AurB
Serine/threonine-protein kinase component of the chromosomal passenger complex (CPC), a complex that acts as a key regulator of mitosis. The CPC complex has essential functions at the centromere in ensuring correct chromosome alignment and segregation and is required for chromatin-induced microtubule stabilization and spindle assembly. Involved in the bipolar attachment of spindle microtubules to kinetochores and is a key regulator for the onset of cytokinesis during mitosis. Required for central/midzone spindle assembly and cleavage furrow formation. Key component of the cytokinesis checkpoint, a process required to delay abscission to prevent both premature resolution of intercellular chromosome bridges and accumulation of DNA damage: phosphorylates CHMP4C, leading to retain abscission-competent VPS4 (VPS4A and/or VPS4B) at the midbody ring until abscission checkpoint signaling is terminated at late cytokinesis. AURKB phosphorylates the CPC complex subunits BIRC5/survivin, CDCA8/borealin and INCENP. Phosphorylation of INCENP leads to increased AURKB activity. Other known AURKB substrates involved in centromeric functions and mitosis are CENPA, DES/desmin, GPAF, KIF2C, NSUN2, RACGAP1, SEPTIN1, VIM/vimentin, HASPIN, and histone H3. A positive feedback loop involving HASPIN and AURKB contributes to localization of CPC to centromeres. Phosphorylation of VIM controls vimentin filament segregation in cytokinetic process, whereas histone H3 is phosphorylated at 'Ser-10' and 'Ser-28' during mitosis (H3S10ph and H3S28ph, respectively). A positive feedback between HASPIN and AURKB contributes to CPC localization. AURKB is also required for kinetochore localization of BUB1 and SGO1. Phosphorylation of p53/TP53 negatively regulates its transcriptional activity. Key regulator of active promoters in resting B- and T-lymphocytes: acts by mediating phosphorylation of H3S28ph at active promoters in resting B-cells, inhibiting RNF2/RING1B-mediated ubiquitination of histone H2A and enhancing binding and activity of the USP16 deubiquitinase at transcribed genes. Belongs to the protein kinase superfamily. Ser/Thr protein kinase family. Aurora subfamily. High level expression seen in the thymus. It is also expressed in the spleen, lung, testis, colon, placenta and fetal liver. Expressed during S and G2/M phase and expression is up-regulated in cancer cells during M phase. 5 alternatively spliced human isoforms have been reported. Note: This description may include information from UniProtKB.
Protein type: AUR family; EC 2.7.11.1; Kinase, protein; Other group; Protein kinase, Other; Protein kinase, Ser/Thr (non-receptor)
Molecular Function: ATP binding; histone H3S28 kinase activity; kinase activity; kinase binding; nucleotide binding; protein binding; protein kinase activity; protein serine/threonine kinase activity; transferase activity
Biological Process: cell cycle; cell cycle G2/M phase transition; cell division; cellular response to UV; cleavage furrow formation; mitotic cell cycle; mitotic cytokinesis; mitotic spindle midzone assembly; mitotic spindle organization; negative regulation of B cell apoptotic process; negative regulation of innate immune response; negative regulation of protein binding; negative regulation of transcription by RNA polymerase II; phosphorylation; positive regulation of attachment of mitotic spindle microtubules to kinetochore; positive regulation of cytokinesis; positive regulation of lateral attachment of mitotic spindle microtubules to kinetochore; positive regulation of mitotic cell cycle spindle assembly checkpoint; positive regulation of mitotic cytokinesis; positive regulation of mitotic sister chromatid segregation; positive regulation of mitotic sister chromatid separation; positive regulation of protein phosphorylation; positive regulation of telomerase activity; positive regulation of telomere capping; positive regulation of telomere maintenance via telomerase; post-translational protein modification; protein localization to kinetochore; protein phosphorylation; regulation of cytokinesis; spindle organization
