a member of the AUR family of kinases. A cell cycle-regulated serine/threonine protein kinase that is overexpressed in many tumor cell lines. Regulated by phosphorylation-dependent proteasomal degradation. Localized to mitotic centrosomes and spindle microtubules and is required for centrosome maturation. Loss of Aurora A leads to defective mitotic spindles and gross errors in chromosome segregation. Required for centrosome duplication and chromosome segregation. Overexpression in culture drives transformation and aneuploidy, and negatively regulates p53. Amplified or overexpressed in many tumors or cell lines. Found as a skin tumor susceptibility gene in mouse, and a human SNP in a degradation domain is weakly cancer-associated and undergoes allele-specific amplification. Inhibitors: VX-680, ZM447439, Hesperadin, SNS-595. Note: This description may include information from UniProtKB.
Protein type: Kinase, protein; EC 184.108.40.206; Protein kinase, Other; Protein kinase, Ser/Thr (non-receptor); Other group; AUR family
Cellular Component: centrosome; spindle microtubule; perinuclear region of cytoplasm; spindle; spindle pole centrosome; midbody; cytosol; nucleus
Molecular Function: protein serine/threonine kinase activity; protein binding; ubiquitin protein ligase binding; protein serine/threonine/tyrosine kinase activity; protein kinase binding; ATP binding; protein kinase activity
Biological Process: mitosis; regulation of centrosome cycle; phosphoinositide-mediated signaling; positive regulation of mitosis; protein amino acid autophosphorylation; regulation of protein stability; cell cycle; protein amino acid phosphorylation; spindle organization and biogenesis; response to estradiol stimulus; cell projection organization and biogenesis; cell division; anaphase-promoting complex-dependent proteasomal ubiquitin-dependent protein catabolic process; mitotic cell cycle
SS: The number of records in which this modification site was determined using site-specific methods. SS methods include amino acid sequencing, site-directed mutagenesis, modification site-specific antibodies, specific MS strategies, etc.