Disease relevance of Aurkb

• In addition, nuclear expression of Aurora-B in prostatic intraepithelial neoplasia lesions correlated with clinical staging of the tumor (rho = -0.4, P = 0.0474) whereas cytoplasmic expression in tumors correlated with seminal vesicle invasion (rho = 0.282, P = 0.0098) [1].
• Here, we report that Aurora-A and Aurora-B are highly expressed in primary human and mouse prostate cancers and prostate cancer cell lines [1].

High impact information on Aurkb

• We show that mammalian cells lacking survivin are unable to align their chromosomes, fail to recruit Aurora B to kinetochores and become polyploid at a very high frequency [2].
• We show here that sustained G(2)/M arrest induced by the genotoxic agent doxorubicin is E2F-dependent and involves a decrease in expression of two mitotic regulators, Stathmin and AIM-1 [3].
• Reduced hepatoblast mitosis was associated with decreased protein levels of the Polo-like kinase 1 and Aurora B kinase, which phosphorylate regulatory proteins essential for orchestrating mitosis and cytokinesis [4].
• STK-1 mRNA is detected in testis, intestine and spleen, tissues that contain a large number of proliferating cells, but not in other tissues [5].
• These findings suggest a role for STK-1 in cell growth [5].

Biological context of Aurkb

• Nevertheless, STK-1 is conserved throughout phylogeny with hybridizing sequences being detected in DNA from mammals, amphibians, insects and yeast [5].
• We have cloned a novel putative serine/threonine kinase-encoding gene, designed STK-1, from murine embryonic stem (ES) cell and testis cDNA libraries [5].
• We found that the mitotic cell death symptoms correlated with attenuated expression of survivin, a member of the chromosomal passenger complex, and mislocalization of Aurora B, the partner of survivin in the chromosomal passenger complex [6].

Anatomical context of Aurkb

• Cell lines and primary tumors derived from the TRAMP model were also found to express high levels of Aurora-A and Aurora-B [1].
• In NIH 3T3 cells, STK-1 is expressed in a cell-cycle-dependent fashion [5].

References