Anti-Phospho-Aurora B pT232 Aurkb Antibody

Store Phospho Specific Antibody at -20°C prior to opening. Aliquot contents and freeze at -20°C or below for extended storage. Avoid cycles of freezing and thawing. Centrifuge product if not completely clear after standing at room temperature. This product is stable for several weeks at 4°C as an undiluted liquid. Dilute only prior to immediate use. Expiration date is one (1) year from date of opening.

Liquid (sterile filtered)

Phospho pT232 Aurora B antibody has been tested for use in ELISA, immunohistochemistry, and by western blot. See below for specific protocol. Expect a band approximately 39 kDa in size corresponding to Aurora Kinase B by western blotting in the appropriate cell lysate or extract. HeLa cell lysate can be used as a positive control.

AURKB

Aurora Kinase B (Aurora-B) is a Ser/Thr protein kinase member of the Aurora subfamily that may be directly involved in regulating the cleavage of polar spindle microtubules and is a key regulator for the onset of cytokinesis during mitosis. Aurora Kinase B is localized to the midzone of central spindle in late anaphase and concentrated into the midbody in telophase and cytokinesis and is colocalized with gamma tubulin in the mid-body. High levels of Aurora B expression are seen in the thymus, although it is also expressed in the spleen, lung, testis, colon, placenta and fetal liver. Aurora B is expressed during S and G2/M phase and expression is up-regulated in cancer cells during M phase. Anti-AUROA B pT232 Antibody is useful for researchers interested in gene expression, DNA damage, cytokinesis, and transcription activities.

0.02 M Potassium Phosphate, 0.15 M Sodium Chloride, pH 7.2, 0.01% (w/v) Sodium Azide

0.87 mg/mL by UV absorbance at 280 nm

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, 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). 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.

Boster Bio Anti-Phospho-Aurora B pT232 Aurkb Antibody (Catalog # P00762). Tested in ELISA, IHC, WB applications. This antibody reacts with Human, Monkey.

Expressed in testis, intestine and spleen. All of them are tissues that contain a large number of proliferating cells. Expressed during S phase, in a cell-cycle-dependent fashion.