- CITATIONS: 1
|Application ||WB, IHC|
|Calculated MW||39311 Da|
|Other Names||Aurora kinase B, Aurora 1, Aurora- and IPL1-like midbody-associated protein 1, AIM-1, Aurora/IPL1-related kinase 2, ARK-2, Aurora-related kinase 2, STK-1, Serine/threonine-protein kinase 12, Serine/threonine-protein kinase 5, Serine/threonine-protein kinase aurora-B, AURKB, AIK2, AIM1, AIRK2, ARK2, STK1, STK12, STK5|
|Target/Specificity||A synthetic peptide corresponding to residues near the N-terminus of human Aurora-B was used as an immunogen.|
|Format||50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 40% Glycerol, 0.01% sodium azide and 0.05% BSA.|
|Storage||Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||Aurora-B Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||AIK2, AIM1, AIRK2, ARK2, STK1, STK12, ST|
|Function||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 (PubMed:22422861, PubMed:24814515). 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, SEPT1, VIM/vimentin, GSG2/Haspin, and histone H3. A positive feedback loop involving GSG2 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 GSG2 and AURKB contributes to CPC localization. AURKB is also required for kinetochore localization of BUB1 and SGOL1. 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.|
|Cellular Location||Nucleus. Chromosome. Chromosome, centromere. Cytoplasm, cytoskeleton, spindle. Midbody. Note=Localizes on chromosome arms and inner centromeres from prophase through metaphase and then transferring to the spindle midzone and midbody from anaphase through cytokinesis. Colocalized with gamma tubulin in the mid-body. Proper localization of the active, Thr-232- phosphorylated form during metaphase may be dependent upon interaction with SPDYC. Colocalized with SIRT2 during cytokinesis with the midbody|
|Tissue Location||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|
Provided below are standard protocols that you may find useful for product applications.
Aurora-B is a member of a novel family of serine/threonine kinases that have been identified as key regulators of the mitotic cell division process. Aurora-B is known to be involved in the regulation of centrosome function, bipolar spindle assembly and chromosome segregation. Aurora kinases are localized at the centrosomes of interphase cells, at the poles of the bipolar spindle and in the midbody of the mitotic apparatus. Substrates identified for the Aurora-B kinases include a kinesin-like motor protein, spindle apparatus proteins, histone H3 protein, kinetochore protein and the tumor suppressor protein p53 (1). Overexpression of aurora B produced multinuclearity and induced aggressive metastasis, suggesting that overexpressed aurora B has multiple functions in cancer development. Identification of Aurora kinases as RasGAP Src homology 3 domain binding protein, also implicates these kinases as potential effectors in the Ras pathway relevant to oncogenesis (2).
1. Katayama H, et al. Cancer Metastasis Rev. 22(4): 451-64, 2003
2. Abdulla A, et al. Cancer Cell International 5(31), 2005
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