AURKB

AURKB

A gene on chromosome 17p13.1 that encodes Aurora kinase B, which is involved in regulating many mitotic events. Aurora B is the catalytic component of the chromosomal passenger complex (CPC), which is critical for the correct progression through and completion of mitosis. It phosphorylates the CPC subunits BIRC5/survivin, CDCA8/borealin and INCENP, the last of which increases AURKB activity.
References in periodicals archive ?
Los resultados muestran que el tratamiento con DAAs revierte la fosforilacion de serina 10 en la histona H3 inducida por HCV a traves la actividad quinasa de Aurora quinasa B (AURKB).
The AURKs are serine/threonine kinases that are involved mainly in checkpoint regulation in the cell cycle.[sup][34] Three mammalian AURKs have been identified: AURKA, AURKB, and AURKC.
Alisertib (MLN8237), a selective AURKA inhibitor, induced a treatment response in six out of 35 patients (17%) with relapsed/refractory AML, while 49% achieved stable disease.[sup][36] Both AZD1152 (barasertib) and ZM447439, selective AURKB inhibitors, showed apoptosis-inducing effects in preclinical research.[sup][37] In a 2013 Phase I study, barasertib, used in combination with low-dose chemotherapy, demonstrated a therapeutic benefit in patients aged ≥60 years.[sup][38] The positive effects of barasertib were also demonstrated in advanced AML[sup][39] and newly diagnosed, relapsed, or refractory AML.[sup][40]
For instance, genes located at 17p13.1 include those codifying for the aurora kinase B (AURKB), a centrosome-associated kinase that plays an important role as regulator of chromosome segregation and cytokinesis, and, for the tumor protein p53, a protein that causes cells with damaged DNA to arrest at the G1 phase of cell cycle (TP53).
In the recent reclassification of breast cancers on the basis of copy number expression analysis, the 5q loss is associated with a strong basal-specific signature, including aurora kinase B (AURKB), B-cell CLL/lymphoma 2 (BCL2), BUB1 mitotic checkpoint serine/threonine kinase (BUB1), cell division cycle associated 3 (CDCA3), cell division cycle associated 4 (CDCA4), cell division cycle 20 (CDC20), cell division cycle 45 (CDC45), checkpoint kinase 1 (CHEK1), forkhead box M1 (FOXM1), histone deacetylase 2 (HDAC2), insulin-like growth factor 1 receptor (IGF1R), kinesin family member 2C (KIF2C), kinesin family member C1 (KIFC1), methylenetetrahydrofolate dehydrogenase (NADP+ dependent) 1-like (MTHFD1L), TTK protein kinase (TTK), and ubiquitin-conjugating enzyme E2C (UBE2C).
Similarly, it has been suggested that activation of the MAPK in pancreatic cancer cells leads to the transcriptional activation of the AURKA and AURKB promoters via ETS2 transcription factors [16].
A second response phase is characterized by a wave of mitosis and DNA synthesis, which occurs 16-24 hr after [E.sub.2] treatment and is correlated with the late-phase cell cycle regulators, including Aurkb (aurora kinase B) and Ccnb2 (cyclin B2) (Hewitt et al.
Aurora kinases A and B (AURKA and AURKB) are serine/threonine kinases that play an important role in chromosome alignment, segregation, and cytokinesis during mitosis.
The probe set IDs of TaqMan probe and primer sets for ACLY, AURKB, CD74, CDKN2D, E2F1, EFEMP1, LIF, and TGM2 are provided in Table 1.
Ube2c, Ccnb2, Cdc2a, and Aurkb are all associated with the G2/M phases of the cell cycle, and are also all increased in the WT uterus by [E.sub.2] after 24 hr.
Several genes in the set of 11 confirmed genes are known to be up-regulated or involved in other cancers: CCNB1 (cyclin B1) (16,17), AURKB (aurora B kinase) (18), SPINT2 (serine protease inhibitor 2) (19), OAZ1 (ornithine decarboxylase antizyme 1) (20), and HPV16 E7 (the E7 protein of human papillomavirus 16) (21).
Consistently, the network of downregulated genes contained a cluster of regulators of sister chromatid cohesion containing PDS5A, CENPE, BUB3, and AURKB (Figure 3(b)).