (2009) Nat. Cell Biol.11(9):1057-68(2009).
8. Takitoh T, Kumamoto K,Toba S, Wynshaw-Boris A, Hiroutsune S. Activation of Aurora-A is essential for neuronal migration via modulation of microtubule organization. J. Neurosci. 32(32):11050-66 (2012).
9. Marumoto T, Honda S, Hara T, Nitta M, Hirota T, Kohmura E, Saya H. Aurora-A kinase maintains the fidelity of early and late mitotic events in HeLa cells. J. Biol. Chem. 278(51): 5178-95 (2003).