Anti-Aurora A

0.5mg/ml if reconstituted with 0.2ml sterile DI water. Aurora kinase A, also called ARK1, AURKA, AIK , AURORA2 ,BTAK, PPP1R47, STK7, STK15, and STK6, is a mitotic centrosomal protein kinase. The main role of AURKA in tumor development is in controlling chromosome segregation during mitosis. Aurora A is a member of a family of mitotic serine/threonine kinases. Cell cycle and Northern blot analyses showed that peak expression of the protein occurs during the G2/M phase and then decreases. By fluorescence in situ hybridization, the gene is represented by 2 signals in chromosome bands 20q13.2-q13.3 and 1q41-q42. It is overexpressed in many human cancers. Ectopic overexpression of Aurora A in mammalian cells induces centrosome amplification, chromosome instability, and oncogenic transformation, a phenotype characteristic of loss-of-function mutations of p53. Depletion of Ajuba prevented activation of AURKA at centrosomes in late G2 phase and inhibited mitotic entry. Activation of the kinase was independently sufficient to induce rapid ciliary resorption, and AURKA acted in this process through phosphorylation of HDAC6, leading to HDAC6-dependent tubulin deacetylation and destabilization of the ciliary axoneme. Protein function: Mitotic serine/threonine kinase that contributes to the regulation of cell cycle progression. Associates with the centrosome and the spindle microtubules during mitosis and plays a critical role in various mitotic events including the establishment of mitotic spindle, centrosome duplication, centrosome separation as well as maturation, chromosomal alignment, spindle assembly checkpoint, and cytokinesis. Required for normal spindle positioning during mitosis and for the localization of NUMA1 and DCTN1 to the cell cortex during metaphase. Required for initial activation of CDK1 at centrosomes. Phosphorylates numerous target proteins, including ARHGEF2, BORA, BRCA1, CDC25B, DLGP5, HDAC6, KIF2A, LATS2, NDEL1, PARD3, PPP1R2, PLK1, RASSF1, TACC3, p53/TP53 and TPX2. Regulates KIF2A tubulin depolymerase activity. Required for normal axon formation. Plays a role in microtubule remodeling during neurite extension. Important for microtubule formation and/or stabilization. Also acts as a key regulatory component of the p53/TP53 pathway, and particularly the checkpoint-response pathways critical for oncogenic transformation of cells, by phosphorylating and stabilizing p53/TP53. Phosphorylates its own inhibitors, the protein phosphatase type 1 (PP1) isoforms, to inhibit their activity. Necessary for proper cilia disassembly prior to mitosis. Regulates protein levels of the anti-apoptosis protein BIRC5 by suppressing the expression of the SCF(FBXL7) E3 ubiquitin-protein ligase substrate adapter FBXL7 through the phosphorylation of the transcription factor FOXP1. [The UniProt Consortium]